PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9068053-1 1997 The effects of exogenous naloxone and adrenocorticotropin (ACTH) on circulating concentrations of corticosterone and glucose in broilers were determined. Glucose 117-124 proopiomelanocortin Homo sapiens 59-63 9068053-8 1997 Glucose levels were significantly elevated at 60 min in birds receiving ACTH i.v., but remained elevated through 90 min in birds pretreated with naloxone. Glucose 0-7 proopiomelanocortin Homo sapiens 72-76 8931651-9 1996 The increase in beta-endorphin levels was also attenuated in well-controlled IDDM patients (4 +/- 1 pmol/L at plasma glucose 5.0 mmol/L to 11 +/- 4 pmol/L at plasma glucose 2.2 mmol/L) versus poorly controlled IDDM patients (5 +/- 1 pmol/L to 26 +/- 7 pmol/L) and healthy subjects (8 +/- 1 pmol/L to 56 +/- 13 pmol/L). Glucose 117-124 proopiomelanocortin Homo sapiens 16-30 8931651-9 1996 The increase in beta-endorphin levels was also attenuated in well-controlled IDDM patients (4 +/- 1 pmol/L at plasma glucose 5.0 mmol/L to 11 +/- 4 pmol/L at plasma glucose 2.2 mmol/L) versus poorly controlled IDDM patients (5 +/- 1 pmol/L to 26 +/- 7 pmol/L) and healthy subjects (8 +/- 1 pmol/L to 56 +/- 13 pmol/L). Glucose 165-172 proopiomelanocortin Homo sapiens 16-30 8931651-10 1996 The plasma glucose threshold required for stimulation of beta-endorphin release was again lower in well-controlled IDDM versus poorly controlled IDDM patients (2.2 +/- 0.1 v 3.0 +/- 0.3 mmol/L) and healthy subjects (2.5 +/- 0.4 mmol/L, P < .05 between IDDM groups). Glucose 11-18 proopiomelanocortin Homo sapiens 57-71 8931651-11 1996 In conclusion, prolactin and beta-endorphin responses to a standardized hypoglycemic stimulus (plasma glucose, 2.2 mmol/L) are reduced and plasma glucose levels required to stimulate release of prolactin and beta-endorphin are lower in well-controlled IDDM compared with poorly controlled IDDM and healthy subjects. Glucose 102-109 proopiomelanocortin Homo sapiens 29-43 8931651-11 1996 In conclusion, prolactin and beta-endorphin responses to a standardized hypoglycemic stimulus (plasma glucose, 2.2 mmol/L) are reduced and plasma glucose levels required to stimulate release of prolactin and beta-endorphin are lower in well-controlled IDDM compared with poorly controlled IDDM and healthy subjects. Glucose 146-153 proopiomelanocortin Homo sapiens 208-222 8856392-1 1996 OBJECTIVE: To establish the possible role of hyperinsulinemia in the elevation of plasma beta-endorphin (beta-EP) levels observed in obese patients after an oral glucose load. Glucose 162-169 proopiomelanocortin Homo sapiens 89-103 8856392-1 1996 OBJECTIVE: To establish the possible role of hyperinsulinemia in the elevation of plasma beta-endorphin (beta-EP) levels observed in obese patients after an oral glucose load. Glucose 162-169 proopiomelanocortin Homo sapiens 105-112 8856392-5 1996 RESULTS: In the six obese patients undergoing the OGTT a significant elevation of beta-EP plasma levels was observed between 60 and 90 min after glucose ingestion. Glucose 145-152 proopiomelanocortin Homo sapiens 82-89 8636289-5 1996 At the nadir glucose level (2.2 mmol/L), ACTH, cortisol, and epinephrine levels were significantly lower in well controlled IDDM compared to healthy controls, and the glucose levels required for significant secretion of ACTH, cortisol, and epinephrine also were lower in well controlled IDDM compared to those in both poorly controlled IDDM and healthy volunteers (P < 0.05). Glucose 13-20 proopiomelanocortin Homo sapiens 41-45 8636289-5 1996 At the nadir glucose level (2.2 mmol/L), ACTH, cortisol, and epinephrine levels were significantly lower in well controlled IDDM compared to healthy controls, and the glucose levels required for significant secretion of ACTH, cortisol, and epinephrine also were lower in well controlled IDDM compared to those in both poorly controlled IDDM and healthy volunteers (P < 0.05). Glucose 167-174 proopiomelanocortin Homo sapiens 220-224 8706296-11 1996 Plasma glucose (P < 0.001) and CRH (P < 0.05) and PRL (P < 0.05) increased significantly during beta-endorphin compared to normal saline. Glucose 7-14 proopiomelanocortin Homo sapiens 105-119 8636293-5 1996 The low rate of beta-endorphin infusion induced physiological elevations of plasma opioid levels in both groups; no significant change in plasma glucose and pancreatic products in control subjects; and a significant (at least P < 0.05) rise in plasma insulin, C peptide, and glucagon concentrations in relatives of the obese. Glucose 145-152 proopiomelanocortin Homo sapiens 16-30 8636293-6 1996 The high rate of beta-endorphin infusion produced pharmacological elevations of opioid plasma levels in both groups; significant (at least P < 0.05) increments in plasma glucose and glucagon levels and no appreciable modification of plasma insulin and C peptide levels in the control group; and a significant (at least P < 0.05) positive response of plasma glucose, insulin, C peptide, and glucagon levels in relatives of obese subjects. Glucose 173-180 proopiomelanocortin Homo sapiens 17-31 8636293-6 1996 The high rate of beta-endorphin infusion produced pharmacological elevations of opioid plasma levels in both groups; significant (at least P < 0.05) increments in plasma glucose and glucagon levels and no appreciable modification of plasma insulin and C peptide levels in the control group; and a significant (at least P < 0.05) positive response of plasma glucose, insulin, C peptide, and glucagon levels in relatives of obese subjects. Glucose 363-370 proopiomelanocortin Homo sapiens 17-31 8706296-12 1996 After insulin administration, glucose reached a similar nadir during beta-endorphin and normal saline (2.1 +/- 0.1 and 1.9 +/- 0.15 mmol/l, respectively) but the fall in plasma glucose was delayed during beta-endorphin (P < 0.01 by ANOVA). Glucose 30-37 proopiomelanocortin Homo sapiens 69-83 8706296-17 1996 Intravenous beta-endorphin increases plasma glucose and delays the onset of hypoglycaemia following insulin but does not result in significant inhibition of the ACTH and cortisol response. Glucose 44-51 proopiomelanocortin Homo sapiens 12-26 7556777-8 1995 infusion of glucose quickly produced moderate hyperglycemia and an increase in plasma insulin, and inhibited secretions of CRH, ACTH and cortisol. Glucose 12-19 proopiomelanocortin Homo sapiens 128-132 8871183-3 1996 After a glucose load, PCOS women had greater beta-EP and Dyn A responses in group 1 and impaired SS response in group 2 as compared with the control. Glucose 8-15 proopiomelanocortin Homo sapiens 45-52 7579009-4 1995 After glucose load, plasma beta-endorphin in CRF patients tended to decline, whereas in normal subjects increased. Glucose 6-13 proopiomelanocortin Homo sapiens 27-41 7579009-5 1995 The fasting and the mean OGTT plasma beta-endorphin values negatively correlated with insulin initial response to glucose, insulin and C-peptide mean OGTT values, but not with glucose OGTT mean values. Glucose 114-121 proopiomelanocortin Homo sapiens 37-51 8106616-0 1994 Insulin, C-peptide, androgens, and beta-endorphin response to oral glucose in patients with polycystic ovary syndrome. Glucose 67-74 proopiomelanocortin Homo sapiens 35-49 7927190-9 1994 We conclude that the lack of cortisol (secondary to ACTH deficiency) and GH in hypopituitary patients may be primarily responsible for the slow recovery of plasma glucose after acute hypoglycemia; and plasma glucagon, E, and NE responses are not impaired. Glucose 163-170 proopiomelanocortin Homo sapiens 52-56 8106616-1 1994 We examined the effects of an oral glucose load on plasma insulin, androgens, and beta-endorphin (beta EP) concentrations in patients carefully selected as having polycystic ovary syndrome (PCOS) and normal glucose tolerance. Glucose 35-42 proopiomelanocortin Homo sapiens 82-96 1471704-9 1992 After oral glucose was given, elevated fasting insulin levels increased significantly in patients with polycystic ovary syndrome (p < 0.01), as did immunoreactive beta-endorphin levels (p < 0.05). Glucose 11-18 proopiomelanocortin Homo sapiens 166-180 8304539-4 1994 ACTH responses to hypoglycemia were significantly increased in the pregnant ewes, and the relation between plasma glucose and plasma ACTH was shifted to the right, indicating greater ACTH responses for a given level of hypoglycemia in the pregnant state. Glucose 114-121 proopiomelanocortin Homo sapiens 133-137 8304539-4 1994 ACTH responses to hypoglycemia were significantly increased in the pregnant ewes, and the relation between plasma glucose and plasma ACTH was shifted to the right, indicating greater ACTH responses for a given level of hypoglycemia in the pregnant state. Glucose 114-121 proopiomelanocortin Homo sapiens 133-137 8228790-9 1993 In multiple regression analyses, BMI and the 2-h ACTH response to glucose were significant predictors of WHR and, in addition, the cortisol ratio, WHR, and BMI of insulin. Glucose 66-73 proopiomelanocortin Homo sapiens 49-53 1320581-8 1992 Plasma glucose levels increased approximately 36% by 3 hr after ACTH infusion, remained elevated following the second ACTH treatment, and then declined to approximately the initial levels by 96 hr. Glucose 7-14 proopiomelanocortin Homo sapiens 118-122 1320581-8 1992 Plasma glucose levels increased approximately 36% by 3 hr after ACTH infusion, remained elevated following the second ACTH treatment, and then declined to approximately the initial levels by 96 hr. Glucose 7-14 proopiomelanocortin Homo sapiens 64-68 1352555-0 1992 Neuroanatomical sites mediating the central actions of beta-endorphin as mapped by changes in glucose utilization: involvement of mu opioid receptors. Glucose 94-101 proopiomelanocortin Homo sapiens 55-69 1352555-4 1992 beta-END was found to produce profound increases in glucose utilization in limbic regions such as the lateral septal nucleus, the amygdalo-hippocampal transition area, the nucleus accumbens and the hippocampal formation. Glucose 52-59 proopiomelanocortin Homo sapiens 0-8 1352555-8 1992 The effects of beta-END on local cerebral glucose utilization were blocked by pretreatment with the mu antagonist, CTOP, whereas the selective delta opioid antagonist ICI 174,864 was less effective. Glucose 42-49 proopiomelanocortin Homo sapiens 15-23 1736041-0 1992 Physiological elevations of plasma beta-endorphin alter glucose metabolism in obese, but not normal-weight, subjects. Glucose 56-63 proopiomelanocortin Homo sapiens 35-49 1363137-1 1992 Abnormal growth hormone (GH) and adrenocorticotropic hormone (ACTH)/cortisol secretory patterns in response to a glucose load have been observed in underweight anorectic women. Glucose 113-120 proopiomelanocortin Homo sapiens 33-60 1324968-1 1992 We report on a patient with isolated ACTH deficiency accompanying deficient insulin response to glucose. Glucose 96-103 proopiomelanocortin Homo sapiens 37-41 1885266-0 1991 Beta-endorphin plasma levels and their dependence on gender during an enteral glucose load in lean subjects as well as in obese patients before and after weight reduction. Glucose 78-85 proopiomelanocortin Homo sapiens 0-14 1662196-10 1991 4: 299-307, 1984), when the blood glucose concentrations decreased to less than 3.3 mM, plasma concentrations of CRF, ACTH, and cortisol showed a significant increase. Glucose 34-41 proopiomelanocortin Homo sapiens 118-122 1662196-12 1991 These results demonstrate that decreases in blood glucose concentration trigger the pituitary-adrenocortical axis to enhance secretion of ACTH and cortisol during low-intensity prolonged exercise in humans. Glucose 50-57 proopiomelanocortin Homo sapiens 138-142 1885266-4 1991 We compared beta-endorphin plasma levels during an oral glucose load in 60 obese, non-diabetic patients and in 20 normal weight controls. Glucose 56-63 proopiomelanocortin Homo sapiens 12-26 1885266-10 1991 (2) During the oral glucose tolerance test the beta-endorphin plasma values remained constant in the obese group. Glucose 20-27 proopiomelanocortin Homo sapiens 47-61 2028070-0 1991 [Plasma levels of beta-endorphin in obese subjects with normal glucose tolerance test and in diabetics]. Glucose 63-70 proopiomelanocortin Homo sapiens 18-32 1653194-11 1991 Injecting YOUNG steers with ACTH before fasting alone or fasting plus transit increased plasma fibrinogen (P less than .10) and serum glucose (P less than .05) concentrations more than ACTH injections in OLD steers. Glucose 134-141 proopiomelanocortin Homo sapiens 28-32 2003375-3 1991 In both obese and post-obese subjects, the infusion of beta-endorphin caused significant increases in peripheral plasma glucose, insulin, C-peptide and glucagon concentrations. Glucose 120-127 proopiomelanocortin Homo sapiens 55-69 34737351-1 2021 Previous studies indicate that the activity of hypothalamic POMC neurons can be regulated by glucose via intracellular mechanisms, but its regulation by lactate is poorly understood. Glucose 93-100 proopiomelanocortin Homo sapiens 60-64 2226124-1 1990 In this study aiming to clarify the relationships between beta-endorphin and glucose levels, beta-endorphin levels were determined in children in acute stress. Glucose 77-84 proopiomelanocortin Homo sapiens 58-72 2098658-4 1990 We have investigated the responses of plasma glucose, insulin, C-peptide and glucagon to an infusion of human beta-endorphin in formerly obese subjects who had obtained by dieting the normalization of body weight and in lean controls. Glucose 45-52 proopiomelanocortin Homo sapiens 110-124 2551176-3 1989 Glucose-induced glucagon suppression was significantly lower during beta-endorphin, a fact that could have contributed to the reduced glucose utilization rates. Glucose 134-141 proopiomelanocortin Homo sapiens 68-82 2551176-4 1989 The infusion of theophylline (150 mg + 350 mg/h) to increase the intracellular cAMP activity by inhibiting phosphodiesterase completely reversed the inhibitory effect of beta-endorphin on glucose-induced insulin secretion. Glucose 188-195 proopiomelanocortin Homo sapiens 170-184 2551176-8 1989 These data confirm that beta-endorphin stimulates glucagon and inhibits basal and glucose-stimulated insulin secretion and suggest that the opioid influences the intraislet adenylate cyclase activity. Glucose 82-89 proopiomelanocortin Homo sapiens 24-38 2528500-2 1989 We tested the yet unknown influence of physiological fluctuations in beta-endorphin serum levels on glucose homeostasis by stimulating the pituitary secretion with CRF. Glucose 100-107 proopiomelanocortin Homo sapiens 69-83 2528500-5 1989 We conclude that only a pharmacological dose of beta-endorphin influences glucose homeostasis. Glucose 74-81 proopiomelanocortin Homo sapiens 48-62 2970411-6 1988 beta-Endorphin also inhibited glucose suppression of glucagon levels and augmented the glucagon response to arginine. Glucose 30-37 proopiomelanocortin Homo sapiens 0-14 2551176-1 1989 The present studies were undertaken to characterize further the influence of synthetic human beta-endorphin (0.5 mg/h) on insulin and glucagon responses to intravenous glucose in humans. Glucose 168-175 proopiomelanocortin Homo sapiens 93-107 2551176-2 1989 Infusion of beta-endorphin in 10 normal volunteers caused a clear-cut inhibition of the overall insulin responses to a glucose pulse (0.33 g/kg iv) with values of glucose disappearance rates in the diabetic range [0.89 +/- 0.09 (P less than 0.01) vs. saline 1.82 +/- 0.15%/min]. Glucose 119-126 proopiomelanocortin Homo sapiens 12-26 2551176-2 1989 Infusion of beta-endorphin in 10 normal volunteers caused a clear-cut inhibition of the overall insulin responses to a glucose pulse (0.33 g/kg iv) with values of glucose disappearance rates in the diabetic range [0.89 +/- 0.09 (P less than 0.01) vs. saline 1.82 +/- 0.15%/min]. Glucose 163-170 proopiomelanocortin Homo sapiens 12-26 2551176-3 1989 Glucose-induced glucagon suppression was significantly lower during beta-endorphin, a fact that could have contributed to the reduced glucose utilization rates. Glucose 0-7 proopiomelanocortin Homo sapiens 68-82 2970411-0 1988 Beta-endorphin-induced inhibition and stimulation of insulin secretion in normal humans is glucose dependent. Glucose 91-98 proopiomelanocortin Homo sapiens 0-14 2970411-2 1988 Infusion of 0.5 mg/h beta-endorphin caused a significant rise in plasma glucose concentrations preceded by a significant increase in peripheral glucagon levels. Glucose 72-79 proopiomelanocortin Homo sapiens 21-35 2970411-4 1988 Acute insulin and C-peptide responses to intravenous pulses of different glucose amounts (0.33 g/kg and 5 g) and arginine (3 g) were significantly reduced by beta-endorphin infusion (P less than .01). Glucose 73-80 proopiomelanocortin Homo sapiens 158-172 2969000-5 1988 Infusion of beta-endorphin in the same subjects caused plasma glucose and glucagon to rise, but insulin and C-peptide levels did not change. Glucose 62-69 proopiomelanocortin Homo sapiens 12-26 2847736-2 1988 ACTH caused a sustained increase in the liberation of lactate as well as a stimulation of both basal and glucose-induced fructose 2,6-bisphosphate content. Glucose 105-112 proopiomelanocortin Homo sapiens 0-4 2826568-1 1987 Intracisternal administration of synthetic human beta-endorphin to conscious, ambulatory adult male rats caused dose-related increases in plasma glucose concentration. Glucose 145-152 proopiomelanocortin Homo sapiens 49-63 2826568-2 1987 The largest dose of beta-endorphin examined, 7.25 nmol, increased plasma glucose concentration within 7 min and this effect lasted 2.5 h. On the other hand, only 58 pmol was required to induce transient hyperglycemia, when compared to the response observed in saline-injected control rats. Glucose 73-80 proopiomelanocortin Homo sapiens 20-34 2826568-5 1987 A significant positive correlation was demonstrated between plasma glucose and plasma epinephrine responses to increasing doses of intracisternally administered beta-endorphin. Glucose 67-74 proopiomelanocortin Homo sapiens 161-175 2826568-9 1987 This further supports the thesis that intracerebral beta-endorphin increases plasma glucose concentration by activation of the central autonomic outflow. Glucose 84-91 proopiomelanocortin Homo sapiens 52-66 2826568-11 1987 Both of these glucose counterregulatory hormones may play minor roles in modulating beta-endorphin-induced hyperglycemia. Glucose 14-21 proopiomelanocortin Homo sapiens 84-98 2958673-5 1987 An infusion of human beta-endorphin (0.05 mg/h) produced only minor changes in plasma glucose, insulin, glucagon, and C-peptide concentrations in lean subjects, but caused marked increments in obese. Glucose 86-93 proopiomelanocortin Homo sapiens 21-35 2828082-7 1987 Replacement therapy with dexamethasone or administration of ACTH led to elevation of the blood glucose to normal, and the plasma cortisol also reached normal levels. Glucose 95-102 proopiomelanocortin Homo sapiens 60-64 2805586-2 1989 Selective antagonists of beta-endorphin have been reported to correct the impaired insulin secretory response to glucose seen in non-insulin dependent diabetes. Glucose 113-120 proopiomelanocortin Homo sapiens 25-39 2969000-11 1988 In the same subjects, beta-endorphin produced elevations of plasma glucose, insulin, C-peptide, and glucagon. Glucose 67-74 proopiomelanocortin Homo sapiens 22-36 2896134-1 1987 The present study was aimed at characterizing the effects of beta-endorphin on plasma glucose, insulin and glucagon plasma levels in subjects with type-2 diabetes mellitus. Glucose 86-93 proopiomelanocortin Homo sapiens 61-75 2896134-2 1987 Infusion of 0.5 mg/h human beta-endorphin produced significant and simultaneous increments in both insulin and glucagon concentrations and decreased plasma glucose levels (-18 +/- 4 mg/dl, 60 min level, p less than 0.01). Glucose 156-163 proopiomelanocortin Homo sapiens 27-41 2885994-2 1987 Infusion of 143 nmol/h beta-endorphin in 7 subjects caused a significant rise in plasma glucose concentrations (+ 1.7 +/- 0.3 mmol/l) which was preceded by a significant increase in peripheral plasma glucagon levels (+ 44 +/- 13 ng/l). Glucose 88-95 proopiomelanocortin Homo sapiens 23-37 2952663-0 1987 Hyperglycemia and obesity as determinants of glucose, insulin, and glucagon responses to beta-endorphin in human diabetes mellitus. Glucose 45-52 proopiomelanocortin Homo sapiens 89-103 2952663-1 1987 The effect of human beta-endorphin on plasma glucose, insulin, and glucagon concentrations was studied in patients with noninsulin-dependent diabetes mellitus and in normal subjects. Glucose 45-52 proopiomelanocortin Homo sapiens 20-34 2952663-3 1987 In lean subjects, infusion of 0.5 mg/h beta-endorphin caused significant increases in peripheral plasma glucose and glucagon levels, but no change in plasma insulin. Glucose 104-111 proopiomelanocortin Homo sapiens 39-53 2952663-5 1987 In lean diabetic patients, beta-endorphin produced significant simultaneous increments in both insulin and glucagon concentrations and significantly decreased plasma glucose levels. Glucose 166-173 proopiomelanocortin Homo sapiens 27-41 2952663-7 1987 There was a significant correlation (r = 0.61; P less than 0.01) between fasting plasma glucose levels and the integrated insulin area in response to beta-endorphin. Glucose 88-95 proopiomelanocortin Homo sapiens 150-164 2952663-8 1987 The infusion of a lower dose of beta-endorphin (0.05 mg/h) in diabetic patients produced similar increments in both insulin and glucagon levels and also decreased plasma glucose concentration. Glucose 170-177 proopiomelanocortin Homo sapiens 32-46 2952663-9 1987 These results indicate that beta-endorphin may have important glucoregulatory effects in man depending on the dose administered, the presence of obesity, and the prevailing plasma glucose concentration. Glucose 180-187 proopiomelanocortin Homo sapiens 28-42 3035302-1 1987 Synthetic human beta-endorphin potentiates insulin secretion by the isolated perfused rat pancreas when glucose is present in the perfusate at concentrations of either 125 or 200 mg/dl, whereas it fails to exert any effect on insulin secretion in the presence of a substimulatory concentration of 100 mg/dl. Glucose 104-111 proopiomelanocortin Homo sapiens 16-30 3034755-0 1987 Plasma beta-endorphin in response to oral glucose tolerance test in obese patients. Glucose 42-49 proopiomelanocortin Homo sapiens 7-21 2951394-0 1987 Beta-endorphin infusion restores acute insulin responses to glucose in type-2 diabetes mellitus. Glucose 60-67 proopiomelanocortin Homo sapiens 0-14 2951394-2 1987 The iv infusion of human beta-endorphin at a dose of 0.5 mg/h for 2 h in type-2 non-insulin-dependent diabetic patients (n = 12) raised plasma insulin and glucagon levels and slightly but significantly lowered plasma glucose concentrations. Glucose 217-224 proopiomelanocortin Homo sapiens 25-39 2951394-3 1987 beta-Endorphin infusion also resulted in reappearance of a clear-cut acute insulin response to glucose, while second phase insulin release was increased and glucose disposal accelerated. Glucose 95-102 proopiomelanocortin Homo sapiens 0-14 3028959-3 1986 In the present study, the direct action of ACTH on glucose uptake by pigeon hepatocytes has been studied by in vitro technique. Glucose 51-58 proopiomelanocortin Homo sapiens 43-47 2951394-3 1987 beta-Endorphin infusion also resulted in reappearance of a clear-cut acute insulin response to glucose, while second phase insulin release was increased and glucose disposal accelerated. Glucose 157-164 proopiomelanocortin Homo sapiens 0-14 2943957-7 1986 Resting beta-EP at basal glucose concentrations was 3.8 +/- 0.7 fmol X ml-1 (mean +/- se) and prior exercise either 2h (3.2 +/- 0.5 fmol X ml-1) or 48 h (4.3 +/- 0.7 fmol X ml-1) before a clamp study did not effect these levels, (p greater than 0.05). Glucose 25-32 proopiomelanocortin Homo sapiens 8-15 2945622-3 1986 The plasma beta-endorphin of the obese subjects was significantly higher than controls one hour and four and one half hours after glucose infusion. Glucose 130-137 proopiomelanocortin Homo sapiens 11-25 3023222-0 1986 Effects of pro-opiomelanocortin-derived peptides on plasma levels of glucagon, insulin and glucose. Glucose 91-98 proopiomelanocortin Homo sapiens 11-31 3023222-2 1986 POMC-derived peptides have been demonstrated in many tissues, including the hypothalamus and the endocrine pancreas, which play important roles in the control of plasma levels of glucagon, insulin and glucose. Glucose 201-208 proopiomelanocortin Homo sapiens 0-4 3023222-3 1986 This article reviews the present knowledge concerning in vitro and in vivo effects of POMC-derived peptides on glucagon, insulin and glucose levels involving several possible mechanisms: direct effects on the endocrine pancreas (including endocrine, paracrine and peptidergic regulation) and glucose production, and indirect effects involving the hypothalamus, the autonomic nervous system and the adrenal gland. Glucose 133-140 proopiomelanocortin Homo sapiens 86-90 3023222-3 1986 This article reviews the present knowledge concerning in vitro and in vivo effects of POMC-derived peptides on glucagon, insulin and glucose levels involving several possible mechanisms: direct effects on the endocrine pancreas (including endocrine, paracrine and peptidergic regulation) and glucose production, and indirect effects involving the hypothalamus, the autonomic nervous system and the adrenal gland. Glucose 292-299 proopiomelanocortin Homo sapiens 86-90 3028959-0 1986 Effect of ACTH on glucose uptake by hepatic cells and its effect on hepatic enzymes in presence of insulin and acetylcholine. Glucose 18-25 proopiomelanocortin Homo sapiens 10-14 2938204-1 1986 The plasma beta-endorphin response to glucose ingestion was compared in 8 bulimics and 8 controls. Glucose 38-45 proopiomelanocortin Homo sapiens 11-25 3008142-4 1986 Since ACTH has been shown to regulate glucose uptake and utilization, its implication in the adaptative response to stress situations, such as cerebral hypoxia, deserves further investigations. Glucose 38-45 proopiomelanocortin Homo sapiens 6-10 3009976-6 1986 Glucose concentration in the aqueous was increased by glucocorticoid administration as well as by stimulation of their secretion by ACTH. Glucose 0-7 proopiomelanocortin Homo sapiens 132-136 3028959-4 1986 The results have shown that ACTH has a direct influence on glucose uptake and this action is not additive in presence of insulin. Glucose 59-66 proopiomelanocortin Homo sapiens 28-32 3028959-5 1986 Glucose uptake in presence ACTH with Acetylcholine was not any more than what was obtained with ACTH alone. Glucose 0-7 proopiomelanocortin Homo sapiens 27-31 3028959-6 1986 These observations have been taken to indicate a non-existence of synergistic action of ACTH with insulin or acetylcholine in promoting glucose uptake by avian liver cells. Glucose 136-143 proopiomelanocortin Homo sapiens 88-92 3936737-3 1985 Met-enkephalin, catecholamines and prostaglandin E (PGE) have all been reported to inhibit the acute insulin response to glucose in normal humans. Glucose 121-128 proopiomelanocortin Homo sapiens 0-14 6099096-0 1984 Plasma immunoreactive beta-endorphin response to glucose ingestion in human obesity. Glucose 49-56 proopiomelanocortin Homo sapiens 22-36 2991079-0 1985 Elevation of plasma glucose, alanine, and urea levels by mammalian ACTH in the American bullfrog (Rana catesbeiana). Glucose 20-27 proopiomelanocortin Homo sapiens 67-71 2991079-1 1985 The effects of a single infusion of mammalian ACTH on plasma glucose, alanine, urea, and lactate were determined in the American bullfrog (Rana catesbeiana). Glucose 61-68 proopiomelanocortin Homo sapiens 46-50 6099096-1 1984 Following the oral administration of 100 g of glucose, morbidly-obese subjects and non-obese controls demonstrated increased levels of plasma immunoreactive beta-endorphin. Glucose 46-53 proopiomelanocortin Homo sapiens 157-171 6339212-1 1983 In pentobarbital-anesthetized rabbits, iv injection of 9 nmol (31 micrograms) human beta-endorphin (beta h-endorphin)/kg BW caused a significant (P less than 0.05) increase in serum glucose and a significant decline in serum insulin during the subsequent 60 min. Glucose 182-189 proopiomelanocortin Homo sapiens 84-98 6088160-8 1984 The results of the present study suggest that serum ACTH and cortisol concentration during low intensity prolonged exercise may be dependent on blood glucose concentration. Glucose 150-157 proopiomelanocortin Homo sapiens 52-56 6323537-0 1984 Beta-endorphin inhibits glucose production in the conscious dog. Glucose 24-31 proopiomelanocortin Homo sapiens 0-14 6323537-6 1984 We conclude that the naturally occurring opioid peptide, beta-endorphin, inhibits glucose production by the liver in vivo. Glucose 82-89 proopiomelanocortin Homo sapiens 57-71 6339212-11 1983 These findings, when compared with previously described structure-activity relationships for opioid receptors, indicate the presence of a novel receptor for beta-endorphin in rabbit pancreas, the activation of which inhibits glucose-stimulated secretion of insulin. Glucose 225-232 proopiomelanocortin Homo sapiens 157-171 6296674-4 1983 In both groups, beta-endorphin increased plasma glucagon concentrations, and this rise was accompanied by a significant increase in plasma glucose concentrations. Glucose 139-146 proopiomelanocortin Homo sapiens 16-30 6303639-2 1983 ACTH administration was associated with urinary sodium retention, hypokalaemia, elevation of fasting blood glucose, lymphopaenia and eosinopaenia. Glucose 107-114 proopiomelanocortin Homo sapiens 0-4 6281031-0 1982 Alterations in local cerebral glucose utilization during chronic treatment with an ACTH 4-9 analog. Glucose 30-37 proopiomelanocortin Homo sapiens 83-87 6274894-6 1982 Augmentation of the ACTH and cortisol responses to insulin hypoglycemia may be the result of an alteration by SS of recognition of glucose levels by glucose-sensitive cells of the brain, and effect which could be due to the inhibition of prostaglandin synthesis. Glucose 131-138 proopiomelanocortin Homo sapiens 20-24 6274894-6 1982 Augmentation of the ACTH and cortisol responses to insulin hypoglycemia may be the result of an alteration by SS of recognition of glucose levels by glucose-sensitive cells of the brain, and effect which could be due to the inhibition of prostaglandin synthesis. Glucose 149-156 proopiomelanocortin Homo sapiens 20-24 6296674-6 1983 The threshold dose of beta-endorphin for producing increased plasma concentrations of glucose and glucagon was 0.005 mg--a dose that acutely increased plasma concentrations of beta-endorphin by approximately 40-fold. Glucose 86-93 proopiomelanocortin Homo sapiens 22-36 6296674-7 1983 Glucose, glucagon, and insulin responses to beta-endorphin could not be blocked by intravenous naloxone. Glucose 0-7 proopiomelanocortin Homo sapiens 44-58 7013105-7 1981 Enhanced glucose demand by tumour cells may also lead to an increased hepatic gluconeogenesis, as will the production of ectopic ACTH. Glucose 9-16 proopiomelanocortin Homo sapiens 129-133 6256217-0 1980 [Insulin response to glucose and arginine in patients with isolated ACTH deficiency (author"s transl)]. Glucose 21-28 proopiomelanocortin Homo sapiens 68-72 7248753-1 1981 Synthetic human beta-endorphin increased plasma glucose concentration when administered intracisternally in chronically cannulated, conscious, unrestrained, adult male rats. Glucose 48-55 proopiomelanocortin Homo sapiens 16-30 7248753-3 1981 Adrenal denervation blocked the beta-endorphin-induced increase in plasma glucose, supporting a thesis that this effect is mediated at least in part by increased epinephrine secretion. Glucose 74-81 proopiomelanocortin Homo sapiens 32-46 226351-6 1979 The transport rate under T3 and ACTH replacement therapy continues to proceed at a maximal rate, so that basal glucose incorporation is high but not further enhanced by insulin. Glucose 111-118 proopiomelanocortin Homo sapiens 32-36 226351-9 1979 This suggests 1) that enzyme activities responsible for the lipogenetic capacity of the fat cell are decreased in hypox rats and returned toward normal by the combined T3/ACTH treatment, and 2) that the limitation of glucose transport in the fat cell is controlled by GH. Glucose 217-224 proopiomelanocortin Homo sapiens 171-175 182712-4 1976 The peak response of ACTH and cortisol was preceded by a significant rise of plasma insulin, by a fall of the blood glucose, which was initially increased by the administration of glucagon, and by the symptoms of nausea and sweating. Glucose 116-123 proopiomelanocortin Homo sapiens 21-25 233664-9 1978 In contrast to the usual presentation of the ectopic ACTH syndrome as primarily hypokalemic alkalosis and glucose intolerance, patients with relatively benign and indolent ACTH-secreting tumors, such as certain cases of medullary carcinoma of the thyroid, may present with more typical signs and symptoms of Cushing"s syndrome. Glucose 106-113 proopiomelanocortin Homo sapiens 53-57 182480-3 1976 After application of 5 IU ACTH/kg body weight, there was in newborn as in 5-day-old piglets an increase in the concentration of cortisol, while an influence on the level of glucose in plasma could not be detected in 0-day-old animals. Glucose 173-180 proopiomelanocortin Homo sapiens 26-30 174896-3 1976 Hyperosmolar solutions prepared by the addition of either NaCL, glucose or mannitol enhanced the ACTH effect on cAMP to the same extent as did the hyperosmolar sucrose solution, but hyperosmolar urea solutions did not have such an effect. Glucose 64-71 proopiomelanocortin Homo sapiens 97-101 165982-5 1975 On the one hand, insulin action (glucose transport) is inhibited by compounds (cholera toxin, ACTH, glucagon and L-norepinephrine) that stimulate adenylate cyclase; conversely, insulin both inhibits the lipolytic action of these compounds, and raises cellular levels of cyclic GMP. Glucose 33-40 proopiomelanocortin Homo sapiens 94-98 4345753-0 1972 The influence of blood glucose on ACTH secretion in man. Glucose 23-30 proopiomelanocortin Homo sapiens 34-38 4357729-0 1973 Elevation of plasma glucose levels by mammalian ACTH in the spiny dogfish shark (Squalus acanthias). Glucose 20-27 proopiomelanocortin Homo sapiens 48-52 4342121-2 1972 The site of ACTH stimulation of glucose metabolism. Glucose 32-39 proopiomelanocortin Homo sapiens 12-16 4392266-0 1970 Role of glucose in facilitating the acute steroidogenic action of adrenocorticotropic hormone (ACTH). Glucose 8-15 proopiomelanocortin Homo sapiens 66-93 4392266-0 1970 Role of glucose in facilitating the acute steroidogenic action of adrenocorticotropic hormone (ACTH). Glucose 8-15 proopiomelanocortin Homo sapiens 95-99 4327656-0 1968 [The effect of adrenalin and ACTH on glucose metabolism in the brain]. Glucose 37-44 proopiomelanocortin Homo sapiens 29-33 13874317-0 1962 Modifying influence of glucose on fatty acid-mobilizing activities of epinephrine, ACTH and growth hormone in vitro. Glucose 23-30 proopiomelanocortin Homo sapiens 83-87 13645000-0 1959 [Cerebrospinal fluid sugar levels following intravenous dextrose loading in childhood tuberculous meningoencephalitis treated with ACTH]. Glucose 56-64 proopiomelanocortin Homo sapiens 131-135 13271530-0 1955 Effect of intravenous injection of fructose, with and without ACTH administration, on the level of blood glucose. Glucose 105-112 proopiomelanocortin Homo sapiens 62-66 13279087-0 1955 [Effect of cortisone and ACTH on intestinal absorption of glucose]. Glucose 58-65 proopiomelanocortin Homo sapiens 25-29 14383607-0 1955 [Effect of ACTH on blood sugar and glucose tolerance test in children]. Glucose 35-42 proopiomelanocortin Homo sapiens 11-15 14383608-0 1955 [Effect of intradermal and intramuscular administration of ACTH on the double blood sugar and blood pyruvic acid curves in glucose tolerance test]. Glucose 123-130 proopiomelanocortin Homo sapiens 59-63 14362637-0 1955 [The effect of cortisone and ACTH on the intestinal absorption of glucose]. Glucose 66-73 proopiomelanocortin Homo sapiens 29-33 13227650-2 1955 Effect of hydrocortisone and corticotropin (ACTH) on the metabolic effects of administered glucose in patients with chronic schizophrenic and manic-depressive psychoses. Glucose 91-98 proopiomelanocortin Homo sapiens 44-48 13211814-1 1954 V. Responses of 17-hydroxycorticosteroids, eosinophils, and glucose to ACTH and epinephrine. Glucose 60-67 proopiomelanocortin Homo sapiens 71-75 13013068-0 1952 [Behavior of the basal glycemia and glycemic curve due to glucose overload in normal children after administration of ACTH]. Glucose 58-65 proopiomelanocortin Homo sapiens 118-122 14844345-0 1951 Effect of ACTH on decreased serum inorganic phosphorus induced by insulin and glucose. Glucose 78-85 proopiomelanocortin Homo sapiens 10-14 18128849-3 1949 However, under the conditions of our experiment, instead of producing a transient state of diabetes mellitus, as it does in the normal subject, the ACTH appeared merely to reverse the hypoglycemic tendency, with return of the fasting blood sugar levels and the glucose tolerance curve to normal. Glucose 261-268 proopiomelanocortin Homo sapiens 148-152 31869841-5 2019 Indeed, POMC and NPY/AgRP neurons are inversely regulated by glucose and metabolic hormones including insulin and leptin. Glucose 61-68 proopiomelanocortin Homo sapiens 8-12 33848536-12 2021 Glucose-sensitive mucosal pro-opiomelanocortin (POMC) cells provide a local source of alpha-MSH that is essential for glucose-induced GLP-1 secretion in small intestine. Glucose 0-7 proopiomelanocortin Homo sapiens 26-46 33848536-12 2021 Glucose-sensitive mucosal pro-opiomelanocortin (POMC) cells provide a local source of alpha-MSH that is essential for glucose-induced GLP-1 secretion in small intestine. Glucose 0-7 proopiomelanocortin Homo sapiens 48-52 33848536-12 2021 Glucose-sensitive mucosal pro-opiomelanocortin (POMC) cells provide a local source of alpha-MSH that is essential for glucose-induced GLP-1 secretion in small intestine. Glucose 118-125 proopiomelanocortin Homo sapiens 26-46 33848536-12 2021 Glucose-sensitive mucosal pro-opiomelanocortin (POMC) cells provide a local source of alpha-MSH that is essential for glucose-induced GLP-1 secretion in small intestine. Glucose 118-125 proopiomelanocortin Homo sapiens 48-52 4322666-4 1971 ACTH-induced paralysis was preceded by rising serum inorganic P, and associated with increased plasma glucose, blood lactate, and serum creatine phosphokinase concentrations. Glucose 102-109 proopiomelanocortin Homo sapiens 0-4 32451760-1 2020 PURPOSE OF REVIEW: In this brief review, we highlight studies that have contributed to our current understanding of glucose homeostasis by the central nervous system (CNS) leptin-melanocortin system, particularly proopiomelanocortin neurons and melanocortin-4 receptors (MC4R). Glucose 116-123 proopiomelanocortin Homo sapiens 213-232 32138354-5 2020 Herein, we found that glucose significantly reduced the melanin content of alpha-melanocyte-stimulating hormone (MSH)-stimulated B16 cells and darkly pigmented normal human melanocytes with no signs of cytotoxicity. Glucose 22-29 proopiomelanocortin Homo sapiens 75-111 32138354-5 2020 Herein, we found that glucose significantly reduced the melanin content of alpha-melanocyte-stimulating hormone (MSH)-stimulated B16 cells and darkly pigmented normal human melanocytes with no signs of cytotoxicity. Glucose 22-29 proopiomelanocortin Homo sapiens 113-116 31798882-4 2019 In this regard, POC glucose meters are becoming valuable tools for conservation physiologists, as glucose can be a useful indicator of stress response. Glucose 20-27 proopiomelanocortin Homo sapiens 16-19 27792263-7 2019 In the 18- to 40-year age group with impaired glucose regulation (IGR), both ACTH and PTC levels were higher than the control group (P < 0.05). Glucose 46-53 proopiomelanocortin Homo sapiens 77-81 31057490-10 2019 In contrast, POMC neurons would not directly respond to glucose through GK and would require presynaptic inputs to sense glucose. Glucose 121-128 proopiomelanocortin Homo sapiens 13-17 30304668-4 2018 In vivo POMC-specific Cacna1e knockdown increased hepatic glucose production and insulin resistance, while body weight, feeding, or leptin-induced suppression of food intake were not changed. Glucose 58-65 proopiomelanocortin Homo sapiens 8-12 32185321-9 2018 We will assess the effect of ACTH vs betamethasone on several metabolic parameters concentrating on glucose homeostasis. Glucose 100-107 proopiomelanocortin Homo sapiens 29-33 22260204-2 2012 Recently, it has been demonstrated that morning glucose ingestion stimulates pulsatile cortisol and adrenocorticotropic hormone (ACTH) secretion, thus elevating their mean concentrations. Glucose 48-55 proopiomelanocortin Homo sapiens 100-127 29184506-5 2017 This review will particularly discuss whether pro-opiomelanocortin (POMC) neurons from the arcuate nucleus are directly glucose-sensing. Glucose 120-127 proopiomelanocortin Homo sapiens 46-66 29184506-5 2017 This review will particularly discuss whether pro-opiomelanocortin (POMC) neurons from the arcuate nucleus are directly glucose-sensing. Glucose 120-127 proopiomelanocortin Homo sapiens 68-72 28028078-4 2017 We also demonstrate that loss of Ire1alpha in Pomc neurons impaired whole-body glucose and insulin tolerance as well as hepatic insulin sensitivity. Glucose 79-86 proopiomelanocortin Homo sapiens 46-50 27688995-4 2016 METHODS: We established glucose-stimulated alpha-MSH secretion using humans, non-human primates, and mouse models. Glucose 24-31 proopiomelanocortin Homo sapiens 43-52 25383463-7 2014 The moderate increase in [Ca]i with 5 mM glucose was suppressed by NPY, but further increased by alpha-MSH in the PVN neurons that were shown to be immunoreactive to nesfatin-1/NUCB2. Glucose 41-48 proopiomelanocortin Homo sapiens 97-106 25017942-3 2014 We also demonstrate that constitutive expression of Xbp1s in Pomc neurons contributes to improved hepatic insulin sensitivity and suppression of endogenous glucose production. Glucose 156-163 proopiomelanocortin Homo sapiens 61-65 24045480-13 2013 Old and young mares had lower plasma glucose concentrations posttraining during DEX/ACTH (P<0.001 and P=0.05, respectively) and DEX/CRF (P<0.001 and P=0.003, respectively) compared to pretraining. Glucose 37-44 proopiomelanocortin Homo sapiens 84-88 23425018-6 2013 RESULTS: ACTH and cortisol levels were positively associated with systolic and diastolic blood pressure, triglycerides, fasting glucose and insulin resistance. Glucose 128-135 proopiomelanocortin Homo sapiens 9-13 23425018-8 2013 When adjusted for confounding factors, an association between ACTH and 2 h post-oral glucose tolerance test glucose was revealed. Glucose 85-92 proopiomelanocortin Homo sapiens 62-66 23425018-8 2013 When adjusted for confounding factors, an association between ACTH and 2 h post-oral glucose tolerance test glucose was revealed. Glucose 108-115 proopiomelanocortin Homo sapiens 62-66 30390291-5 2018 Therefore, in this review we will mainly discuss those established theories and recent progresses in this area, demonstrating the possible physiological mechanism by which glucose, leptin, and insulin affect neuronal excitability of POMC and AgRP neurons. Glucose 172-179 proopiomelanocortin Homo sapiens 233-237 28606559-10 2017 These results demonstrate that adiponectin enhances IPSC onto NPY neurons to attenuate action potential firing in NPY neurons in a glucose-independent manner, being contrasted to its glucose-dependent effect on POMC neurons. Glucose 183-190 proopiomelanocortin Homo sapiens 211-215 27609221-2 2016 Central leptin-melanocortin signaling via hypothalamic arcuate proopiomelanocortin (POMC) neurons is crucial for the regulation of energy and glucose balance. Glucose 142-149 proopiomelanocortin Homo sapiens 63-82 27609221-2 2016 Central leptin-melanocortin signaling via hypothalamic arcuate proopiomelanocortin (POMC) neurons is crucial for the regulation of energy and glucose balance. Glucose 142-149 proopiomelanocortin Homo sapiens 84-88 27503800-0 2016 Glucose level determines excitatory or inhibitory effects of adiponectin on arcuate POMC neuron activity and feeding. Glucose 0-7 proopiomelanocortin Homo sapiens 84-88 27503800-7 2016 We found that adiponectin at high glucose inhibited POMC neurons and increased food intake while at low glucose it exerted opposite effects. Glucose 34-41 proopiomelanocortin Homo sapiens 52-56 27503800-8 2016 The results demonstrate that glucose level determines excitatory or inhibitory effects of adiponectin on arcuate POMC neuron activity and feeding. Glucose 29-36 proopiomelanocortin Homo sapiens 113-117 26038394-4 2015 ACTH induced an elevation in cortisol, aldosterone, glucose, and fatty acids within 2 h, with complete recovery observed within 24 h of administration. Glucose 52-59 proopiomelanocortin Homo sapiens 0-4 25808323-0 2015 Interplay between glucose and leptin signalling determines the strength of GABAergic synapses at POMC neurons. Glucose 18-25 proopiomelanocortin Homo sapiens 97-101 25808323-3 2015 Here we show that leptin"s action on GABA release to POMC neurons is influenced by glucose levels. Glucose 83-90 proopiomelanocortin Homo sapiens 53-57 25808323-6 2015 However, postsynaptic TRPC channel opening by the PI3K-PLC signalling pathway in POMC neurons enhances spontaneous GABA release via activation of presynaptic MC3/4 and mGlu receptors at 2.5 mM glucose. Glucose 193-200 proopiomelanocortin Homo sapiens 81-85 25808323-8 2015 Our data indicate that the interplay between glucose and leptin signalling in glutamatergic POMC neurons is critical for determining the strength of inhibitory tone towards POMC neurons. Glucose 45-52 proopiomelanocortin Homo sapiens 92-96 25808323-8 2015 Our data indicate that the interplay between glucose and leptin signalling in glutamatergic POMC neurons is critical for determining the strength of inhibitory tone towards POMC neurons. Glucose 45-52 proopiomelanocortin Homo sapiens 173-177 25127258-0 2014 Glucose rapidly induces different forms of excitatory synaptic plasticity in hypothalamic POMC neurons. Glucose 0-7 proopiomelanocortin Homo sapiens 90-94 25127258-3 2014 Brain glucose-sensing plays an essential role in the maintenance of normal body weight and metabolism; however, the effect of glucose on synaptic transmission in POMC neurons is largely unknown. Glucose 126-133 proopiomelanocortin Homo sapiens 162-166 25127258-4 2014 Here we identified three types of POMC neurons (EPSC(+), EPSC(-), and EPSC(+/-)) based on their glucose-regulated spontaneous excitatory postsynaptic currents (sEPSCs), using whole-cell patch-clamp recordings. Glucose 96-103 proopiomelanocortin Homo sapiens 34-38 25127258-10 2014 These data indicate that glucose induces distinct excitatory synaptic plasticity in different subpopulations of POMC neurons. Glucose 25-32 proopiomelanocortin Homo sapiens 112-116 23215896-1 2013 OBJECTIVES: To evaluate the usefulness of continuous glucose monitoring (CGM) to identify nocturnal hypoglycaemia in children affected by combined ACTH and GH deficiency and to optimize the hydrocortisone replacement therapy in these patients. Glucose 53-60 proopiomelanocortin Homo sapiens 147-151 22260204-2 2012 Recently, it has been demonstrated that morning glucose ingestion stimulates pulsatile cortisol and adrenocorticotropic hormone (ACTH) secretion, thus elevating their mean concentrations. Glucose 48-55 proopiomelanocortin Homo sapiens 129-133 22285542-5 2012 Lack of Atg7 in POMC neurons caused higher postweaning body weight, increased adiposity, and glucose intolerance. Glucose 93-100 proopiomelanocortin Homo sapiens 16-20 19038501-6 2009 Independent of sleep, glucose infusion reduced levels of ACTH (P<0.01) and cortisol (P<0.02) during the second night half. Glucose 22-29 proopiomelanocortin Homo sapiens 57-61 21969806-2 2011 This cross-sectional study aimed to analyze the relationship of morning plasma cortisol and adrenocorticotropic hormone (ACTH) levels with body mass index (BMI) and glucose tolerance. Glucose 165-172 proopiomelanocortin Homo sapiens 92-119 21969806-2 2011 This cross-sectional study aimed to analyze the relationship of morning plasma cortisol and adrenocorticotropic hormone (ACTH) levels with body mass index (BMI) and glucose tolerance. Glucose 165-172 proopiomelanocortin Homo sapiens 121-125 21969806-11 2011 Both ACTH and cortisol increased as fasting plasma glucose increased. Glucose 51-58 proopiomelanocortin Homo sapiens 5-9 20068134-4 2010 RESULTS: Upregulation of Socs3 in POMC neurons leads to impairment of STAT3 and mammalian target of rapamycin (mTOR)-S6K-S6 signaling, with subsequent leptin resistance, obesity, and glucose intolerance. Glucose 183-190 proopiomelanocortin Homo sapiens 34-38 19709691-2 2009 We hypothesized that glucose infusion might acutely down-regulate increased ACTH secretion in patients with Addison disease. Glucose 21-28 proopiomelanocortin Homo sapiens 76-80 19770186-0 2009 Hormone and glucose signalling in POMC and AgRP neurons. Glucose 12-19 proopiomelanocortin Homo sapiens 34-38 19770186-6 2009 Thus, this review attempts to offer an integrative overview about how peripheral signals, particularly leptin, insulin and glucose, converge on a molecular level in POMC and AgRP neurons of the arcuate nucleus of the hypothalamus to control energy homeostasis. Glucose 123-130 proopiomelanocortin Homo sapiens 165-169 21752898-0 2011 Glucose ingestion selectively amplifies ACTH and cortisol secretory-burst mass and enhances their joint synchrony in healthy men. Glucose 0-7 proopiomelanocortin Homo sapiens 40-44 21752898-2 2011 HYPOTHESIS: Glucose ingestion elevates cortisol secretion by 1) augmenting pulsatile ACTH release; and/or 2) enhancing ACTH-cortisol synchrony or dose-responsiveness. Glucose 12-19 proopiomelanocortin Homo sapiens 85-89 21752898-2 2011 HYPOTHESIS: Glucose ingestion elevates cortisol secretion by 1) augmenting pulsatile ACTH release; and/or 2) enhancing ACTH-cortisol synchrony or dose-responsiveness. Glucose 12-19 proopiomelanocortin Homo sapiens 119-123 21752898-7 2011 Glucose ingestion abolished both relationships but amplified pulsatile ACTH (P = 0.009) and cortisol (P = 0.001) secretion. Glucose 0-7 proopiomelanocortin Homo sapiens 71-75 21752898-8 2011 Glucose exposure selectively augmented the mass of ACTH (P < 0.001) and of cortisol (P = 0.004) secreted per burst without altering burst number or basal secretion. Glucose 0-7 proopiomelanocortin Homo sapiens 51-55 21752898-11 2011 According to approximate entropy analysis, glucose input also enhanced the joint synchrony of ACTH-cortisol secretory patterns (P <= 0.001). Glucose 43-50 proopiomelanocortin Homo sapiens 94-98 21752898-13 2011 CONCLUSION: Conjoint augmentation of the mass of ACTH and cortisol secreted per burst and enhancement of ACTH-cortisol synchrony underlie glucose-induced glucocorticoid secretion in healthy men. Glucose 138-145 proopiomelanocortin Homo sapiens 49-53 21752898-13 2011 CONCLUSION: Conjoint augmentation of the mass of ACTH and cortisol secreted per burst and enhancement of ACTH-cortisol synchrony underlie glucose-induced glucocorticoid secretion in healthy men. Glucose 138-145 proopiomelanocortin Homo sapiens 105-109 19508605-0 2009 The impact of blood glucose levels on stimulated adrenocorticotropin hormone and growth hormone release in healthy subjects. Glucose 20-27 proopiomelanocortin Homo sapiens 49-76 19508605-2 2009 In the present study the impact of physiological and elevated blood glucose levels on adrenocorticotropin hormone (ACTH) and growth hormone release are investigated. Glucose 68-75 proopiomelanocortin Homo sapiens 86-113 19508605-2 2009 In the present study the impact of physiological and elevated blood glucose levels on adrenocorticotropin hormone (ACTH) and growth hormone release are investigated. Glucose 68-75 proopiomelanocortin Homo sapiens 115-119 19380749-1 2009 "Glucose regulates the effects of leptin on hypothalamic POMC neurons". Glucose 1-8 proopiomelanocortin Homo sapiens 57-61 18599453-0 2008 Glucose regulates the effects of leptin on hypothalamic POMC neurons. Glucose 0-7 proopiomelanocortin Homo sapiens 56-60 18599453-2 2008 We show here that at 11 mM glucose leptin excites POMC cells. Glucose 27-34 proopiomelanocortin Homo sapiens 50-54 18599453-5 2008 However, at high glucose concentrations (11 mM), activation of POMC cells may contribute to the appetite-suppressing effects of leptin. Glucose 17-24 proopiomelanocortin Homo sapiens 63-67 18417651-6 2008 ARC expression levels of POMC and CART genes, but none of the other genes, were positively correlated with fetal plasma glucose concentrations. Glucose 120-127 proopiomelanocortin Homo sapiens 25-29 18283269-7 2008 ACTH levels increased with weight (r = 0.13, p = 0.02), systolic blood pressure (r = 0.21, p = 0.002), diastolic blood pressure (r = 0.17, p = 0.01), fasting glucose (r = 0.17, p = 0.01). Glucose 158-165 proopiomelanocortin Homo sapiens 0-4 17332528-0 2007 Glucose regulates AMP-activated protein kinase activity and gene expression in clonal, hypothalamic neurons expressing proopiomelanocortin: additive effects of leptin or insulin. Glucose 0-7 proopiomelanocortin Homo sapiens 119-138 17908553-2 2007 New studies (Parton et al., 2007; Claret et al., 2007) disrupting glucose sensing in pro-opiomelanocortin neurons via differing methods have yielded disparate energy and glucose homeostasis phenotypes, suggesting that neuronal glucose sensing is not critical for these processes. Glucose 66-73 proopiomelanocortin Homo sapiens 85-105 17908553-2 2007 New studies (Parton et al., 2007; Claret et al., 2007) disrupting glucose sensing in pro-opiomelanocortin neurons via differing methods have yielded disparate energy and glucose homeostasis phenotypes, suggesting that neuronal glucose sensing is not critical for these processes. Glucose 170-177 proopiomelanocortin Homo sapiens 85-105 17932770-6 2007 The production of AAs in response to ACTH appears to be closely related to altered factors regulating glucose-mediated glucose disposal, increased peripheral metabolism of cortisol, and to a less extent to the effects of extra-adrenal androgens, insulin resistance, hyperinsulinemia or obesity. Glucose 102-109 proopiomelanocortin Homo sapiens 37-41 17932770-6 2007 The production of AAs in response to ACTH appears to be closely related to altered factors regulating glucose-mediated glucose disposal, increased peripheral metabolism of cortisol, and to a less extent to the effects of extra-adrenal androgens, insulin resistance, hyperinsulinemia or obesity. Glucose 119-126 proopiomelanocortin Homo sapiens 37-41 16921546-0 2007 High glucose activates pituitary proopiomelanocortin gene expression: possible role of free radical-sensitive transcription factors. Glucose 5-12 proopiomelanocortin Homo sapiens 33-52 16921546-4 2007 RESULTS: We found that high glucose concentration (24 mM) significantly stimulated the 5"-promoter activity of POMC gene. Glucose 28-35 proopiomelanocortin Homo sapiens 111-115 16921546-6 2007 Furthermore, the stimulatory effect of high glucose on POMC gene was eliminated by NF-kappaB and AP1 inhibitors, suggesting the involvement of the transcriptional factors. Glucose 44-51 proopiomelanocortin Homo sapiens 55-59 16921546-9 2007 CONCLUSIONS: Our data suggest that hyperglycemia activates POMC gene expression, at least partly, via NF-kappaB/AP1, and that high-glucose-induced free radical generation may mediate the activation of these transcription factors, which in turn stimulates the transcription of POMC gene. Glucose 131-138 proopiomelanocortin Homo sapiens 59-63 16921546-9 2007 CONCLUSIONS: Our data suggest that hyperglycemia activates POMC gene expression, at least partly, via NF-kappaB/AP1, and that high-glucose-induced free radical generation may mediate the activation of these transcription factors, which in turn stimulates the transcription of POMC gene. Glucose 131-138 proopiomelanocortin Homo sapiens 276-280 17332528-5 2007 The N-43/5 POMC neurons may therefore be an appropriate cell model to study glucose-sensing mechanisms in the hypothalamus. Glucose 76-83 proopiomelanocortin Homo sapiens 11-15 17332528-6 2007 In N-43/5 POMC neurons, increasing glucose concentrations decreased phospho-AMPK activity. Glucose 35-42 proopiomelanocortin Homo sapiens 10-14 17332528-7 2007 As a relevant downstream effect, we found that POMC transcription increased with 2.8 and 16.7 mM glucose. Glucose 97-104 proopiomelanocortin Homo sapiens 47-51 16955632-3 2006 It is only possible to check precision of POC devices for glucose in external quality assessment (EQA) surveys for POC devices for blood glucose. Glucose 58-65 proopiomelanocortin Homo sapiens 42-45 12571170-8 2003 Stepwise regression analysis, after exclusion of testosterone, revealed significant correlations between the groups (lean controls, obese controls, infertility) and ACTH-stimulated 11-deoxycortisol/cortisol ratio (P < 0.05), but not with fasting glucose, insulin, cortisol, 11-deoxycortisol and baseline 11-deoxycortisol/cortisol ratios. Glucose 249-256 proopiomelanocortin Homo sapiens 165-169 16268954-7 2005 Glucose concentration was significantly decreased on the second day of ACTH administration (P < 0.001) and on day 9 after treatment (P < 0.001). Glucose 0-7 proopiomelanocortin Homo sapiens 71-75 12639916-0 2003 Hypothalamic proopiomelanocortin neurons are glucose responsive and express K(ATP) channels. Glucose 45-52 proopiomelanocortin Homo sapiens 13-32 12639916-8 2003 This pharmacological and molecular profile suggested that POMC neurons might be sensitive to metabolic inhibition, and indeed, we found that their firing rate varied with changes in glucose concentrations. Glucose 182-189 proopiomelanocortin Homo sapiens 58-62 11979399-1 2002 The objective of the current study was to examine the potential impact of a cryptic trinucleotide repeat polymorphism in exon 3 of proopiomelanocortin (POMC) on serum leptin levels and salivary cortisol, as well as obesity and estimates of insulin, glucose, and lipid metabolism in 284 unrelated Swedish men born in 1944. Glucose 249-256 proopiomelanocortin Homo sapiens 131-150 11979399-1 2002 The objective of the current study was to examine the potential impact of a cryptic trinucleotide repeat polymorphism in exon 3 of proopiomelanocortin (POMC) on serum leptin levels and salivary cortisol, as well as obesity and estimates of insulin, glucose, and lipid metabolism in 284 unrelated Swedish men born in 1944. Glucose 249-256 proopiomelanocortin Homo sapiens 152-156 11412339-2 2001 This study aimed to investigate the temporal relationship between a rapid decrease in plasma glucose and the corresponding rise in plasma adenocorticotropic hormone (ACTH), and to assess the reproducibility of hormone responses to hypoglycemia in normal humans. Glucose 93-100 proopiomelanocortin Homo sapiens 166-170 11888847-8 2002 Furthermore, cortisol and ACTH levels increased paradoxically in patients after glucose; this was more pronounced in patients with long CTG repeat expansions. Glucose 80-87 proopiomelanocortin Homo sapiens 26-30 11888847-9 2002 CONCLUSIONS: This study showed that the GLP-1 and ACTH/cortisol responses to oral glucose are abnormal in insulin-resistant DM1 patients and that CTG triplet repeats are linked to GIP release. Glucose 82-89 proopiomelanocortin Homo sapiens 50-54 11412339-9 2001 In the seven tests performed with frequent sampling, an ACTH rise never preceded the glucose nadir, but occurred at the nadir, or up to 15 min after. Glucose 85-92 proopiomelanocortin Homo sapiens 56-60 11232008-5 2001 Features of the metabolic syndrome were independently associated with enhanced adrenal responsiveness to ACTH-(1-24) (raised blood pressure, P = 0.02; glucose intolerance, P = 0.09; hypertriglyceridemia, P = 0.02), with trends to increased urinary cortisol metabolite excretion, but not with differences in plasma cortisol after dexamethasone. Glucose 151-158 proopiomelanocortin Homo sapiens 105-109 11093286-2 2000 However, circulating alpha-MSH concentrations in obese men and their relationship with clinical indicators of obesity and glucose metabolism have not as yet been evaluated. Glucose 122-129 proopiomelanocortin Homo sapiens 21-30 10218877-2 1999 The power of the 6.5-14.0 Hz physiological "alpha" rhythm of the electroencephalogram (EEG) proved inverted-U correlated with the ACTH concentration (with maximum power at 12-14 pmol/l ACTH) but was independent from the extent of ACTH change or from cortisol/glucose concentrations. Glucose 259-266 proopiomelanocortin Homo sapiens 130-134 10657503-3 1999 An insulin injection decreased the plasma glucose level, which followed a prompt rise in plasma ACTH level and an increase in serum CINC level. Glucose 42-49 proopiomelanocortin Homo sapiens 96-100 10379939-6 1999 ACTH administration resulted in higher plasma glucose (Glu) compared to a control, although only steers housed at -5 degrees C evidently showed lower plasma inorganic phosphorus (IP). Glucose 46-53 proopiomelanocortin Homo sapiens 0-4 10379939-6 1999 ACTH administration resulted in higher plasma glucose (Glu) compared to a control, although only steers housed at -5 degrees C evidently showed lower plasma inorganic phosphorus (IP). Glucose 55-58 proopiomelanocortin Homo sapiens 0-4 9768684-10 1998 Plasma ACTH levels increased significantly at 60-120 min after IFN-beta injection compared with the levels before IFN-beta injection and in the control study using glucose injection. Glucose 164-171 proopiomelanocortin Homo sapiens 7-11 10340296-7 1999 beta-endorphin effects glucose metabolism in the limbic system, CCK increases the release of beta-endorphin from the anterior pituitary, NPY is a powerful anxiolytic that regulates beta-endorphin and insulin, while VIP indirectly regulates the expression of TNF-alpha through the inhibition of interleukin-4 (IL-4). Glucose 23-30 proopiomelanocortin Homo sapiens 0-14 9878302-0 1998 The effect of vertical banded gastroplasty on glucose-induced beta-endorphin response. Glucose 46-53 proopiomelanocortin Homo sapiens 62-76 9878302-2 1998 In this study, we investigated glucose-induced beta-endorphin, insulin, and glucose responsiveness in morbidly obese patients and the effect of surgically induced weight loss. Glucose 31-38 proopiomelanocortin Homo sapiens 47-61 9878302-9 1998 CONCLUSION: Morbidly obese patients have an increased glucose-stimulated response of beta-endorphin, insulin, and glucose which is partially corrected with weight loss following vertical banded gastroplasty. Glucose 54-61 proopiomelanocortin Homo sapiens 85-99 10195378-6 1999 ACTH levels decreased during the 5% dextrose in water and the EDTA infusions but increased during the calcium infusion. Glucose 36-44 proopiomelanocortin Homo sapiens 0-4 10874362-0 1998 Effect of Met-enkephalin on blood glucose level. Glucose 34-41 proopiomelanocortin Homo sapiens 10-24 9526708-0 1998 Beta-endorphin response to oral glucose tolerance test in obese and non-obese pre- and postmenopausal women. Glucose 32-39 proopiomelanocortin Homo sapiens 0-14 9702443-5 1998 RESULTS: The threshold for release of epinephrine, norepinephrine, ACTH, and cortisol occurred at higher plasma glucose levels in NIDDM than in IDDM patients (P < 0.05-0.01). Glucose 112-119 proopiomelanocortin Homo sapiens 67-71 9526708-3 1998 Previous clinical studies have demonstrated high plasma beta-EP levels in obese subjects and increased beta-EP release after an oral glucose tolerance test (OGTT) in normal or obese women. Glucose 133-140 proopiomelanocortin Homo sapiens 103-110 9526708-10 1998 A significant increase in plasma beta-EP levels, at 30 and 60 minutes after oral glucose ingestion, was shown in control premenopausal women. Glucose 81-88 proopiomelanocortin Homo sapiens 33-40