PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
9143863-1	1997	OBJECTIVE: To investigate a long-term colchicine treatment in inhibiting normal release of insulin, in response to a glucose load.	Colchicine	38-48	insulin	Homo sapiens	91-98	
14706815-6	2004	The enhancement of cephalexin uptake by the insulin pretreatment was inhibited by genistein, a tyrosine kinase inhibitor, and colchicine, an agent that disrupts protein translocation.	Colchicine	126-136	insulin	Homo sapiens	44-51	
9143863-4	1997	METHODS: A standard oral glucose tolerance test (OGTT) was performed to study the effect of long-term colchicine treatment on glucose-induced insulin response.	Colchicine	102-112	insulin	Homo sapiens	142-149	
6378371-10	1984	Cell cycle analysis after the addition of colchicine to prevent mitosis and the reentry of cells into G1 demonstrates a shortened G1 in response to insulin.	Colchicine	42-52	insulin	Homo sapiens	148-155	
34978374-9	2022	CONCLUSIONS: In adults with obesity and MetS, colchicine appears to improve insulin regulation of lipolysis and reduce markers of systemic inflammation independent of an effect on local leukocyte distributions in SAT.	Colchicine	46-56	insulin	Homo sapiens	76-83	
3073092-3	1988	So, for instance, drugs that increase prostaglandins synthesis as colchicine or furosemide inhibit insulin secretion while non steroid anti-inflammator drugs, mainly salicylates, which inhibit cyclo-oxygenase, enhance the insulin response to various stimuli.	Colchicine	66-76	insulin	Homo sapiens	99-106	
6796445-2	1981	Acute insulin response to glucose (0.33 g/kg) was significantly decreased by colchicine (3 mg i.v.).	Colchicine	77-87	insulin	Homo sapiens	6-13	
6796445-3	1981	In fact, this response (mean change 2-10 min insulin) was 44 +/- 8 microunits/ml before and 32 +/- 6 microunits/ml after colchicine administration (P less than 0.01).	Colchicine	121-131	insulin	Homo sapiens	45-52	
6796445-5	1981	Infusion of lysine acetylsalicylate (LAS), an inhibitor of endogenous PG synthesis, completely reversed the inhibitory effect of colchicine upon insulin secretion and also augmented acute insulin response to glucose (response before colchicine + LAS = 45 +/- 8 microunits/ml; response after colchicine + LAS = 51 +/- 9 microunits/ml, P less than 0.05).	Colchicine	129-139	insulin	Homo sapiens	145-152	
7002671-8	1980	Colchicine (10(-8) M to 10(-4) M) inhibited insulin release in a dose-dependent manner.	Colchicine	0-10	insulin	Homo sapiens	44-51	
7002671-9	1980	Maximum inhibition of insulin release (by about 40%) by colchicine (10(-4) M) required 60 min.	Colchicine	56-66	insulin	Homo sapiens	22-29	
27241260-8	2016	Given these findings, we hypothesize that, in at-risk individuals (those with obesity-induced inflammation and metabolic dysregulation), long-term colchicine use will lead to suppression of inflammation and thus cause improvements in insulin sensitivity and other obesity-related metabolic impairments.	Colchicine	147-157	insulin	Homo sapiens	234-241	
488360-0	1979	Effect of colchicine and vinblastine on the coupling of insulin binding and insulin action in fat cells.	Colchicine	10-20	insulin	Homo sapiens	56-83	
1227510-1	1975	When isolated fat-cells are incubated at 25 degrees C in serum-based media containing glucose, insulin and heparin, the rise that occurs in the clearing-factor lipase activity of the incubation medium is inhibited by colchicine.	Colchicine	217-227	insulin	Homo sapiens	95-102	
1098658-3	1975	Incubation of islets of Langerhans in vitro in the presence of colchicine produced a progressive inhibition of the insulin-secretory response to glucose, which was dependent on the time of incubation.	Colchicine	63-73	insulin	Homo sapiens	115-122	
1098658-8	1975	After an initial 30 min delay, the time-course of the binding of [3-H]colchicine to islet-cell proteins paralleled that for the inhibitory effect of colchicine on insulin release.	Colchicine	70-80	insulin	Homo sapiens	163-170	
557047-4	1977	Of the inhibitors tested, vinblastine and cytocalasin B abolished the growth promoting activity of insulin, while colchicine inhibited the activity of both serum and insulin.	Colchicine	114-124	insulin	Homo sapiens	166-173	
780246-3	1976	Vinblastine and cold treatment, which have been shown to cause disaggregation of microtubules into subunits and to inhibit insulin release from islets, increased the number of colchicine binding subunits.	Colchicine	176-186	insulin	Homo sapiens	123-130	
30869182-8	2019	However, changes in some secondary outcomes, including homeostatic model assessment of insulin resistance (P = 0.0499), fasting insulin (P = 0.07) and glucose effectiveness (P = 0.08), suggested metabolic improvements in the colchicine versus placebo group.	Colchicine	225-235	insulin	Homo sapiens	87-94	
30869182-8	2019	However, changes in some secondary outcomes, including homeostatic model assessment of insulin resistance (P = 0.0499), fasting insulin (P = 0.07) and glucose effectiveness (P = 0.08), suggested metabolic improvements in the colchicine versus placebo group.	Colchicine	225-235	insulin	Homo sapiens	128-135	
30869182-11	2019	These results suggest a larger, adequately powered study should be conducted to determine whether colchicine improves insulin resistance and other measures of metabolic health in at-risk individuals.	Colchicine	98-108	insulin	Homo sapiens	118-125	
22607032-6	2012	Colchicine or nocodazole treatment abolished insulin-induced INM targeting of cav-2.	Colchicine	0-10	insulin	Homo sapiens	45-52