PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19125755-0	2009	Pregnancy outcome in patients with raised blood glucose due to a heterozygous glucokinase gene mutation.	Blood Glucose	42-55	glucokinase	Homo sapiens	78-89	
28458896-13	2017	LEARNING POINTS: Gain-of-function mutations in GCK cause familial hyperinsulinemic hypoglycemia.Hypoglycemia during pregnancy may have serious health implications for mother and fetus.Pregnancy with hyperinsulinism represents a medical dilemma as hypoglycemia as well as octreotide treatment may pose a risk of fetal growth restriction.In some cases of familial hyperinsulinemic hypoglycemia, blood glucose levels can be successfully managed through diet only.	Blood Glucose	393-406	glucokinase	Homo sapiens	47-50	
25802718-5	2015	Since 2003, many glucokinase activators (GKAs) have been developed, and their ability to lower the blood glucose has been shown in several animal models of type 2 diabetes.	Blood Glucose	99-112	glucokinase	Homo sapiens	17-28	
12228011-5	2002	Normal blood glucose levels were observed after gene transfer, and glucose tolerance was substantially enhanced compared with diabetic control animals, suggesting that hepatic GK expression is a feasible mechanism to enhance glucose disposal.	Blood Glucose	7-20	glucokinase	Homo sapiens	176-178	
25935773-7	2015	Seven-point home blood glucose monitoring over a 7-day period in each trimester demonstrated higher fasting and postprandial glycemic excursions in the first trimester of GCK pregnancies when compared to HNF-1alpha pregnancies (fasting 104 [90-115] mg/dL vs 84 [77-88] mg/dL; P = .01 and postprandial 154 [135-196] mg/dL vs 111 [100-131] mg/dL; P = .04) despite insulin treatment.	Blood Glucose	17-30	glucokinase	Homo sapiens	171-174