PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29077483-4	2017	Normally, the high level of plasma cholesterol is downregulated by HGMCR inhibition as the result of degradation of LDL, but in abnormal conditions, for example, high blood glucose, the HMGCR over activated resulting in uncontrolled blood cholesterol.	Glucose	173-180	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	186-191	
26959703-3	2016	RECENT FINDINGS: In a major Mendelian randomization study of variants in the HMGCR gene, which encodes the protein through which statins exert their effect, two polymorphisms associated with lower LDL-cholesterol were also associated with higher weight, higher waist circumference, higher glucose and higher diabetes risk.	Glucose	289-296	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	77-82	
21881526-14	2011	This effect, partially amplified in the presence of high glucose and FFA, is reversed by rosuvastatin, suggesting another potential therapeutic application for this 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor.	Glucose	57-64	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	165-212	
26566492-6	2015	The underlying mechanisms are not completely understood but modulation of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA)-reductase may play a central role as genetic data indicate that mutations resulting in lower HMG CoA-reductase activity are also associated with obesity, higher glucose concentrations and diabetes.	Glucose	283-290	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	74-131	
26566492-6	2015	The underlying mechanisms are not completely understood but modulation of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA)-reductase may play a central role as genetic data indicate that mutations resulting in lower HMG CoA-reductase activity are also associated with obesity, higher glucose concentrations and diabetes.	Glucose	283-290	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	215-232	
16787330-3	2005	Here we show that 3-hydroxy-3-methylglutaryl CoA reductase inhibitor (statin) attenuates both high glucose level-induced and angiotensin II (Ang II)-induced activation of p42/44 mitogen-activated kinase (MAP kinase) in cultured human mesangial cells through inhibition of NAD(P)H oxidase activity.	Glucose	99-106	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	18-58	
16013027-7	2005	Mesangial cell proliferation induced by high glucose can be reverted by 3-hydroxy-3-methylglutaryl CoA reductase inhibitor which blocks the synthesis of prenyl groups and consequently Ras activation.	Glucose	45-52	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	72-112	
8999918-2	1997	Exposure of glucose- and T3-treated hepatocytes to a spot 14 antisense oligonucleotide inhibited induction of mRNAs encoding malic enzyme, ATP citrate-lyase, fatty acid synthase, liver-type pyruvate kinase, phosphoenolpyruvate carboxykinase, and type I deiodinase but not hydroxymethylglutaryl-CoA reductase, cytochrome c, and actin mRNAs.	Glucose	12-19	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	272-307	
15146374-9	2004	CONCLUSIONS: The HMG CoA reductase inhibitor cerivastatin lowers total and LDL cholesterol and the concentration of dense LDL in patients with elevated fasting glucose, impaired glucose tolerance or type 2 diabetes.	Glucose	160-167	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	17-34