Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.9 (glucose-6-phosphatase)
 3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of pioglitazone (5-[4-[2-(5-etyl-2-pyridyl)ethoxy] benzyl]-2,4-thiazolidinedione, AD-4833, also known as U-72, 107E) on peripheral and hepatic insulin resistance were examined using genetically obese-hyperglycemic rats, Wistar fatty. Pioglitazone was administered to fatty rats (3 mg/kg/d) and lean rats (10 mg/kg/d) for 6 days. Pioglitazone decreased hyperglycemia and hypertriglyceridemia without affecting hyperinsulinemia in the fatty rats, and significantly reduced plasma levels of triglyceride and insulin without altering normoglycemia in the lean rats. The same rats were subjected to an isotopic method combined with a euglycemic clamp technique for assessing insulin sensitivity in hepatic glucose production (HGP) and peripheral glucose utilization (PGU). HGP decreased and PGU increased in response to infused insulin in the lean rats but did not in the fatty rats, indicating that insulin resistance was present in the liver and peripheral tissues of the fatty rats. Treatment with pioglitazone restored the responses of HGP and PGU to infused insulin in the fatty rats, but did not produce any changes in the lean rats. When the same levels of glycemia and insulinemia were established by 480 mU/h of insulin in both treated and control fatty groups, PGU was 1.5-fold higher and HGP was 3-fold lower in the pioglitazone treated group. Pioglitazone also corrected the abnormality in hepatic enzyme regulation by insulin of the fatty rats: glucose-6-phosphatase decreased and glucokinase increased, suggesting the increased response of the liver to insulin and the resultant suppression of HGP. Therefore, pioglitazone is expected to be useful for treating abnormal glucose and lipid metabolism in non-insulin-dependent diabetes mellitus through reducing insulin resistance of the peripheral tissues and liver.
 ...
PMID:Effects of pioglitazone on hepatic and peripheral insulin resistance in Wistar fatty rats. 219 15

Insulin resistance has been implicated in the pathogenesis of type 2 diabetes. High fat diets cause insulin resistance. Both metformin and pioglitazone are considered "insulin sensitizers" and used as antihyperglycemic agents for type 2 diabetes treatment. The aim of this study is to Compare pioglitazone and metformin effects on carbohydrate metabolism and insulin sensitivity in diabetic and glucose intolerant rats on high fat diet. Male albino rats were randomized to seven groups. The 1st group received high carbohydrate diet (control). The 2nd, 3rd and 4th groups received high sunflower oil diets for 6 weeks and either left untreated, or given pioglitazone or metformin during the last 3 weeks. The 5th, 6th, and 7th groups were made diabetic by STZ injection on day 15 of the 6 weeks-high fat diet regimen. They were either left untreated, or given pioglitazone or metformin during the last 3 weeks. High-fat diet induced glucose intolerance; represented by increase of serum glucose associated with increase in liver glucose-6-phosphatase and decreases in liver glucose-6-phosphate dehydrogenase and glucokinase activities. No significant differences were observed between pioglitazone and metformin. In diabetic rats, both pioglitazone and metformin decreased elevated serum glucose by approximately 30%. Only metformin increased hepatic glycogen, and normalized glucose-6-phosphatase activity. On the other hand, pioglitazone normalized elevated renal glycogen content and increased glucose-6-phosphate dehydrogenase activity. High sunflower oil diet impaired glucose tolerance. Pioglitazone and metformin had comparable effects on estimates of carbohydrate metabolism and insulin sensitivity in high-fat fed rats, but different effects in diabetic rats.
 ...
PMID:Pioglitazone versus metformin in two rat models of glucose intolerance and diabetes. 2056 45