Influence of PPAR-alpha agonist fenofibrate on insulin sensitivity and selected adipose tissue-derived hormones in obese women with type 2 diabetes
Language English Country Czech Republic Media print-electronic
Document type Controlled Clinical Trial, Journal Article, Research Support, Non-U.S. Gov't
PubMed
17184146
DOI
10.33549/physiolres.931058
PII: 1058
Knihovny.cz E-resources
- MeSH
- Adipokines blood MeSH
- Adiponectin blood MeSH
- Time Factors MeSH
- Diabetes Mellitus, Type 2 blood complications drug therapy physiopathology MeSH
- Fenofibrate pharmacology therapeutic use MeSH
- Glucose Clamp Technique MeSH
- Glycated Hemoglobin metabolism MeSH
- Cholesterol, HDL blood MeSH
- Hypolipidemic Agents pharmacology therapeutic use MeSH
- Body Mass Index MeSH
- Insulin Resistance * MeSH
- Blood Glucose drug effects MeSH
- Humans MeSH
- Obesity blood complications drug therapy physiopathology MeSH
- PPAR gamma agonists MeSH
- Resistin blood MeSH
- Case-Control Studies MeSH
- Triglycerides blood MeSH
- Adipose Tissue drug effects metabolism MeSH
- Treatment Outcome MeSH
- Check Tag
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Controlled Clinical Trial MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Adipokines MeSH
- Adiponectin MeSH
- ADIPOQ protein, human MeSH Browser
- Fenofibrate MeSH
- Glycated Hemoglobin A MeSH
- Cholesterol, HDL MeSH
- Hypolipidemic Agents MeSH
- Blood Glucose MeSH
- PPAR gamma MeSH
- Resistin MeSH
- RETN protein, human MeSH Browser
- Triglycerides MeSH
PPAR-alpha agonists improve insulin sensitivity in rodent models of obesity/insulin resistance, but their effects on insulin sensitivity in humans are less clear. We measured insulin sensitivity by hyperinsulinemic-isoglycemic clamp in 10 obese females with type 2 diabetes before and after three months of treatment with PPAR-alpha agonist fenofibrate and studied the possible role of the changes in endocrine function of adipose tissue in the metabolic effects of fenofibrate. At baseline, body mass index, serum glucose, triglycerides, glycated hemoglobin and atherogenic index were significantly elevated in obese women with type 2 diabetes, while serum HDL cholesterol and adiponectin concentrations were significantly lower than in the control group (n=10). No differences were found in serum resistin levels between obese and control group. Fenofibrate treatment decreased serum triglyceride concentrations, while both blood glucose and glycated hemoglobin increased after three months of fenofibrate administration. Serum adiponectin or resistin concentrations were not significantly affected by fenofibrate treatment. All parameters of insulin sensitivity as measured by hyperinsulinemic-isoglycemic clamp were significantly lower in an obese diabetic group compared to the control group before treatment and were not affected by fenofibrate administration. We conclude that administration of PPAR-alpha agonist fenofibrate for three months did not significantly affect insulin sensitivity or resistin and adiponectin concentrations in obese subjects with type 2 diabetes mellitus. The lack of insulin-sensitizing effects of fenofibrate in humans relative to rodents could be due to a generally lower PPAR-alpha expression in human liver and muscle.
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