Effect of telmisartan on selected adipokines, insulin sensitivity, and substrate utilization during insulin-stimulated conditions in patients with metabolic syndrome and impaired fasting glucose
Language English Country Great Britain, England Media print-electronic
Document type Journal Article, Randomized Controlled Trial, Research Support, Non-U.S. Gov't
PubMed
20630944
DOI
10.1530/eje-10-0436
PII: EJE-10-0436
Knihovny.cz E-resources
- MeSH
- Adipokines blood MeSH
- Benzimidazoles therapeutic use MeSH
- Benzoates therapeutic use MeSH
- Adult MeSH
- Glucose Clamp Technique MeSH
- Hypoglycemic Agents therapeutic use MeSH
- Angiotensin-Converting Enzyme Inhibitors therapeutic use MeSH
- Insulin therapeutic use MeSH
- Insulin Resistance physiology MeSH
- Blood Glucose drug effects metabolism MeSH
- Middle Aged MeSH
- Humans MeSH
- Metabolic Syndrome blood drug therapy MeSH
- Glucose Intolerance blood drug therapy MeSH
- Telmisartan MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Randomized Controlled Trial MeSH
- Names of Substances
- Adipokines MeSH
- Benzimidazoles MeSH
- Benzoates MeSH
- Hypoglycemic Agents MeSH
- Angiotensin-Converting Enzyme Inhibitors MeSH
- Insulin MeSH
- Blood Glucose MeSH
- Telmisartan MeSH
OBJECTIVE: Telmisartan improves glucose and lipid metabolism in rodents. This study evaluated the effect of telmisartan on insulin sensitivity, substrate utilization, selected plasma adipokines and their expressions in subcutaneous adipose tissue (SAT) in metabolic syndrome. DESIGN AND METHODS: Twelve patients with impaired fasting glucose completed the double-blind, randomized, crossover trial. Patients received telmisartan (160 mg/day) or placebo for 3 weeks and vice versa with a 2-week washout period. At the end of each period, a hyperinsulinemic euglycemic clamp (HEC) combined with indirect calorimetry was performed. During HEC (0, 30, and 120 min), plasma levels of adipokines were measured and a needle biopsy (0 and 30 min) of SAT was performed. RESULTS: Fasting plasma glucose was lower after telmisartan compared with placebo (P<0.05). There were no differences in insulin sensitivity and substrate utilization. We found no differences in basal plasma adiponectin, resistin and tumour necrosis factor α (TNFα), but an increase was found in basal leptin, after telmisartan treatment. Insulin-stimulated plasma adiponectin (P<0.05), leptin and resistin (P<0.001) were increased, whereas TNFα was decreased (P<0.05) after telmisartan treatment. Expression of resistin, but not adiponectin, TNFα and leptin was increased after telmisartan treatment. CONCLUSIONS: Despite the decrease in fasting plasma glucose, telmisartan does not improve insulin sensitivity and substrate utilization. Telmisartan increases plasma leptin as well as insulin-stimulated plasma adiponectin, leptin and resistin, and decreases plasma TNFα during HEC. Changes in plasma adipokines cannot be explained by their expressions in SAT. The changes in plasma adipokines might be involved in the metabolic effects of telmisartan in metabolic syndrome.
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