Fol. Biol. 2002, 48, 237-241
Rosiglitazone Improves Insulin Resistance, Lipid Profile and Promotes Adiposity in a Genetic Model of Metabolic Syndrome X
RSG is a member of the TZD group of drugs widely used in treatment of type 2 diabetes. The underlying mechanism of TZD action in insulin-sensitive tissues is not fully understood. In this study we show that 14-day RSG administration in a new rodent model of metabolic syndrome X, polydactylous rat strain (PD/Cub), substantially improves its lipid profile (serum TGs 4.20 ± 0.23 vs 2.34 ± 0.14 mmol/l, P < 0.0001; FFA 0.46 ± 0.05 vs 0.33 ± 0.02 mmol/l, P = 0.017), diminishes the liver TG depots (15.76 ± 0.60 vs 8.44 ± 0.55 µmol/g, P < 0.0001), serum insulin concentrations (1.10 ± 0.08 vs 0.63 ± 0.02 nmol/l, P < 0.0001) and promotes visceral adiposity (adiposity index 1.28 ± 0.03 vs 1.85 ± 0.07, P < 0.0001). No changes were observed in serum or liver concentrations of cholesterol. Concomitantly, both basal and insulin-stimulated glycogen synthesis in red-fibre type muscle (m. soleus) was enhanced, as well as glucose uptake into adipose tissue. However, glucose oxidation in soleus (basal and insulin-stimulated) remained unchanged. In consent with previously published data we suggest the current pharmacogenetic study as a further proof of substantial influence of genetic background on the physiological outcome of TZD therapy.
Keywords
rosiglitazone, metabolic syndrome X, genetic models, PD/Cub.
Funding
This work was supported by following grants: GAUK 7/2000/C from the Grant Agency of Charles University, No. 303/01/1010 and No. 204/98/K015 from the Grant Agency of the Czech Republic, and No. 6367-3 from the Internal Grant Agency of the Ministry of Health of the Czech Republic.
References
Copyright
This is an open-access article distributed under the terms of the Creative Commons Attribution License.