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 micromol/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.