Submitted on March 9, 2006
Revised on September 7, 2006
Accepted on September 11, 2006
Acute hyperinsulinemia inhibits intramyocellular triglyceride synthesis in high fat-fed obese rats
ZengKui Guo, Lianzhen Zhou, and Michael D. Jensen
Internal Medicine, Mayo Clinic, Rochester, MN 55905
Corresponding Author: guo.zengkui{at}mayo.edu
Hyperinsulinemia is common in obesity but whether it plays a role in intramyocellular triglyceride (imcTG) buildup is unknown. In this study, hyperinsulinemic-euglycemic clamp experiments were performed in overnight-fasted lean and high fat-fed obese rats, awake, to determine the effect of insulin on imcTG synthesis (incorporation of 14C-glycerol, 14C-glucose and 3H-oleate). Insulin infusion at 25 (low insulin) and 100 (high insulin) pmol/kg/min increased plasma insulin by 5 and 16 fold, respectively, while plasma and intramyocellular glycerol, free fatty acids, triglycerides and glucose levels were maintained at their basal levels by co-infusion of exogenous glycerol, free fatty acids and triglycerides at fixed rates and glucose at varying rate. In obese rats, insulin suppressed incorporation of glycerol into imcTG-glycerol moiety dose-dependently (P<0.01 – P<0.001) in gastrocnemius and tibialis anterior, but only the high insulin suppressed it in soleus (P<0.05). The low insulin suppressed glucose incorporation into imcTG-glycerol in all three muscles (P=0.01 – P<0.01). However, the low insulin did not affect (P>0.05) and the high insulin suppressed (P<0.05 – P<0.01) fatty acid incorporation into imcTG in all three muscles. Insulin also suppressed glycerol incorporation in lean rats (P<0.01 – P<0.04). On the other hand, imcTG pool size was not affected by insulin (P>0.05). The observations suggested that acute hyperinsulinemia inhibits imcTG synthesis and thus does not appear to promote imcTG accumulation via synthetic pathway at least in short term.
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