A possible hepatic factor in the control of plasma free fatty acid levels.
Insulin acts as a regulator of lipid metabolism by inhibiting the rate of lipolysis. Hyperinsulinemia, produced by the peripheral infusion of glucose, therefore, causes a lowering of plasma free fatty acids (FFA) by decreasing the mobilization of fats from peripheral deposits. Based on previous studies, it was postulated that a lowering of plasma FFA could be produced, in the absence of hyperinsulinemia, by the infusion of glucose directly into the liver. This study was undertaken to investigate the existence of endogenous factors other than insulin, which inhibit lipolysis. It was determined that glucose at a dosage of 0.125 gm/kg/hr could be infused into the portal vein of dogs without increasing plasma insulin levels. This dosage significantly lowered plasma FFA levels when injected into the portal vein but had no effect on plasma FFA when infused peripherally. There were significant decreases in FFA turnover following portal glucose administration, with no changes in fractional turnover. This indicated that the lowered plasma FFA concentrations found following portal infusions of glucose, were due to reduced lipid mobilization from adipose tissue, rather than increased tissue uptake of FFA. These results suggested the existence of an hepatic factor, stimulated by portal glucose infusion, which lowered FFA mobilization from adipose tissue.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004285:Dogs; D005230:Fatty Acids, Nonesterified / Q000097:blood*; D005947:Glucose; D007328:Insulin / Q000097:blood; D008099:Liver / Q000378:metabolism*; D011169:Portal Vein
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D005947:Glucose