Corticoid release and gluconeogenesis following triglyceride ingestion in the rat

Abstract

Following a 5.0 ml triglyceride (cottonseed oil) gavage, there was a 60% elevation in the blood glucose concentration by the seventh hour in naturally occurring hypertriglyceridemic rats of the Long Evans strain. Glycogenolysis from liver or gastrocnemius muscle glycogen did not seem to be the source of this glucose. A significant elevation in the plasma total amino acid concentration concomitant with a peak in the blood urea nitrogen concentration by the fifth hour after gavage implicated gluconeogenesis. A prolonged plasma total corticoid elevation from hours 1 1/2 through 3 post‐ingestion, which did not occur in non‐fed or mineral oil‐fed cohorts, supported gluconeogenesis. The serum total protein concentration rose significantly and progressively to a peak by the eighth hour due to an elevation in the albumin concentration. These elevations in serum proteins appeared to support glucocorticoid mediated gluconeogenesis. Adrenalectomy appeared to negate triglyceride‐induced elevation in serum free amino acids, urea nitrogen, total protein and albumin.

Lipid metabolism following triglyceride ingestion in intact and adrenalectomized rats

“…Seven hours after triglyceride ingestion there was a 64% rise in plasma glucose, P< 0.05, compared to the zero time level, while in the adrenalectomized rat a 29% drop was noted in plasma glucose, P < 0.01. In the intact rat, this glucose rise was traced to glucocorticoid release and gluconeogenesis from amino acids (5). It was further noted that plasma phospholipids and cholesterol rose dur- ing the first 4 hr after triglyceride loading in intact rats, but not in the adrenalectomized rats.…”