Key result
Triglyceride gavage raises blood glucose ~60% in hypertriglyceridemic rats via corticoid release.
Why the study?
The metabolic effects of triglyceride ingestion on corticoid release and gluconeogenesis in hypertriglyceridemic rats were not fully understood.
Answers are grounded in this paper and cite their sources.
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.
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Lenz et al. (1970) studied Hypertriglyceridemia (animal model). Triglyceride (cottonseed oil) gavage vs. Non-fed or mineral oil-fed cohorts was evaluated on Blood glucose concentration. Triglyceride gavage in hypertriglyceridemic rats resulted in a 60% elevation in blood glucose concentration and prolonged corticoid release, implicating glucocorticoid-mediated gluconeogenesis.
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