The intestine's contribution to endogenous, triglyceride (TG)-rich lipoprotein production was compared in control and diabetic rats. Male rats were given either streptozotocin (45 mg. per kilogram) or saline. After one week, hyperglycemic animals were divided into a moderately diabetic group (glucose < 300 mg. per deciliter) and a severely diabetic group (glucose > 300 mg. per deciliter). In some animals, mesenteric lymph duct fistulas were prepared, and rats were restrained and given saline intraduodenally. After an overnight fast, lymph was collected in three two-hour periods for quantification of intestinal TG production. Other animals subjected to sham, lymph duct surgery and overnight restraint were injected with Triton WR 1339, and the ensuing increment in plasma TG concentration was used to quantify total body TG secretion. Results in control rats subjected to surgery and restraint showed the mean (± S.E.) intestinal TG secretion rate to be 3.2 ± 0.2 mg. per hour; this value represented 11 per cent of total body TG secretion. Under identical conditions, intestinal TG secretion increased (p < 0.01) by 70 per cent in moderately diabetic rats; this value represented 24 per cent of total TG secretion. In contrast, intestinal TG secretion in severely diabetic rats represented only 11 per cent of the total TG secretion: this value reflected a significant (p < 0.01) reduction in both intestinal and total body TG secretion. Electron microscopy indicated that the lymph lipoprotein particles in all animals studied were of very low density (VLDL) size. Thus, although the intestine contributes a relatively small amount of VLDL-TG to the plasma pool in control and severely diabetic rats, it appears to be a significant source of very low density lipoprotein–triglyceride (VLDL-TG) in animals with moderate insulin deficiency.

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