Bypass of large segments of the small intestine to produce weight loss in morbidly obese human subjects has been associated with increased lipid accumulation in the liver. Congenital and nutritional obese rat models were employed to evaluate hepatic lipid accumulation following bypass of 90% of the small intestine. When small intestinal bypass was performed on nutritionally obese rats ingesting a high-fat diet (17%) supplemented with choline dihydrogen citrate (3,4 g/kg diet), a 59% loss of weight at 1 mo was unassociated with increased hepatic lipid accumulation when compared to sham-operated controls. When small intestinal bypass was performed on a nutritionally obese rat fed a relative choline-methionine-deficient diet following intestinal bypass, marked increases in total hepatic lipid and hepatic triglyceride content were evident when compared to the lipid content in sham-operated controls ingesting a similar choline-deficient diet. Hepatic steatosis following small intestinal bypass could be produced in a rat model only by a deficiency in a required substrate for triglyceride conversion to phospholipid and suggests that similar deficiencies may contribute to the increased hepatic lipid accumulation occurring in human subjects following intestinal bypass.

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