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Research Article Free access | 10.1172/JCI106227
Thorndike Memorial Laboratory and the Second and Fourth (Harvard) Medical Services, Boston City Hospital, Boston, Massachusetts 02118
Gastroenterology Research Laboratory, Madison Veterans Administration Hospital, Boston, Massachusetts 02118
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02118
Department of Medicine, University of Wisconsin, Madison, Wisconsin 53706
Find articles by Olsen, W. in: JCI | PubMed | Google Scholar
Thorndike Memorial Laboratory and the Second and Fourth (Harvard) Medical Services, Boston City Hospital, Boston, Massachusetts 02118
Gastroenterology Research Laboratory, Madison Veterans Administration Hospital, Boston, Massachusetts 02118
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02118
Department of Medicine, University of Wisconsin, Madison, Wisconsin 53706
Find articles by Rosenberg, I. in: JCI | PubMed | Google Scholar
Published January 1, 1970 - More info
The specificity and mechanism of altered intestinal transport of diabetic rats was studied with an everted ring technique. Increased intracellular accumulation of amino acids, as well as galactose and 3-O-methylglucose, was demonstrated in diabetes. The greater accumulation by diabetic intestine could not be attributed to a direct effect of the agent used to induce diabetes or to an alteration in food consumption. Although the changes were related to the severity of diabetes and could be reversed with treatment with insulin, they could not be modified by addition of insulin in vitro. The changes could not be induced in control intestine either with hyperglycemia from glucose infusion or preincubation with glucose in vitro.
Although the higher concentration gradients of amino acids, galactose, and 3-O-methylglucose could result from increased energy utilization by diabetic intestine, an alteration of cell membrane function, as well, is suggested by the demonstration with kinetic studies of increased influx with an increase in Vmax.