Secretin, glucagon, insulin-antibodies, islet-cell exhaustion and diabetes mellitus: a hypothesis

Malhotra, S. L. (1982) Secretin, glucagon, insulin-antibodies, islet-cell exhaustion and diabetes mellitus: a hypothesis Medical Hypotheses, 8 (1). pp. 105-110. ISSN 0306-9877

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Official URL: http://linkinghub.elsevier.com/retrieve/pii/030698...

Related URL: http://dx.doi.org/10.1016/0306-9877(82)90093-7

Abstract

There are many studies that show that important and interesting differences exist in the patterns of diabetes mellitus, not only between countries but from group to group in the same country. Such big differences suggest the causes may be environmental, most of which are dietary and, therefore, preventable. In these dietary factors it is perhaps the pattern of eating, the presence or absence of cellulose, roughage and vegetable fibre, milk and fermented milk products such as yoghurt, which are of crucial importance. There is a quicker rise of blood glucose in the case of "non-masticatory-roughage-poor" dietary regimens as compared with "masticatory" milk, milk-products and roughage-rich regimens on account of faster gastric emptying in the former and slower gastric emptying in the latter. The hyperchlorhydria caused by fibre-poor non-masticatory meals produces an instantaneous secretin-release which results in hyperinsulinism. Such "sucrose-induced hyperinsulinism" leads to formation of insulin antibodies. Diabetes is caused by this excessive inactivation of insulin by antibodies, brought about by dietary factors, setting up the vicious cycle of hurried meals - hyperchlorhydria and secretin resulting in instantaneous insulin-release -neoglucogenesis more insulin-release -insulin antibodies and a further secretion of insulin -insulin antagonism - islet cell exhaustion - diabetes mellitus. There is evidence of an alternative mechanism in which diabetes appears to be caused by interference with insulin-release even though islets manufacture insulin normally.

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