The premature induction of BBM enzymes by exogenous insulin is mediated by the binding of the hormone to its intestinal receptor. Binding of insulin to the extramembra-nous domain of the intestinal receptor induces a conformational change allowing phosphorylation of the tyrosine kinase domain. This binding of insulin to its receptor is higher in the crypt than in villus cells, and is higher in the ileum than in the jejunum. The BBM activities of lactase and sucrase fall with age, by a process that likely involves a post-transcriptional process. The age-related decrease in insulin binding is the result of a decline in low and high affinity receptor classes, without any change in the affinity constants.
Insulin suppresses the development of diabetes in non-obese diabetic mice and alters the balance from a T helper (Th) 1 to a Th2 type cytokine pattern in inflamed pancreatic islets. When low doses of oral insulin are given in conjunction with an adjuvant, there is upregulation of IL-4 Th2 cells in infiltrated islets and sustained local IL-2 gene expression. The same shift to the Th2 type reactivity and downregulation of inducible NOS in the intestine is also observed with low doses of insulin.
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BB rats spontaneously develop insulin-dependent diabetes mellitus around or after puberty. The nature of the insulinitis may vary between ‘benign’ and ‘beta-cell destructive’ damage. Th2-type cytokines such as IL-4 and IL-10 are associated with benign insulinitis. Th1-type cytokines such as IFN-y and IL-2 dominate during destructive insulinitis and are associated with progression to diabetes — buy diabetes drugs. The nature of the dietary fat may influence the development of diabetes in BB rats; changing the type of fat in the diet does not affect the rise of IFN-y gene expression or the influx of leukocytes into the islets, but all the fat-enriched diets lead to significantly higher IL-10 mRNA levels.