Milk and Meat Signalling in the Pathogenesis of Type 2 Diabetes

来源 :MIT`s 1st Annual World Congress of Diabetes-2012(2012第一届糖尿病大 | 被引量 : 0次 | 上传用户:fei000chong
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  Increased dairy protein and meat consumption will be presented as an overlooked fundamental environmental risk factor of Western diet promoting the development of type 2 diabetes.Mammalian milk exerts important endocrine functions as an inulinotropic, anabolic and mitogenic signalling system promoting species-dependent neonatal growth and development.Milk stimulates neonates pancreatic beta-cell proliferation and insulin secretion by activating the nutrient-sensitive kinase mTORC1 (mammalian target of rapamycin complex 1).The recent finding, that adult rodent beta-cells only proliferate by self-duplication, is of crucial importance, because permanent milk consumption in combination with high meat intake may over-stimulate beta-cell replication thereby accelerating early onset ofreplicative beta-cell senescence.Whey proteins (14%) and casein proteins (10%) and meat proteins (8%) are rich sources of the essential amino acid leucine, which stimulates insulin secretion and beta-cell proliferation by activation of mTORC1.The long-term use ofleucine-rich milk proteins after the weaning period as well as increased consumption of leucine-rich meat, both staples of Western diet, explain exaggerated mTORC1-dependent beta-cell proliferation, early onset of replicative beta-cell senescence and beta-cell apoptosis, both hallmarks of type 2 diabetes.The annual total per capita leucine uptake has triplicated in Germany from 1960 to 2011 in parallel to the increasing prevalence of type 2 diabetes.Dietary limitation of leucine-rich dairy and animal proteins to levels of traditional vegetable-rich Chinese diet offers a great chance for the prevention of type 2 diabetes by attenuating beta-cell mTORC1 signalling.
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