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Almost always, obesity is an obligate prerequisite for the development of type 2 diabetes mellitus. Loss of a well-known lipid phosphatase appears to prevent insulin-resistant diabetes in mice by removal of a positive regulator of adiposity.
Birnbaum
Morris J
MJ
Department of Medicine and Howard Hughes Medical Institute, University of Pennsylvania, 415 Curie Boulevard, Philadelphia, Pennsylvania 19104, USA.
D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D050356:Lipid Metabolism; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D008954:Models, Biological; D009765:Obesity / Q000235:genetics* / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D000072183:Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases; D010744:Phosphoric Monoester Hydrolases / Q000235:genetics / Q000378:metabolism / Q000502:physiology*
D007328:Insulin; D019869:Phosphatidylinositol 3-Kinases; D010744:Phosphoric Monoester Hydrolases; C098706:INPPL1 protein, human; D000072183:Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases