作者: Lisanne M.M. Gommers , Joost G.J. Hoenderop , René J.M. Bindels , Jeroen H.F. de Baaij
DOI: 10.2337/DB15-1028
关键词: Insulin receptor 、 Hypomagnesemia 、 Internal medicine 、 Type 2 diabetes 、 Endocrinology 、 Biology 、 Insulin resistance 、 Diabetes mellitus 、 Magnesium deficiency (medicine) 、 Insulin 、 Type 2 Diabetes Mellitus
摘要: Over the past decades, hypomagnesemia (serum Mg(2+) <0.7 mmol/L) has been strongly associated with type 2 diabetes mellitus (T2DM). Patients show a more rapid disease progression and have an increased risk for complications. Clinical studies demonstrate that T2DM patients reduced pancreatic β-cell activity are insulin resistant. Moreover, dietary supplementation improves glucose metabolism sensitivity. Intracellular regulates glucokinase, KATP channels, L-type Ca(2+) channels in β-cells, preceding secretion. receptor autophosphorylation is dependent on intracellular concentrations, making direct factor development of resistance. Conversely, important regulator homeostasis. In kidney, activates renal channel transient potential melastatin 6 determines final urinary excretion. Consequently, enter vicious circle which causes resistance reduces serum concentrations. This Perspective provides systematic overview molecular mechanisms underlying effects secretion signaling. addition to providing review current knowledge, we provide novel directions future research identify previously neglected contributors T2DM.