冰雹
发表于 2025-3-27 00:18:36
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和谐
发表于 2025-3-27 02:45:06
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Atrium
发表于 2025-3-27 05:52:32
Regulation of the insulin signalling pathway by cellular protein-tyrosine phosphatases,lar studies, the transmembrane, receptor-type PTPase LAR and the intracellular, non-receptor enzyme PTP1B have been shown to have a direct impact on insulin action in intact cell models. Since insulin signalling can be enhanced by reducing the abundance or activity of specific PTPases, pharmaceutica
斜
发表于 2025-3-27 11:21:48
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错误
发表于 2025-3-27 15:16:19
Multifunctional actions of vanadium compounds on insulin signaling pathways: Evidence for preferentanism of insulin action as well as the means to overcome the biochemical defects responsible for the resistance. Vanadium compounds have been discovered to mimic many of the metabolic actions of insulin both . and . and improve glycemic control in human subjects with diabetes mellitus. Apart from it
Matrimony
发表于 2025-3-27 20:28:32
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结果
发表于 2025-3-28 00:10:38
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规范就好
发表于 2025-3-28 04:19:58
Metabolic and therapeutic lessons from genetic manipulation of GLUT4,e homeostasis. Three mouse models are discussed including MLC-GLUT4 mice which overexpress GLUT4 specifically in skeletal muscle, GLUT4 null mice which express no GLUT4, and the MLC-GLUT4 null mice which express GLUT4 only in skeletal muscle. Overexpressing GLUT4 specifically in the skeletal muscle
尊严
发表于 2025-3-28 09:59:22
Insulin action in skeletal muscle from patients with NIDDM,pheral glucose uptake in NIDDM patients can be localized to defects in insulin action on glucose transport in skeletal muscle. Following short term . exposure to both submaximal and maximal concentrations of insulin, 3-O-methylglucose transport rates are 40–50% lower in isolated skeletal muscle stri
美学
发表于 2025-3-28 12:34:25
,Genetic manipulation of insulin action and β-cell function in mice,by manipulating insulin action or pancreatic β-cell function in the mouse. The availability of such mutant mice will allow in the future to develop animal models in which the pathophysiologies resulting from polygenic defects might be reconstituted and studied in detail. Such animal models hopefully