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麩醯胺對於肥胖下肢缺血小鼠肝臟葡萄糖代謝之影響

為了解決Komeda jp的問題，作者戴安娜 這樣論述：

Background and aims: Obesity is a growing worldwide health problem. High fat diet-induced obesity can disturb hepatic glucose metabolism through alteration of the PI3K-Akt pathway in the liver. Moreover, obesity and insulin resistance is the leading cause of type 2 diabetes which is a risk factor f

or the development of the peripheral arterial disease. Glutamine (Gln) is a non-essential amino acid, however, it is considered essential in catabolic conditions. Previous studies found that Gln improved insulin sensitivity and attenuated hyperglycemia in the diabetic state. The aim of this study is

to investigate the effect of Gln administration on the hepatic insulin sensitivity in the obese mice with limb ischemia.Methods: Male C57BL/6 mice were used and high-fat diet was provided for 4 weeks to induce obesity. Mice in the Gln groups were provided with Gln (replaced 25% of the total amino a

cid nitrogen) to the high-fat diet for addition 4 weeks. Left-back limb ischemia operation was performed at the end of experiment and mice were sacrificed at 1 day or 7 days after ischemia operation according to the sacrificed time schedule of the experimental groups. The proteins related to the PI3

K-Akt pathway were measured by western blotting. ELISA was performed to measure plasma insulin level. The fasting blood glucose and epididymal fat were measured to support the hypothesis.Results: The high-fat diet-induced obesity caused impairment of hepatic insulin signaling by inducing the alterat

ion of the PI3K-Akt pathway. Moreover, diet-induced obesity increased fasting blood glucose and plasma insulin levels as an indicator of insulin insensitivity. Based on the western blot analysis, administration of Gln improved the PI3K-pathway by increasing the expression of p-PI3K, p-Akt, PDK1, PRE

X2, GSK3, and p-FOXO1 expression in the cytoplasm and reducing the level of FOXO1, PC, PEPCK, and G6PC in the nucleus. Furthermore, Gln administration also reversed insulin resistance by normalizing blood sugar.Conclusions: High fat diet-induced obesity reduces hepatic insulin signaling which automa

tically induces gluconeogenesis and inhibits glycogen synthesis in the liver. Gln administration reverses those conditions by improving hepatic insulin signaling through regulating PI3K-Akt pathway, mediating glycogen synthesis, and reducing gluconeogenesis in the liver. Moreover, Gln administration

can improve insulin sensitivity in obese mice subjected to limb ischemia.