Genistein ameliorates hyperglycemia in a mouse model of nongenetic type 2 diabetes.

Genistein ameliorates hyperglycemia in a mouse model of nongenetic type 2 diabetes.
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DOI:
10.1139/h2012-005
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发表时间:
2012-06
期刊:
Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme
影响因子:
--
通讯作者:
Liu D
Liu D
中科院分区:
其他
文献类型:
--
作者:
Fu Z;Gilbert ER;Pfeiffer L;Zhang Y;Fu Y;Liu D

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虽然外周胰岛素抵抗在小鼠和人的肥胖和衰老期间是常见的,但进展为2型糖尿病(T2 D)主要是由于通过细胞凋亡的β细胞质量和功能的丧失。我们最近报道,染料木黄酮,一种大豆衍生的黄酮,可以改善胰岛素缺乏的糖尿病小鼠的血糖控制和β细胞功能。然而,它是否可以预防T2 D小鼠的β细胞丢失和糖尿病尚不清楚。我们目前的研究旨在探讨饮食补充染料木黄酮在非遗传性T2 D小鼠模型中的作用。通过高脂饮食和低剂量链脲佐菌素注射产生非遗传性中年肥胖糖尿病小鼠。测定膳食补充染料木黄酮对血糖控制和β细胞质量和功能的影响。膳食摄入金雀异黄素(250 mg·kg-1)可改善肥胖糖尿病小鼠的高血糖、糖耐量和血胰岛素水平,但对体重增加、摄食量、脂肪存款、血脂和外周血胰岛素敏感性无影响。Genistein可增加胰岛中胰岛素阳性β细胞的数量,促进胰岛β细胞的存活,保护胰岛质量。总之,膳食摄入金雀异黄素可以通过对β细胞的直接保护作用预防T2 D,而不改变外周胰岛素敏感性。
While peripheral insulin resistance is common during obesity and aging in mice and people, the progression to type 2 diabetes (T2D) is largely due to loss of β-cell mass and function through apoptosis. We recently reported that genistein, a soy derived isoflavone, can improve glycemic control and β-cell function in insulin-deficient diabetic mice. However, whether it can prevent β-cell loss and diabetes in T2D mice is unknown. Our current study aimed to investigate the effect of dietary supplemented genistein in a nongenetic T2D mouse model. Nongenetic, middle-aged obese diabetic mice were generated by high fat diet and a low dose of streptozotocin injection. The effect of dietary supplementation of genistein on glycemic control and β-cell mass and function was determined. Dietary intake of genistein (250 mg·kg–1 diet) improved hyperglycemia, glucose tolerance, and blood insulin level in obese diabetic mice, whereas it did not affect body weight gain, food intake, fat deposit, plasma lipid profile, and peripheral insulin sensitivity. Genistein increased the number of insulin-positive β-cell in islets, promoted islet β-cell survival, and preserved islet mass. In conclusion, dietary intake of genistein could prevent T2D via a direct protective action on β-cells without alteration of periphery insulin sensitivity.
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