高脂肪饮食对β细胞增殖和β细胞量的调节
High Fat Diet Regulation of β-Cell Proliferation and β-Cell Mass.
作者信息
Golson M L, Misfeldt A Ackermann, Kopsombut U G, Petersen C P, Gannon M
机构信息
Department of Medicine, Division of Diabetes, Endocrinology, and Metabolism, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
出版信息
Open Endocrinol J. 2010;4. doi: 10.2174/1874216501004010066.
Type 2 Diabetes (T2D) is characterized by relative insulin insufficiency, caused when peripheral tissues such as liver, muscle, and adipocytes have a decreased response to insulin. One factor that elevates the risk for insulin resistance and T2D is obesity. In obese patients without T2D and initially in people who develop T2D, pancreatic β-cells are able to compensate for insulin resistance by increasing β-cell mass, effected by increased proliferation and hypertrophy, as well as increased insulin secretion per β-cell. In patients that go on to develop T2D, however, this initial period of compensation is followed by β-cell failure due to decreased proliferation and increased apoptosis. The forkhead box transcription factor FoxM1 is required for β-cell replication in mice after four weeks of age, during pregnancy, and after partial pancreatectomy. We investigated whether it is also required for β-cell proliferation due to diet-induced obesity.
2型糖尿病（T2D）的特征是相对胰岛素不足，这是由肝脏、肌肉和脂肪细胞等外周组织对胰岛素的反应降低所致。增加胰岛素抵抗和T2D风险的一个因素是肥胖。在没有T2D的肥胖患者以及最初患T2D的人群中，胰腺β细胞能够通过增加β细胞质量来补偿胰岛素抵抗，这是通过增殖增加、肥大以及每个β细胞的胰岛素分泌增加来实现的。然而，在继续发展为T2D的患者中，这种最初的补偿期之后会出现β细胞功能衰竭，原因是增殖减少和凋亡增加。叉头框转录因子FoxM1在小鼠4周龄后、怀孕期间以及部分胰腺切除术后的β细胞复制中是必需的。我们研究了饮食诱导的肥胖导致的β细胞增殖是否也需要它。
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