High fat diet regulation of β-cell proliferation and β-cell mass

ML Golson, AA Misfeldt, UG Kopsombut… - The open …, 2010 - pmc.ncbi.nlm.nih.gov
ML Golson, AA Misfeldt, UG Kopsombut, CP Petersen, M Gannon
The open endocrinology journal, 2010pmc.ncbi.nlm.nih.gov
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 …
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.
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