期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 99, 期 24, 页码 15644-15648出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.202612199
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资金
- NICHD NIH HHS [R01 HD007857, HD07857] Funding Source: Medline
- NIDDK NIH HHS [1-P01-DK59820-01, P01 DK059820] Funding Source: Medline
Gestational diabetes coincides with elevated circulating progesterone levels. We show that progesterone accelerates the progression of diabetes in female db/db mice. In contrast, RU486, an antagonist of the progesterone receptor (PR), reduces blood glucose levels in both female WT and db/db mice. Furthermore, female, but not male, PR-/- mice had lower fasting glycemia than PR+/+ mice and showed higher insulin levels on glucose injection. Pancreatic islets from female PR-/- mice were larger and secreted more insulin consequent to an increase in beta-cell mass due to an increase in beta-cell proliferation. These findings demonstrate an important role of progesterone signaling in insulin release and pancreatic function and suggest that it affects the susceptibility to diabetes.
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