| Intermittent protein restriction protects islet 13 cells and improves glucose homeostasis in diabetic mice |
| 論文作者 |
Wei, SY; Li, CC; Luo, XM; Yang, LZX; Yu, L; Wang, QT; Meng, ZX; Wang, T; Chen, Y |
| 期刊/會(huì)議名稱 |
SCIENCE BULLETIN |
| 論文年度 |
2022 |
| 論文類別 |
Article |
| 摘要 |
Diabetes is caused by the interplay between genetics and environmental factors, tightly linked to lifestyle and dietary patterns. In this study, we explored the effectiveness of intermittent protein restriction (IPR) in diabetes control. IPR drastically reduced hyperglycemia in both streptozotocin-treated and leptin receptor-deficient db/db mouse models. IPR improved the number, proliferation, and function of 13 cells in pancreatic islets. IPR reduced glucose production in the liver and elevated insulin signaling in the skeletal muscle. IPR elevated serum level of FGF21, and deletion of the Fgf21 gene in the liver abrogated the hypoglycemic effect of IPR without affecting 13 cells. IPR caused less lipid accumulation and damage in the liver than that caused by continuous protein restriction in streptozotocin-treated mice. Single-cell RNA sequencing using mouse islets revealed that IPR reversed diabetes-associated 13 cell reduction and immune cell accumulation. As IPR is not based on calorie restriction and is highly effective in glycemic control and 13 cell protection, it has promising translational potential in the future.(c) 2021 Science China Press. Published by Elsevier B.V. and Science China Press. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
| 期 |
7 |
| 卷 |
67 |
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