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Intermittent protein restriction protects isletβcells and improves glucose homeostasis in diabetic mice

Science Bulletin 2022年第7期67卷 733-747页

作者： Siying Wei Chenchen Li Xuemei Luo lanzexin yang Long Yu Qintao Wang Zhuo-Xian Meng Tao Wang Yan Chen CAS Key Laboratory of Nutrition Metabolism and Food SafetyShanghai Institute of Nutrition and HealthUniversity of Chinese Academy of SciencesChinese Academy of SciencesShanghai 200031China School of Life Science and Technology ShanghaiTech UniversityShanghai 201210China Huzhou R&D Center for Nutrition and Health Shanghai Institute of Nutrition and HealthChinese Academy of SciencesHuzhou 313000China Department of Pathology and Pathophysiology Key Laboratory of Precision Diagnosis and Treatment for Hepatobiliary and Pancreatic Tumor of Zhejiang ProvinceFirst Affliated HospitalSchool of MedicineZhejiang UniversityHangzhou 310058China

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 β 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 β 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 β cell reduction and immune cell accumulation. As IPR is not based on calorie restriction and is highly effective in glycemic control and β cell protection, it has promising translational potential in the future.

关键词： Nutritional intervention Diabetes intervention Protein restriction Islets scRNA-seq

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