PMID- 38287719 OWN - NLM STAT- MEDLINE DCOM- 20240131 LR - 20240206 IS - 1520-7560 (Electronic) IS - 1520-7552 (Linking) VI - 40 IP - 1 DP - 2024 Jan TI - The role of autophagy in insulin resistance and glucolipid metabolism and potential use of autophagy modulating natural products in the treatment of type 2 diabetes mellitus. PG - e3762 LID - 10.1002/dmrr.3762 [doi] AB - Type 2 diabetes mellitus (T2DM) is a severe, long-term condition characterised by disruptions in glucolipid and energy metabolism. Autophagy, a fundamental cellular process, serves as a guardian of cellular health by recycling and renewing cellular components. To gain a comprehensive understanding of the vital role that autophagy plays in T2DM, we conducted an extensive search for high-quality publications across databases such as Web of Science, PubMed, Google Scholar, and SciFinder and used keywords like 'autophagy', 'insulin resistance', and 'type 2 diabetes mellitus', both individually and in combinations. A large body of evidence underscores the significance of activating autophagy in alleviating T2DM symptoms. An enhanced autophagic activity, either by activating the adenosine monophosphate-activated protein kinase and sirtuin-1 signalling pathways or inhibiting the mechanistic target of rapamycin complex 1 signalling pathway, can effectively improve insulin resistance and balance glucolipid metabolism in key tissues like the hypothalamus, skeletal muscle, liver, and adipose tissue. Furthermore, autophagy can increase beta-cell mass and functionality in the pancreas. This review provides a narrative summary of autophagy regulation with an emphasis on the intricate connection between autophagy and T2DM symptoms. It also discusses the therapeutic potentials of natural products with autophagy activation properties for the treatment of T2DM conditions. Our findings suggest that autophagy activation represents an innovative approach of treating T2DM. CI - (c) 2024 John Wiley & Sons Ltd. FAU - Yang, Xiaoxue AU - Yang X AD - School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China. FAU - Ding, Wenwen AU - Ding W AD - School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China. FAU - Chen, Ziyi AU - Chen Z AD - School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China. FAU - Lai, Kaiyi AU - Lai K AD - School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China. FAU - Liu, Ying AU - Liu Y AUID- ORCID: 0000-0002-0543-0099 AD - School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China. LA - eng PT - Journal Article PT - Review PL - England TA - Diabetes Metab Res Rev JT - Diabetes/metabolism research and reviews JID - 100883450 RN - 0 (Insulin) RN - 0 (Biological Products) SB - IM MH - Humans MH - *Diabetes Mellitus, Type 2/drug therapy/metabolism MH - *Insulin Resistance MH - Insulin/therapeutic use MH - *Biological Products/therapeutic use MH - Autophagy OTO - NOTNLM OT - autophagy OT - cell metabolism OT - insulin resistance OT - natural products OT - type 2 diabetes mellitus EDAT- 2024/01/30 06:42 MHDA- 2024/01/31 06:43 CRDT- 2024/01/30 02:14 PHST- 2023/11/19 00:00 [revised] PHST- 2023/09/06 00:00 [received] PHST- 2023/11/30 00:00 [accepted] PHST- 2024/01/31 06:43 [medline] PHST- 2024/01/30 06:42 [pubmed] PHST- 2024/01/30 02:14 [entrez] AID - 10.1002/dmrr.3762 [doi] PST - ppublish SO - Diabetes Metab Res Rev. 2024 Jan;40(1):e3762. doi: 10.1002/dmrr.3762.