Ginsenoside CK improves skeletal muscle insulin resistance by activating DRP1/PINK1-mediated mitophagy

Li, Weili; Li, Haiyang; Zheng, Lujuan; Xia, Jing; Yang, Xiaoxuan; Men, Shuhan; Yuan, Ye; Fan, Yuying

doi:10.1039/d2fo02026b

Cited by 12 publications

(11 citation statements)

References 51 publications

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“…55 Fan et al found that ginsenoside CK improved skeletal muscle insulin resistance by activating Pink1/Parkin-induced mitophagy and restoring Pink1/Parkin-enhanced autophagy flow. 56 In our previous study, we determined that linolenic acid ameliorated mitochondrial function in C. elegans with sarcopenia by inducing Pink1/Parkin-mediated mitochondrial autophagy. 57 In this study, we report that GA, EA, and NA promoted mitophagy by mediating the LC3-I to LC3-II transition, elevating the expression of ATG5 and decreasing the expression of p62 via enhancement of the Pink1/Parkin pathway in oxaliplatin-induced RSC96 cells.…”

Section: Discussionmentioning

confidence: 98%

Acer truncatum Bunge seed oil ameliorated oxaliplatin-induced demyelination by improving mitochondrial dysfunction via the Pink1/Parkin mitophagy pathway

Cheng,

Wang,

Guo

et al. 2024

Food Funct.

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Section: Discussionmentioning

confidence: 98%

Acer truncatum Bunge seed oil ameliorated oxaliplatin-induced demyelination by improving mitochondrial dysfunction via the Pink1/Parkin mitophagy pathway

Cheng,

Wang,

Guo

et al. 2024

Food Funct.

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“…96 Additionally, ginsenoside compound K (CK), a primary active compound in ginseng, increases insulin sensitivity and alleviates IR by stimulating mitophagy in the skeletal muscle of db/db mice. 97 Moreover, the promotion of autophagy via the SIRT1forkhead box transcription factor O1 signalling pathway has been shown to alleviate abnormal lipid metabolism and attenuate IR in the skeletal muscle of Zucker diabetic fatty rats. 98 These findings underscore the significance of a properly regulated autophagic activity in enhancing insulin sensitivity and balancing glucolipid metabolism within muscle tissues.…”

Section: Skeletal Musclementioning

confidence: 99%

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

Yang,

Ding,

Chen

et al. 2024

Diabetes Metabolism Res

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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 β‐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.

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“…Extensive research has shown that mitophagy can improve MQC by increasing ROS production and inhibiting the inflammatory response in adipocytes, thereby inhibiting hepatic IR and steatosis 8,43 . A recent study found that ginsenoside CK could activate mitophagy in skeletal muscle through the DRP1/PINK1 pathway to maintain MQC, thereby reducing IR in diabetic mice 44 . In brief, mitophagy can exert its inhibitory effects in IR by maintaining MQC, promoting oxidative stress and inhibiting inflammatory responses, but there are still few studies on the related molecular mechanisms, and a large number of experiments are needed to verify them.…”

Section: Mitophagy In Msmentioning

confidence: 99%

Mitophagy in metabolic syndrome

Miao

Han

Liu

2023

J of Clinical Hypertension

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Metabolic syndrome (MS), a chronic and non‐communicable pathological condition, is characterized by a constellation of clinical manifestations including insulin resistance, abdominal adiposity, elevated blood pressure, and perturbations in lipid metabolism. The prevalence of MS has increased dramatically in both developed and developing countries and has now become a truly global problem. Excessive energy intake and concomitant obesity are the main drivers of this syndrome. Mitophagy, in which cells degrade damaged mitochondria through a selective form of autophagy, assumes a crucial position in the regulation of mitochondrial integrity and maintenance. Abnormal mitochondrial quality could result in a spectrum of pathological conditions related to metabolic dysfunction, including metabolic syndrome, cardiovascular ailments, and neoplasms. Recently, there has been a proliferation of research pertaining to the process of mitophagy in the context of MS, and there are various regulatory pathways in MS, including pathways like the ubiquitin‐dependent mechanism and receptor‐mediated mechanisms, among others. Furthermore, studies have uncovered that the process of mitophagy serves a defensive function in the advancement of Metabolic Syndrome, and inhibition of mitophagy exacerbates the advancement of MS. As a result, the regulation of mitophagy holds great promise as a therapeutic approach in the management of Metabolic Syndrome. In this comprehensive analysis, the authors present a synthesis of the diverse regulatory pathways involved in mitophagy in the context of Metabolic Syndrome, as well as its modes of action in metabolic disorders implicated in the development of MS, Including obesity, insulin resistance (IR), and type 2 diabetes mellitus (T2DM), offering novel avenues for the prophylaxis and therapeutic management of MS.

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Ginsenoside CK improves skeletal muscle insulin resistance by activating DRP1/PINK1-mediated mitophagy

Abstract: Skeletal muscle insulin resistance is the main cause of type 2 diabetes, and mitochondria play a key role. Ginsenoside CK is main active compound of ginseng with a variety of...

Cited by 12 publications

References 51 publications

Acer truncatum Bunge seed oil ameliorated oxaliplatin-induced demyelination by improving mitochondrial dysfunction via the Pink1/Parkin mitophagy pathway

Acer truncatum Bunge seed oil ameliorated oxaliplatin-induced demyelination by improving mitochondrial dysfunction via the Pink1/Parkin mitophagy pathway

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

Mitophagy in metabolic syndrome

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