2022
DOI: 10.1016/j.heliyon.2022.e11529
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Regulation of the apoptosis/autophagy switch by propionic acid in ventromedial hypothalamus of rats with type 2 diabetes mellitus

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Cited by 9 publications
(12 citation statements)
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“…reported that metformin inhibited neuronal apoptosis by regulating mitochondrial homeostasis and reducing oxidative stress. [ 67 ] In venous grafts suffering from PVT deprivation, by promoting mitochondrial function, metformin may increase the expression of antioxidant enzymes and reduce the production of ROS, thereafter inhibiting apoptosis of the endothelial cell. What is more, we found that metformin increased the phosphorylation of eNOS through AMPK/mTOR in the endothelial cells, resulting in the enhanced production of NO, which further prevented the endothelial cells from ROS damage.…”
Section: Resultsmentioning
confidence: 99%
See 1 more Smart Citation
“…reported that metformin inhibited neuronal apoptosis by regulating mitochondrial homeostasis and reducing oxidative stress. [ 67 ] In venous grafts suffering from PVT deprivation, by promoting mitochondrial function, metformin may increase the expression of antioxidant enzymes and reduce the production of ROS, thereafter inhibiting apoptosis of the endothelial cell. What is more, we found that metformin increased the phosphorylation of eNOS through AMPK/mTOR in the endothelial cells, resulting in the enhanced production of NO, which further prevented the endothelial cells from ROS damage.…”
Section: Resultsmentioning
confidence: 99%
“…[66] Natrus et al reported that metformin inhibited neuronal apoptosis by regulating mitochondrial homeostasis and reducing oxidative stress. [67] In venous grafts suffering from PVT deprivation, by promoting mitochondrial function, metformin may increase the expression of antioxidant enzymes and reduce the production of ROS, thereafter inhibiting apoptosis of the endothelial cell. What is more, we found that metformin Figure 7.…”
Section: Ampk/mtor and Nf𝜿b Signaling Pathway Play Roles In Met-stent...mentioning
confidence: 99%
“…78 Autophagy defects have been identified in these IR-sensitive organs or tissues in diabetic animals, highlighting a significant correlation between autophagy dysfunction and the development of T2DM. [79][80][81][82][83] In the following section, we provide a summary and illustration of the intricate association between autophagy and T2DM (Figure 3).…”
Section: Autophagy In T2dmmentioning
confidence: 99%
“…The hypothalamus is responsible for coordinating hormonal and metabolic signals to balance food intake and energy consumption, thereby maintaining glucose homoeostasis 84 . Studies have demonstrated that promoting autophagy in the hypothalamus can alleviate IR 79 . Particularly, the neurons within the arcuate melanocortin system (AMS), such as those generating pro‐opiomelanocortin (POMC)‐derived peptides, are integral to regulate homoeostatic metabolism 85,86 .…”
Section: Autophagy In T2dmmentioning
confidence: 99%
“…13 Propionic acid can effectively counteract cell death induced by peripheral nervous system injuries in T2DM by converting nerve cell apoptosis into autophagy. 14 In addition, the pathogenesis of T2DM involves multiple gene targets in vivo , such as protein kinase B (AKT-1), glucose transporter 2 (GLUT-2), etc . AKT-1 is a serine/threonine protein kinase, it is a key signaling molecule in the process of hypoglycemic activity of insulin and highly expressed in target tissues containing insulin receptors.…”
Section: Introductionmentioning
confidence: 99%