Serum levels of acetylcholinesterase in metabolic syndrome

Hristova, Mariyana G.

doi:10.14748/adipo.v7.1561

Cited by 2 publications

(3 citation statements)

References 14 publications

(12 reference statements)

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“…Autonomic imbalance is closely associated with obesity and metabolic syndrome, [24,25] and several studies have analyzed the effect of overactivated sympathetic nerves on hepatic steatosis and fibrosis. [15,26] We detected elevated AChE levels in the hepatic tissues of the HFD-fed mice, which is consistent with the observations of Hristova [17] and Rao et al [18] ACh is the principal neurotransmitter of dysfunction can attenuate metabolic disorder. [27] Jung Dae Kim and colleagues showed that altering sympathetic nerve activity in mice with PEGyAMPH, a new derivative of amphetamine, resulted in weight loss via lipolysis and thermogenesis.…”

Section: Discussionsupporting

confidence: 91%

“…Autonomic imbalance is closely associated with obesity and metabolic syndrome, [ 24,25 ] and several studies have analyzed the effect of overactivated sympathetic nerves on hepatic steatosis and fibrosis. [ 15,26 ] We detected elevated AChE levels in the hepatic tissues of the HFD‐fed mice, which is consistent with the observations of Hristova [ 17 ] and Rao et al [ 18 ] ACh is the principal neurotransmitter of the vagus nerve, and a decreased level of ACh indicates depressed vagus nerve activity. Studies show that regulation of autonomic dysfunction can attenuate metabolic disorder.…”

Section: Discussionsupporting

confidence: 91%

“…[13,14] For instance, the sympathetic nerve activity increases by two fold in mice after 10 weeks of high fat diet (HFD) intake, [15] and hepatic vagotomy has been shown to worsen methionine-choline deficient diet-induced steatohepatitis. [16] In addition, serum acetylcholinesterase (AChE) levels are increased during obesity and diabetes, [17,18] indicating that AChE is also a potential target for the prevention of obesity-induced liver diseases. In a previous study, we showed that the AChE inhibitor pyridostigmine (PYR) preserved cardiac function and mitochondrial homeostasis in HFD-fed mice and rats.…”

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confidence: 99%

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Pyridostigmine attenuated high‐fat‐diet induced liver injury by the reduction of mitochondrial damage and oxidative stress via α7nAChR and M3AChR

Xue,

Wu,

Guo

et al. 2024

J Biochem & Molecular Tox

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Obesity is a major cause of nonalcohol fatty liver disease (NAFLD), which is characterized by hepatic fibrosis, lipotoxicity, inflammation, and apoptosis. Previous studies have shown that an imbalance in the autonomic nervous system is closely related to the pathogenesis of NAFLD. In this study, we investigated the effects of pyridostigmine (PYR), a cholinesterase (AChE) inhibitor, on HFD‐induced liver injury and explored the potential mechanisms involving mitochondrial damage and oxidative stress. A murine model of HFD‐induced obesity was established using the C57BL/6 mice, and PYR (3 mg/kg/d) or placebo was administered for 20 weeks. PYR reduced the body weight and liver weight of the HFD‐fed mice. Additionally, the serum levels of IL‐6, TNF‐α, cholesterol, and triglyceride were significantly lower in the PYR‐treated versus the untreated mice, corresponding to a decrease in hepatic fibrosis, lipid accumulation, and apoptosis in the former. Furthermore, the mitochondrial morphology improved significantly in the PYR‐treated group. Consistently, PYR upregulated ATP production and the mRNA level of the mitochondrial dynamic factors OPA1, Drp1 and Fis1, and the mitochondrial unfolded protein response (UPRmt) factors LONP1 and HSP60. Moreover, PYR treatment activated the Keap1/Nrf2 pathway and upregulated HO‐1 and NQO‐1, which mitigated oxidative injury as indicated by decreased 8‐OHDG, MDA and H2O2 levels, and increased SOD activity. Finally, PYR elevated acetylcholine (ACh) levels by inhibiting AChE, and upregulated the α7nAChR and M3AChR proteins in the HFD‐fed mice. PYR alleviated obesity‐induced hepatic injury in mice by mitigating mitochondrial damage and oxidative stress via α7nAChR and M3AChR.

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Section: Discussionsupporting

confidence: 91%

“…Autonomic imbalance is closely associated with obesity and metabolic syndrome, [ 24,25 ] and several studies have analyzed the effect of overactivated sympathetic nerves on hepatic steatosis and fibrosis. [ 15,26 ] We detected elevated AChE levels in the hepatic tissues of the HFD‐fed mice, which is consistent with the observations of Hristova [ 17 ] and Rao et al [ 18 ] ACh is the principal neurotransmitter of the vagus nerve, and a decreased level of ACh indicates depressed vagus nerve activity. Studies show that regulation of autonomic dysfunction can attenuate metabolic disorder.…”

Section: Discussionsupporting

confidence: 91%