<i>Zanthoxylum</i> alkylamides ameliorate protein metabolism in type 2 diabetes mellitus rats by regulating multiple signaling pathways

Wei, Xunyu; Yang, Bing; Chen, Xuhui; Wen, Leyan; Kan, Jianquan

doi:10.1039/d0fo02695f

Cited by 20 publications

(12 citation statements)

References 51 publications

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“…AMPK, mainly expressed in the liver and muscle, plays important roles in energy and carbohydrate metabolism . As reported, AMPK activation promotes the expression of glucose transporter proteins and glucose uptake and utilization, further improving energy metabolism and inhibiting insulin resistance . Hepatic AMPK activation is often accompanied by reduction in hepatic glucose production .…”

Section: Discussionmentioning

confidence: 97%

“…29 As reported, AMPK activation promotes the expression of glucose transporter proteins and glucose uptake and utilization, further improving energy metabolism and inhibiting insulin resistance. 30 Hepatic AMPK activation is often accompanied by reduction in hepatic glucose production. 31 This may be because of the AMPK-mediated suppression of hepatic gluconeogenesis.…”

Section: ■ Discussionmentioning

confidence: 99%

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Lactobacillus acidophilus NX2-6 Improved High-Fat Diet-Induced Glucose Metabolism Disorder Independent of Promotion of Insulin Secretion in Mice

Tang

Cao

Zhao

et al. 2021

J. Agric. Food Chem.

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High-fat diet (HFD) contributes to metabolic inflammation and glucose metabolism disorder, thereby resulting in the pathogenesis of metabolic syndrome. Accumulating evidence has revealed that some probiotics could improve HFD-induced metabolic inflammation and glucose metabolism disorder. Our previous study has discovered that Lactobacillus acidophilus NX2-6 exhibited in vitro lipid-lowering, antioxidative, and anti-inflammatory activities. This study mainly investigated whether L. acidophilus NX2-6 improved HFD-induced glucose metabolism disorder. The results exhibited that L. acidophilus NX2-6 effectively reduced blood glucose levels and improved glucose tolerance by activating the insulin signaling pathway, promoting glucose uptake, glycolysis, and intestinal gluconeogenesis and suppressing hepatic gluconeogenesis, independent of regulation of glycogen synthesis in the liver and muscle. Enhanced insulin sensitivity was associated with L. acidophilus NX2-6-mediated suppression of inflammatory cascades in the target organs. Meanwhile, L. acidophilus NX2-6 also improved hepatic energy metabolism via the FGF21/AMPKα/PGC-1α/NRF1 pathway. However, L. acidophilus NX2-6 did not affect apoptosis, pyroptosis, inflammation, and endoplasmic reticulum stress in the pancreas of HFD-fed mice. In conclusion, our results indicated that L. acidophilus NX2-6 improved glucose metabolism disorder through enhancing insulin sensitivity, suppressing metabolic inflammation, and promoting energy expenditure.

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Section: Discussionmentioning

confidence: 97%

Section: ■ Discussionmentioning

confidence: 99%

Lactobacillus acidophilus NX2-6 Improved High-Fat Diet-Induced Glucose Metabolism Disorder Independent of Promotion of Insulin Secretion in Mice

Tang

Cao

Zhao

et al. 2021

J. Agric. Food Chem.

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“…Multiple studies have revealed the role of Akt/mTOR signaling in regulating β-cell function (Leibowitz et al, 2009;Xie & Herbert, 2012;Yin et al, 2017). The Akt/mTOR pathway has been considered a target for T2DM therapy in recent years (Wei et al, 2021;Xu et al, 2021). the PI3K/Akt pathway in pulmonary arterial hypertension and regulated the proliferation and migration of pulmonary artery smooth muscle cells (Hu et al, 2021b).…”

Section: Discussionmentioning

confidence: 99%

“…Multiple studies have revealed the role of Akt/mTOR signaling in regulating β‐cell function (Leibowitz et al, 2009; Xie & Herbert, 2012; Yin et al, 2017). The Akt/mTOR pathway has been considered a target for T2DM therapy in recent years (Wei et al, 2021; Xu et al, 2021). Furthermore, studies have indicated that TRIM32 modulates the Akt/mTOR pathway in multiple diseases.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of TRIM32 promotes pancreatic β‐cell autophagic cell death through Akt/mTOR pathway under high glucose conditions

Wan

Wang

et al. 2022

Cell Biology International

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Type 2 diabetes mellitus (T2DM) is a growing worldwide epidemic and is characterized by progressive pancreatic β-cell dysfunction and insulin resistance. Tripartite motif protein 32 (TRIM32) belongs to the TRIM family protein and has been shown to be involve in insulin resistance in skeletal muscle and the liver. However, the effect of TRIM32 on pancreatic β-cell dysfunction and its mechanism remains unknown. In the current study, we found that serum TRIM32 concentrations of T2DM in patients were significantly elevated compared to those in healthy controls, which indicated that TRIM32 might be used as a diagnostic biomarker in T2DM patients. In INS-1 cells, exposure to high glucose (HG) conditions caused a significant elevation in TRIM32 expression and TRIM32 was located in the nucleus. Overexpression of TRIM32 in INS-1 cells exacerbated the effects of HG-induced autophagy and impaired insulin secretion. In contrast, the silencing of TRIM32 produced the opposite effect. Furthermore, TRIM32 overexpression decreased the phosphorylation levels of Akt and mTOR under HG conditions. However, the activation of Akt/mTOR by MHY1485 reversed the effects of TRIM32 on HG-treated INS-1 cells. Collectively, the present results suggested that TRIM32 participates in the development of T2DM by modulating autophagic cell death and insulin secretion, which might occur through the Akt/mTOR pathway. Thus, TRIM32 might be a promising target in T2DM therapy.

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“…The weight of the mice was recorded every week. The preliminary studies of this project showed that the intragastric dose of 4~12 mg/kg·bw had an effect on lipids, blood glucose, and protein, among which 8 mg/kg·bw had a significant effect on lipid, sugar, and protein metabolism in mice [ 16 , 19 , 20 ]. Therefore, the intragastric dose in this study was based on the results of previous studies.…”

Section: Methodsmentioning

confidence: 99%

Effects of Hydroxy-Alpha-Sanshool on Intestinal Metabolism in Insulin-Resistant Mice

Zhu

et al. 2022

Foods

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To explore the hydroxy-alpha-sanshool (HAS) effects on the intestinal metabolites of insulin-resistant mice, the blank group (BG), model group (MG), and HAS dose group (DG) were designed. The insulin resistance (IR) model was induced through streptozotocin (STZ) combined with a high-fat and high-sugar diet. Based on the availability of the model, the HAS dose was given by gavage for 28 days. The determination of cecum and key serum indexes was made, including the contents of insulin (INS), triglycerides (TG), total cholesterol (TC), glycosylated serum protein (GSP), and glycosylated hemoglobin (GHb). The changes in gut microbiota and metabolites in cecal contents were detected by 16S rRNA gene amplicon sequencing and UPLC/HRMS technology, respectively. The results that the levels of GSP, GHb, TG, and TC were significantly increased; this was not the case for INS; or for the changes in the gut microbiota and metabolites in MG. However, the intervention of HAS effectively reversed these changes, for instance, it decreased levels of GSP, GHb, TG, TC, and alterations of metabolite composition for linoleic acid and tyrosine metabolism and recovered trends of declining species diversity and richness of the gut microbiota in MG. It was indicated that HAS alleviated IR by regulating the gut microbiota and metabolites and affecting lipid and amino acid metabolism pathways.

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Zanthoxylum alkylamides ameliorate protein metabolism in type 2 diabetes mellitus rats by regulating multiple signaling pathways

Abstract: Type 2 diabetes mellitus (T2DM) can easily induce insulin resistance (IR) in skeletal muscle, causing protein metabolism disorder and inflammation. The present study aimed to investigate whether Zanthoxylum alkylamides...

Cited by 20 publications

References 51 publications

Lactobacillus acidophilus NX2-6 Improved High-Fat Diet-Induced Glucose Metabolism Disorder Independent of Promotion of Insulin Secretion in Mice

Lactobacillus acidophilus NX2-6 Improved High-Fat Diet-Induced Glucose Metabolism Disorder Independent of Promotion of Insulin Secretion in Mice

Overexpression of TRIM32 promotes pancreatic β‐cell autophagic cell death through Akt/mTOR pathway under high glucose conditions

Effects of Hydroxy-Alpha-Sanshool on Intestinal Metabolism in Insulin-Resistant Mice

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