Chlorogenic acid alleviates autophagy and insulin resistance by suppressing JNK pathway in a rat model of nonalcoholic fatty liver disease

Yan, Hua; Gao, Yuan; Zhang, Ying; Wang, Huan; Liu, Guisheng; Lei, Jian-Yuan

doi:10.1007/s12038-018-9746-5

Cited by 47 publications

(28 citation statements)

References 30 publications

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“…In another experiment with the INS-1E insulin-secreting cell line and rat islets of Langerhans, stimulation of insulin secretion was observed after treatment with 50 μg/mL CA; the effect was close to that caused by 5 mM of glucose, whereas in 8.3 mM of glucose, CA significantly increased the secretion of insulin [29]. Rats exposed to a high-fat diet and administered 50 mg/kg CA for 20 weeks showed an increase in insulin secretion and an improvement in insulin resistance [30]. Also, CA treatment of both high-fat diet-induced obese mice and spontaneously obese mice reduced hyperinsulinemia and enhanced insulin sensitivity, suggesting that CA can improve obesity-related insulin resistance [31].…”

Section: Use Of Ca To Prevent and Treat Dmmentioning

confidence: 77%

Use of Chlorogenic Acid against Diabetes Mellitus and Its Complications

Yan

Zhou²,

Ke³

et al. 2020

Journal of Immunology Research

111

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Chlorogenic acid (CA) is a phenolic compound commonly found in human plant-based diets. CA is the main component of many traditional Chinese medicine preparations, and in recent years, it has been found to have hypoglycemic, hypolipidemic, anti-inflammatory, antioxidant, and other pharmacological properties. Specifically, CA relieves the effects of, and prevents, diabetes mellitus (DM). In addition, CA is also beneficial against complications arising from DM, such as diabetic nephropathy (DN), diabetic retinopathy (DR), and diabetic peripheral neuropathy (DPN). Herein, we review the use of CA in the prevention and treatment of DM and its complications, providing a background for further research and medical uses.

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Section: Use Of Ca To Prevent and Treat Dmmentioning

confidence: 77%

Use of Chlorogenic Acid against Diabetes Mellitus and Its Complications

Yan

Zhou²,

Ke³

et al. 2020

Journal of Immunology Research

111

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show abstract

“…Subsequently, we investigated the mechanisms by which DUSP12 inhibits the progression of NAFLD/NASH. Considering that DUSP12 could regulate microbial infection and cardiac hypertrophy through modulating MAPK signaling, MAPK pathways are well known to regulate metabolic dysfunction and hepatic steatosis during the pathogenesis of NAFLD . Thus, we examined whether DUSP12 could regulate MAPK signaling in hepatic steatosis.…”

Section: Resultsmentioning

confidence: 99%

Dual Specificity Phosphatase 12 Regulates Hepatic Lipid Metabolism Through Inhibition of the Lipogenesis and Apoptosis Signal–Regulating Kinase 1 Pathways

Huang

Zhang

et al. 2019

Hepatology

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Nonalcoholic fatty liver disease (NAFLD) has become the most common cause of chronic liver disease worldwide. Due to the growing economic burden of NAFLD on public health, it has become an emergent target for clinical intervention. DUSP12 is a member of the dual specificity phosphatase (DUSP) family, which plays important roles in brown adipocyte differentiation, microbial infection, and cardiac hypertrophy. However, the role of DUSP12 in NAFLD has yet to be clarified. Here, we reveal that DUSP12 protects against hepatic steatosis and inflammation in L02 cells after palmitic acid/oleic acid treatment. We demonstrate that hepatocyte specific DUSP12-deficient mice exhibit high-fat diet (HFD)-induced and high-fat high-cholesterol diet-induced hyperinsulinemia and liver steatosis and decreased insulin sensitivity. Consistently, DUSP12 overexpression in hepatocyte could reduce HFDinduced hepatic steatosis, insulin resistance, and inflammation. At the molecular level, steatosis in the absence of DUSP12 was characterized by elevated apoptosis signal-regulating kinase 1 (ASK1), which mediates the mitogenactivated protein kinase (MAPK) pathway and hepatic metabolism. DUSP12 physically binds to ASK1, promotes its dephosphorylation, and inhibits its action on ASK1-related proteins, JUN N-terminal kinase, and p38 MAPK in order to inhibit lipogenesis under high-fat conditions. Conclusion: DUSP12 acts as a positive regulator in hepatic steatosis and offers potential therapeutic opportunities for NAFLD. (Hepatology 2019;70:1099-1118). SEE EDITORIAL ON PAGE 1091N onalcoholic fatty liver disease (NAFLD) is the most common diffuse liver disease and is characterized by lipid accumulation in hepatocytes in the absence of excessive alcohol consumption. (1) The prevalence of NAFLD increases worryingly with obesity and other diseases of metabolic syndrome (MS) and is expected to be the leading cause of liver failure in the future. (2) Accumulating studies show that NAFLD not only is linked to an increased risk of liver-related mortality or morbidity

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“…plasma glucose through the modulation of adiponectin receptor signaling pathways in diabetic mice (Jin et al, 2015). It also ameliorates IR by suppressing autophagy via inhibiting the JNK pathway in a fatty liver rat model (Yan et al, 2018). Moreover, rutin can exert anti-IR activity through enhancement of insulin receptor kinase activity and glucose transporter 4 translocation (Hsu et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Edgeworthia gardneri (Wall.) Meisn. Water Extract Ameliorates Palmitate Induced Insulin Resistance by Regulating IRS1/GSK3β/FoxO1 Signaling Pathway in Human HepG2 Hepatocytes

et al. 2020

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The flower of Edgeworthia gardneri (Wall.) Meisn is commonly used in beverage products in Tibet and has potential health benefits for diabetes. However, the mechanisms underlying anti-insulin resistance (IR) action of the flower of E. gardneri are not fully understood. This study aims to investigate the effects of the water extract of the flower of E. gardneri (WEE) on IR in palmitate (PA)-exposed HepG2 hepatocytes. WEE was characterized by UPLC analysis. PA-treated HepG2 cells were selected as the IR cell model. The cell viability was determined using MTT assay. Moreover, the glucose consumption and production were measured by glucose oxidase method. The glucose uptake and glycogen content were determined by the 2-NBDG (2-deoxy-2-[(7-nitro-2,1,3-benzoxadiazol-4-yl) amino]-D-glucose) glucose uptake assay and anthrone-sulfuric acid assay, respectively. The intracellular triglyceride content was detected by oxidative enzymic method. Protein levels were examined by Western blotting. Nuclear localization of FoxO1 was detected using immunofluorescence analyses and Western blotting. The expression of FoxO1 target genes was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The viability of PA-treated HepG2 cells was concentrationdependently increased by incubation with WEE for 24 h. WEE treatment remarkably increased the consumption and uptake of glucose in PA-exposed HepG2 cells. Moreover, treatment with WEE significantly decreased the PA-induced overproduction of glucose in HepG2 cells. After exposure of HepG2 cells with PA and WEE, the glycogen content was significantly elevated. The phosphorylation and total levels of IRb, IRS1, and Akt were upregulated by WEE treatment in PA-exposed HepG2 cells. The phosphorylation of GSK3b was elevated after WEE treatment in PA-treated cells. WEE treatment also concentration-dependently downregulated the phosphorylated CREB, ERK, c-Jun, p38

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Chlorogenic acid alleviates autophagy and insulin resistance by suppressing JNK pathway in a rat model of nonalcoholic fatty liver disease

Cited by 47 publications

References 30 publications

Use of Chlorogenic Acid against Diabetes Mellitus and Its Complications

Use of Chlorogenic Acid against Diabetes Mellitus and Its Complications

Dual Specificity Phosphatase 12 Regulates Hepatic Lipid Metabolism Through Inhibition of the Lipogenesis and Apoptosis Signal–Regulating Kinase 1 Pathways

Edgeworthia gardneri (Wall.) Meisn. Water Extract Ameliorates Palmitate Induced Insulin Resistance by Regulating IRS1/GSK3β/FoxO1 Signaling Pathway in Human HepG2 Hepatocytes

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