Effect of trivalent chromium on erythropoietin production and the prevention of insulin resistance in HepG2 cells

Polysaccharides are key bioactive compounds in lotus plumule tea, but their anti-diabetes activities remain unclear. The purpose of this study was to investigate the prebiotic activities of a novel polysaccharide fraction from the Nelumbo nucifera lotus plumule, and to examine its regulation of glucose metabolism in insulin-resistant HepG2 cells. The N. nucifera polysaccharide (NNP) was purified after discoloration, hot water extraction, ethanol precipitation, and DEAE-cellulose chromatography to obtain purified polysaccharide fractions (NNP-2). Fourier transform infrared spectroscopy was used to analyze the main structural characteristics and functional group of NNP-2. Physicochemical characterization indicated that NNP-2 had a molecular weight of 110.47 kDa and consisted of xylose, glucose, fructose, galactose, and fucose in a molar ratio of 33.4:25.7:22.0:10.5:8.1. The prebiotic activity of NNP-2 was demonstrated in vitro using Lactobacillus and Bifidobacterium. Furthermore, NNP-2 showed bioactivity against α-glucosidase (IC50 = 97.32 µg/mL). High glucose-induced insulin-resistant HepG2 cells were used to study the effect of NNP-2 on glucose consumption, and the molecular mechanism of the insulin transduction pathway was studied using RT-qPCR. NNP-2 could improve insulin resistance by modulating the IRS1/PI3K/Akt pathway in insulin-resistant HepG2 cells. Our data demonstrated that the Nelumbo nucifera polysaccharides are potential sources for nutraceuticals, and we propose functional food developments from the bioactive polysaccharides of N. nucifera for the management of diabetes.

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Loureirin B attenuates insulin resistance in HepG2 cells by regulating gluconeogenesis signaling pathway

European Journal of Pharmacology ◽

10.1016/j.ejphar.2021.174481 ◽

2021 ◽

pp. 174481

Author(s):

Yanting Ding ◽

Sijing Xia ◽

Haowen Fang ◽

Bing Niu ◽

Qin Chen

Keyword(s):

Insulin Resistance ◽

Signaling Pathway ◽

Hepg2 Cells ◽

Loureirin B

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PKM2 aggravates palmitate-induced insulin resistance in HepG2 cells via STAT3 pathway

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2017.08.025 ◽

2017 ◽

Vol 492 (1) ◽

pp. 109-115 ◽

Cited By ~ 4

Author(s):

Ling Chen ◽

Zhuqi Tang ◽

Xiaohua Wang ◽

Hong Ma ◽

Dandan Shan ◽

...

Keyword(s):

Insulin Resistance ◽

Hepg2 Cells ◽

Stat3 Pathway

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(‐)‐Epigallocatechin‐3‐gallate Ameliorates Insulin Resistance and Mitochondrial Dysfunction in HepG2 Cells: Involvement of Bmal1

Molecular Nutrition & Food Research ◽

10.1002/mnfr.201700440 ◽

2017 ◽

Vol 61 (12) ◽

pp. 1700440 ◽

Cited By ~ 14

Author(s):

Yashi Mi ◽

Guoyuan Qi ◽

Yuqi Gao ◽

Runnan Li ◽

Yiwen Wang ◽

...

Keyword(s):

Insulin Resistance ◽

Mitochondrial Dysfunction ◽

Hepg2 Cells

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Hypoglycemic Effect of Vitexin in C57BL/6J Mice and HepG2 Models

Journal of Food Quality ◽

10.1155/2021/5535476 ◽

2021 ◽

Vol 2021 ◽

pp. 1-7

Author(s):

Weidong Xu ◽

Jiayao Li ◽

Weipeng Qi ◽

Ye Peng

Keyword(s):

Insulin Resistance ◽

Body Weight ◽

Weight Gain ◽

Blood Glucose ◽

Glucose Uptake ◽

Lipid Content ◽

Hepg2 Cells ◽

Body Weight Gain ◽

Tnf Α ◽

Hepatic Lipid Content

Apigenin-8-C-glucoside (vitexin), a natural phytochemical contained in hawthorn, has been reported to have versatile beneficial bioactivities, such as antioxidation, anticancer property, and adipogenesis inhibition. The present research aimed to determine the influence of vitexin on insulin resistance elicited by HFD in mice and HepG2 cells. Vitexin markedly alleviated body weight gain and improved glucose and insulin intolerance induced by HFD. Vitexin partially normalized blood glucose, cholesterol, TNF-α, and hepatic lipid content. Moreover, vitexin recovered the reduced glucose uptake induced by glucosamine. The present results indicate that vitexin prevents HFD-induced insulin resistance.

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The conception of the probable role of the biological active chromium in the emergence of insulin resistance and alimentary obesity

International Professional Journal Medicine ◽

10.31082/1728-452x-2021-223-1-34-38 ◽

2021 ◽

Vol 1 (223) ◽

pp. 34-38

Author(s):

Bolat Abishev ◽

Keyword(s):

Insulin Resistance ◽

Structural Organization ◽

Redox State ◽

Metabolic Response ◽

Essential Element ◽

Insulin Receptors ◽

Trivalent Chromium ◽

Manual Search ◽

Alimentary Obesity ◽

Search And Selection

The conception of probable alimentary chromium role in connection with metabolic reasons emergence of insulin resistance in the alimentary obesity and type 2 diabetes is represented. The violation of insulin receptors structural organization and conformation with these pathological conditions in connection with redox states of chromium is supposed. Based on information from general chemistry and chromium metabolism, higher biological activity of hexavalent chromium when compared to the activity of trivalent chromium is assumed in insulin-resistant conditions. Aim. To analyze the literature data on the a supposed participation of chromium in food and chromium nutraceuticals in connection with insulin resistance at the metabolic level. Material and methods. The analysis of the literature was carried out by the method of manual search and selection of the most important and significant for the analyzed issue monographs and articles up to 60 years in depth. The search criteria were works directly related to the association of food chromium with the insulin-dependent metabolic response of cells and the activity of insulin receptors. No works published over the past 10 years that introduce principled novelty and are of principled importance for the present problem have not been identified. Results and discussion. The concept of the supposed participation of chromium as an essential element in connection with the metabolic reasons for the formation of insulin resistance and the structural organization of insulin receptors depending on the redox state of chromium is presented. Keywords: hexavalent and trivalent chromium, insulin resistance, redox state, insulin receptor, alimentary obesity, diabetes.

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Visfatin Induces Inflammation and Insulin Resistance via the NF-κB and STAT3 Signaling Pathways in Hepatocytes

Journal of Diabetes Research ◽

10.1155/2019/4021623 ◽

2019 ◽

Vol 2019 ◽

pp. 1-11 ◽

Cited By ~ 15

Author(s):

Yu Jung Heo ◽

Sung-E Choi ◽

Ja Young Jeon ◽

Seung Jin Han ◽

Dae Jung Kim ◽

...

Keyword(s):

Insulin Resistance ◽

Signaling Pathways ◽

Western Blotting ◽

Insulin Signaling ◽

Proinflammatory Cytokine ◽

Hepg2 Cells ◽

Molecular Mechanisms ◽

Immunocytochemical Staining ◽

Mrna Levels ◽

Rt Pcr

Background. It has been suggested that visfatin, which is an adipocytokine, exhibits proinflammatory properties and is associated with insulin resistance. Insulin resistance and inflammation are the principal pathogeneses of nonalcoholic fatty liver disease (NAFLD), but the relationship, if any, between visfatin and NAFLD remains unclear. Here, we evaluated the effects of visfatin on hepatic inflammation and insulin resistance in HepG2 cells and examined the molecular mechanisms involved. Methods. After treatment with visfatin, the inflammatory cytokines IL-6, TNF-α, and IL-1β were assessed by real-time polymerase chain reaction (RT-PCR) and immunocytochemical staining in HepG2 cells. To investigate the effects of visfatin on insulin resistance, we evaluated insulin-signaling pathways, such as IR, IRS-1, GSK, and AKT using immunoblotting. We assessed the intracellular signaling molecules including STAT3, NF-κB, IKK, p38, JNK, and ERK by western blotting. We treated HepG2 cells with both visfatin and either AG490 (a JAK2 inhibitor) or Bay 7082 (an NF-κB inhibitor); we examined proinflammatory cytokine mRNA levels using RT-PCR and insulin signaling using western blotting. Results. In HepG2 cells, visfatin significantly increased the levels of proinflammatory cytokines, reduced the levels of proteins (e.g., phospho-IR, phospho-IRS-1 (Tyr612), phospho-AKT, and phospho-GSK-3α/β) involved in insulin signaling, and increased IRS-1 S307 phosphorylation compared to controls. Interestingly, visfatin increased the activities of the JAK2/STAT3 and IKK/NF-κB signaling pathways but not those of the JNK, p38, and ERK pathways. Visfatin-induced inflammation and insulin resistance were regulated by JAK2/STAT3 and IKK/NF-κB signaling; together with AG490 or Bay 7082, visfatin significantly reduced mRNA levels of IL-6, TNF-α and IL-1β and rescued insulin signaling. Conclusion. Visfatin induced proinflammatory cytokine production and inhibited insulin signaling via the STAT3 and NF-κB pathways in HepG2 cells.

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Wu-Mei-Wan Reduces Insulin Resistance via Inhibition of NLRP3 Inflammasome Activation in HepG2 Cells

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2017/7283241 ◽

2017 ◽

Vol 2017 ◽

pp. 1-10 ◽

Cited By ~ 5

Author(s):

Xueping Yang ◽

Lingli Li ◽

Ke Fang ◽

Ruolan Dong ◽

Jingbin Li ◽

...

Keyword(s):

Insulin Resistance ◽

Insulin Receptor ◽

Insulin Signaling ◽

Nlrp3 Inflammasome ◽

Hepg2 Cells ◽

Glucose Transporter ◽

Interleukin 1 ◽

Serine Phosphorylation ◽

Inflammasome Activation ◽

Glucose Consumption Rate

Wu-Mei-Wan (WMW) is a Chinese herbal formula used to treat type 2 diabetes. In this study, we aimed to explore the effects and mechanisms of WMW on insulin resistance in HepG2 cells. HepG2 cells were pretreated with palmitate (0.25 mM) to impair the insulin signaling pathway. Then, they were treated with different doses of WMW-containing medicated serum and stimulated with 100 nM insulin. Results showed that palmitate could reduce the glucose consumption rate in HepG2 cells and impair insulin signaling related to phosphorylation of insulin receptor (IR) and insulin receptor substrate-1 (IRS-1), thereby regulating the downstream signaling pathways. However, medicated serum of WMW restored impaired insulin signaling, upregulated the expression of phospho-IR (pIR), phosphatidylinositol 3-kinase p85 subunit, phosphoprotein kinase B, and glucose transporter 4, and decreased IRS serine phosphorylation. In addition, it decreased the expression of interleukin-1β and tumor necrosis factor-α, which are the key proinflammatory cytokines involved in insulin resistance; besides, it reduced the expression of NLRP3 inflammasome. These results suggested that WMW could alleviate palmitate-induced insulin resistance in HepG2 cells via inhibition of NLRP3 inflammasome and reduction of proinflammatory cytokine production.

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