Curcumin improves high glucose-induced INS-1 cell insulin resistance via activation of insulin signaling

Song, Zhenyuan; Wang, Huan; Zhu, Lin; Mingbao, Han; Gao, Yuan; Du, Yu; Wen, Yiping

doi:10.1039/c4fo00608a

Cited by 34 publications

(26 citation statements)

References 39 publications

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“…Treatment of INS-1 cells with curcumin for 24 h resulted in increased glucose-induced insulin secretion [111]. Curcumin treatment increased GLUT2 and insulin mRNA, tyrosine phosphorylation of InsR and IRS-1.…”

Section: Effects Of Curcumin: In Vitro Pancreatic Cell Studiesmentioning

confidence: 90%

“…In addition, curcumin treatment significantly increased high glucose treated phosphorylated PI3Kp85 and Akt protein levels and increased the association of PI3K to IRS1. Curcumin treatment significantly increased glucokinase (GCK) and pancreatic and duodenal homeobox-1 (PDX-1) protein levels (Table 4) [111].…”

Section: Effects Of Curcumin: In Vitro Pancreatic Cell Studiesmentioning

confidence: 99%

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Antidiabetic Properties of Curcumin I: Evidence from In Vitro Studies

2020

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Type 2 diabetes mellitus (T2DM) is a growing metabolic disease characterized by insulin resistance and hyperglycemia. Current preventative and treatment strategies for T2DM and insulin resistance lack in efficacy resulting in the need for new approaches to prevent and manage/treat the disease better. In recent years, epidemiological studies have suggested that diets rich in fruits and vegetables have beneficial health effects including protection against insulin resistance and T2DM. Curcumin, a polyphenol found in turmeric, and curcuminoids have been reported to have antioxidant, anti-inflammatory, hepatoprotective, nephroprotective, neuroprotective, immunomodulatory and antidiabetic properties. The current review (I of II) summarizes the existing in vitro studies examining the antidiabetic effects of curcumin, while a second (II of II) review summarizes evidence from existing in vivo animal studies and clinical trials focusing on curcumin’s antidiabetic properties.

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Section: Effects Of Curcumin: In Vitro Pancreatic Cell Studiesmentioning

confidence: 90%

Section: Effects Of Curcumin: In Vitro Pancreatic Cell Studiesmentioning

confidence: 99%

Antidiabetic Properties of Curcumin I: Evidence from In Vitro Studies

2020

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“…The cytotoxicity of OA against the HepG2 cells was assessed by the MTT assay. The MTT viability assay was described previously [ 19 ]. Briefly, HepG2 cells were plated in 96-well plates at 1 × 10 5 cells per well.…”

Section: Methodsmentioning

confidence: 99%

Oleanolic Acid Attenuates Insulin Resistance via NF-κB to Regulate the IRS1-GLUT4 Pathway in HepG2 Cells

Han

Bei

et al. 2015

Evidence-Based Complementary and Alternative Medicine

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The aim of our study is to elucidate the mechanisms of oleanolic acid (OA) on insulin resistance (IR) in HepG2 cells. HepG2 cells were induced with FFA as the insulin resistance model and were treated with OA. Then the glucose content and the levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were analyzed. Moreover, protein expression of nuclear factor kappa B (NF-κB), insulin receptor substrate 1(IRS1), and glucose transporter 4 (GLUT4) in cells treated with OA were measured by Western blot analysis. Additionally, IRS1 protein expression exposed to OA was detected after using pyrrolidine dithiocarbamate (PDTC).Our results revealed that OA decreased the glucose content in HepG2 cells in vitro. Moreover, OA reduced the levels of TNF-α and IL-6 and upregulated IRS1 and GLUT4 protein expression. Furthermore, OA also reduced NF-κB protein expression in insulin-resistant HepG2 cells. After blocking NF-κB, the expression of IRS1 protein had no obvious changes when treated with OA. OA attenuated insulin resistance and decreased the levels of TNF-α and IL-6. Meanwhile, OA decreased NF-κB protein expression and upregulated IRS1 and GLUT4 protein expression. Therefore, regulating the IRS1-GLUT4 pathway via NF-κB was the underlying mechanism of OA on insulin resistance.

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“…I nsulin signa ling pathways, for exa mple the IR/IRS/PI3K/AKT signaling pathway, are important in regulating the expression of GLUT2 (42)(43)(44) and GSK-3 (7,45,46). When insulin binds to IR, the intrinsic tyrosine kinase activity of IR is activated.…”

mentioning

confidence: 99%

3-Deoxyglucosone induces insulin resistance by impairing insulin signaling in HepG2 cells

Liang

Wang

Song

et al. 2016

Molecular Medicine Reports

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3-Deoxyglucosone (3DG), a highly reactive dicarbonyl intermediate generated during glycation, has been confirmed to be markedly elevated in the plasma of patients with diabetes. Our previous study found that there is an association between increasing accumulation of plasma 3DG and impaired glucose regulation in non-diabetic seniors (females, >50 years old; males, >55 years old). It was also found that 3DG led to impaired plasma glucose homeostasis in healthy mice, however, the mechanisms underlying the deleterious effect of 3DG in diabetes remain to be fully elucidated. The present study aimed to investigate the ability of 3DG to cause hepatic insulin resistance in a cell model by assessing glucose uptake and glycogen content. In addition, the molecular signaling events, including the phosphoinositide 3‑kinase (PI3K)/AKT/glucose transporter 2 (GLUT2) and PI3K/AKT/glycogen synthase kinase‑3 (GSK‑3) pathways, which affect hepatic insulin resistance, were further investigated using Western blot analysis. The results showed that 3DG (10‑300 ng/ml) had no significant effect on HepG2 cell viability, however, the viability of the HepG2 cells decreased with exposure to concentrations of 500 and 1,000 ng/ml. Treatment with non‑cytotoxic 3DG concentrations resulted in decreased uptake of glucose and glycogen content with insulin stimulation, but not under basal conditions. The insulin‑induced expression of GLUT2 and p‑GSK‑3 were eliminated by 3DG (80 and 300 ng/ml), in addition to inhibiting the phosphorylation of downstream effectors of the insulin signaling pathway, including insulin receptor substrate 1, PI3K and AKT. In conclusion, the findings of the present study indicated that the addition of exogenous 3DG directly contributed to the induction of insulin resistance by impairing insulin signaling in the HepG2 cells, which suggested that 3DG may be involved in worsening of the diabetic condition.

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Curcumin improves high glucose-induced INS-1 cell insulin resistance via activation of insulin signaling

Cited by 34 publications

References 39 publications

Antidiabetic Properties of Curcumin I: Evidence from In Vitro Studies

Antidiabetic Properties of Curcumin I: Evidence from In Vitro Studies

Oleanolic Acid Attenuates Insulin Resistance via NF-κB to Regulate the IRS1-GLUT4 Pathway in HepG2 Cells

3-Deoxyglucosone induces insulin resistance by impairing insulin signaling in HepG2 cells

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