Development of insulin resistance through sprouting of inflammatory markers during hypoxia in 3T3-L1 adipocytes and amelioration with curcumin

Priyanka, A; Shyni, G. L.; Nair, Anupama; Raj, P. Salin; Anusree, S.S.; Raghu, K.

doi:10.1016/j.ejphar.2017.07.005

Cited by 23 publications

(22 citation statements)

References 49 publications

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“…Resistin and toll-like receptor 4 (TLR-4) mRNA levels, and NF-κB p65 nuclear faction and phosphorylated JNK protein levels were reduced with curcumin treatment, suggesting reduced inflammation. Insulin sensitivity was improved with curcumin treatment, with decreased hypoxic-induced serine phosphorylation of IRS-1 and increased IRS-2 protein levels [67]. In addition, hypoxic-induced glucose uptake and GLUT1 mRNA and protein levels were reduced, while GLUT4 mRNA and protein levels were increased with curcumin treatment.…”

Section: Effects Of Curcumin: In Vitro Adipocyte Studiesmentioning

confidence: 92%

“…Treatment of 3T3-L1 adipocytes with curcumin (20 µM) for 24 h resulted in reduced hypoxic-induced inflammation and angiogenesis [67]. Curcumin treatment reduced MCP-1 and leptin levels, while adiponectin levels were increased.…”

Section: Effects Of Curcumin: In Vitro Adipocyte Studiesmentioning

confidence: 96%

“…In addition, hypoxic-induced glucose uptake and GLUT1 mRNA and protein levels were reduced, while GLUT4 mRNA and protein levels were increased with curcumin treatment. The hypoxic-induced increase in pro-angiogenic factors (MMP-2, MMP-9 and VEGF) and angiopoietin like protein 4 (Angpt4) levels were abolished with curcumin treatment, indicating improve angiogenesis ( Table 1) [67].…”

Section: Effects Of Curcumin: In Vitro Adipocyte Studiesmentioning

confidence: 99%

“…Cellular effects of curcumin on muscle and fat cellular signaling molecules. The figure was created based on the data of the studies[40,41,[43][44][45][46]57,67,73,97,98,101,102]. AKT: protein kinase B; PIP3: phosphatidylinositol-3,4,5-triphosphate; PIP2: phosphatidylinositol 4,5-bisphosphate; ERK: extracellular signal-regulated kinase; PI3K: phosphoinositide 3-kinase; IRS1: insulin receptor substrate 1; TNF-α: tumor necrosis factor-α; AMPK: AMP-activated protein kinase; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; ACC: acetyl-CoA carboxylase; PGC-1: peroxisome proliferator-activated receptor gamma co-activator 1; FFAs: free fatty acids.…”

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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 Adipocyte Studiesmentioning

confidence: 92%

Section: Effects Of Curcumin: In Vitro Adipocyte Studiesmentioning

confidence: 96%

Section: Effects Of Curcumin: In Vitro Adipocyte Studiesmentioning

confidence: 99%

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confidence: 99%

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Antidiabetic Properties of Curcumin I: Evidence from In Vitro Studies

2020

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“…After the particular treatment, the total protein was extracted in RIPA buffer , and quantified using the bicinchoninic acid protein assay kit (BCA kit; Pierce, Rockford, IL, USA). An equal amount of proteins (20 μg) were separated by 10% SDS‐PAGE and transferred to PVDF membranes using the Trans‐Blot ® Turbo™ Transfer system (Bio‐Rad, Hercules, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

High glucose induced calcium overload via impairment of SERCA/PLN pathway and mitochondrial dysfunction leads to oxidative stress in H9c2 cells and amelioration with ferulic acid

Raj

Swapna

Raghu

2019

Fundamemntal Clinical Pharma

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Oxidative stress and associated complications are the major pathological concerns of diabetic cardiomyopathy (DC). We aim to elucidate the mechanisms by which high glucose (HG) induced alteration in calcium homeostasis and evaluation of the beneficial effect of two concentrations (10 and 25 μm) of ferulic acid (FA). HG was induced in H9c2 cardiomyoblast by treating with glucose (33 mm) for 48 h, and FA was co‐treated. Intracellular calcium ([Ca2+]i) overload was found increased significantly with HG. For elucidation of mechanism, the SERCA pathway and mitochondrial integrity (transmembrane potential and permeability transition pore) were explored. Then, we assessed oxidative stress, and cell injury with brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), and lactate dehydrogenase (LDH) release. HG caused significant [Ca2+]i overload through downregulation of SERCA2/1, pPLN, and pPKA C‐α; and upregulation of PLN and PKA C‐α and alteration in the integrity of mitochondria with HG. The [Ca2+]i overload in turn caused oxidative stress via generation of reactive oxygen species, lipid peroxidation, and protein carbonylation. This resulted in cell injury which was evident with significant release of BNP, ANP, and LDH. FA co‐treatment was effective to mitigate all pathological changes caused by HG. From the overall results, we conclude that [Ca2+]i overload via SERCA pathway and altered mitochondrial integrity is the main cause for oxidative stress during HG. Based on our result, we report that FA could be an attractive nutraceutical for DC.

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