A polyphenol rescues lipid induced insulin resistance in skeletal muscle cells and adipocytes

Gogoi, Bhaskarjyoti; Chatterjee, Priyajit; Mukherjee, Sandip; Buragohain, Alak Kumar; Bhattacharya, Samir; Dasgupta, Suman

doi:10.1016/j.bbrc.2014.08.079

Cited by 28 publications

(25 citation statements)

References 35 publications

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“…Our data together with Gogoi et al observations [30] demonstrate that HMGA1, phosphorylated by PKCε, may reside longer in the heterochromatin preferentially interacting with positively charged histones.…”

Section: Discussionsupporting

confidence: 85%

PKCε as a novel promoter of skeletal muscle differentiation and regeneration

Marcantonio

Galli

Carubbi

et al. 2015

Experimental Cell Research

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Introduction Satellite cells are muscle resident stem cells and are responsible for muscle regeneration. In this study we investigate the involvement of PKCε during muscle stem cell differentiation in vitro and in vivo. Here, we describe the identification of a previously unrecognized role for the PKCε – HMGA1 signaling axis in myoblast differentiation and regeneration processes. Methods PKCε expression was modulated in the C2C12 cell line and primary murine satellite cells in vitro, as well as in an in vivo model of muscle regeneration. Immunohistochemistry and immunofluorescence, RT-PCR and shRNA silencing techniques were used to determine the role of PKCε and HMGA1 in myogenic differentiation. Results PKCε expression increases and subsequently re-localizes to the nucleus during skeletal muscle cell differentiation. In the nucleus, PKCε blocks Hmga1 expression to promote Myogenin and Mrf4 accumulation and myoblast formation. Following in vivo muscle injury, PKCε accumulates in regenerating, centrally-nucleated myofibers. Pharmacological inhibition of PKCε impairs the expression of two crucial markers of muscle differentiation, namely MyoD and Myogenin, during injury induced muscle regeneration. Conclusion This work identifies the PKCε – HMGA1 signaling axis as a positive regulator of skeletal muscle differentiation.

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Section: Discussionsupporting

confidence: 85%

PKCε as a novel promoter of skeletal muscle differentiation and regeneration

Marcantonio

Galli

Carubbi

et al. 2015

Experimental Cell Research

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“…4 Met is a suggested candidate for lifespan extension, treatment and prevention of sedentariness damages, insulin resistance, and obesity. 31 Different mechanisms are involved in skeletal muscle's insulin resistance encountered in cases of obesity; impaired skeletal muscle microvascular responses to insulin, 32 oxidative stress caused by obesity that impairs glucose uptake low-grade inflammation and decreased IRS-1 activation. These animals showed significantly increased blood glucose, insulin total cholesterol, triglycerides and calculated HOMA-IR as noted by Sishi et al 4 and Parim et al 30 One of the most important organs responsible for glucose uptake, disposal, and storage is skeletal muscles, which account for about 75% of the whole body's glucose uptake under insulin stimulation.…”

Section: Discussionmentioning

confidence: 99%

Beneficial effects of metformin on muscle atrophy induced by obesity in rats

Hasan

Shalaby

El‐Gendy

et al. 2018

J of Cellular Biochemistry

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Aim A growing interest to understand the signaling pathways mediating obesity‐induced muscle atrophy is given. Metformin (Met) was reported to possess positive effects on preventing muscle damage and promoting muscle mass maintenance. The aim of the present study to investigate pathways involved in Met effect on obesity induced muscle atrophy. Methods Thirty adult male albino rats were assigned into two groups: normal chew diet fed group as control group (C; n = 10) and high‐fat‐diet (HFD) fed group ( n = 20). After 16 weeks, the HFD‐fed animals were subdivided into two groups; HFD group ( n = 10) and HFD fed treated with oral Met (320 mg/day) treatment (Met, n = 10) for 4 weeks. At the end of the experiment; final body weight, visceral fat weight, fasting blood glucose, insulin, lactate, total cholesterol, triglycerides were measured and calculated homeostatic model assessment insulin resistant (HOMA‐IR) for all groups. Soleus muscle weight, histopathlogical examination and expression of peroxisome proliferator‐activated receptor‐γ coactivator‐1α (PGC‐1α), forkhead box O3 (FoxO3), atrogin‐1/MAFbx, and muscle RING finger 1 (MuRF‐1) were performed. Results HFD‐fed animals showed significant increase in final body weight, visceral fat mass, fasting blood glucose, insulin, calculated HOMA‐IR, lactate, total cholesterol and triglycerides with significant decrease in soleus muscle weight, PGC‐1α and significant increase in FoxO3, atrogin‐1/MAFbx, and MuRF‐1 expression. Also, there was significant decrease in fiber diameter, myosin heavy chain (MHC) I content while collagen content and myosin heavy chain IIa were increased compared with control group. Met‐treated group showed a significant decrease in the measured parameters compared with the HFD group. It also restored the gene expression, morphometric measures and MHC composition toward normal. Conclusion The current study is the first to provide evidence that Met could ameliorate muscle atrophy in high‐fat diet induced obesity and this effect may be in part due to regulation of PGC‐1α‐FoxO3 pathway.

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“…Ferulic acid (FA), a phenolic acid commonly found in several plants, has various pharmacological effects such as antioxidant, anti‐inflammatory, and anti‐diabetic activities . A previous study using high‐fat diet (HFD)‐induced obese mouse model has shown that FA administration for 8 weeks reduced weight gain, hyperlipidaemia, oxidative stress, and inflammation in the mice .…”

Section: Introductionmentioning

confidence: 99%

“…The antihyperglycaemic activity of FA in the HFD‐induced obese mice was also reported to be mediated via the regulation of insulin secretion, inhibitions of G‐6‐Pase and PEPCK activities, and the stimulation of glucokinase activity . The FA, purified from the Hibiscus mutabilis leaf, improved the insulin resistance in L6 myotubes by activating the insulin signalling pathway in the saturated fatty acid‐induced insulin resistant condition . A recent study showed that FA reduced the gene expression of hepatic glucose transporter 2 (GLUT2) in the high‐fat and fructose‐induced type 2 diabetic rats by impairing the interaction between SREBP1c, hepatocyte nuclear factor 1 α (HNF1 α ), HNF3 β , and GLUT2 gene promoter .…”

Section: Introductionmentioning

confidence: 99%

Ferulic acid improves lipid and glucose homeostasis in high‐fat diet‐induced obese mice

Naowaboot

Piyabhan

Munkong

et al. 2016

Clin Exp Pharma Physio

101

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Ferulic acid (FA) is a plant phenolic acid that has several pharmacological effects including antihyperglycaemic activity. Thus, the objective of this study is to investigate the effect of FA on glucose and lipid metabolism in high-fat diet (HFD)-induced obese mice. Institute for Cancer Research (ICR) mice were fed a HFD (45 kcal% fat) for 16 weeks. At the ninth week of induction, the obese mice were orally administered with daily FA doses of 25 and 50 mg/kg for the next eight weeks. The results show that FA significantly reduced the elevated blood glucose and serum leptin levels, lowered the insulin resistance, and increased the serum adiponectin level. Moreover, serum lipid level, and liver cholesterol and triglyceride accumulations were also reduced. The histological examination showed clear evidence of a decrease in the lipid droplets in liver tissues and smaller size of fat cells in the adipose tissue in the obese mice treated with FA. Interestingly, FA reduced the expression of hepatic lipogenic genes such as sterol regulatory element-binding protein 1c (SREBP1c), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC). It could also up-regulate hepatic carnitine palmitoyltransferase 1a (CPT1a) gene and peroxisome proliferator-activated receptor alpha (PPARα) proteins. The FA treatment was also found to suppress the protein expressions of hepatic gluconeogenic enzymes, phosphoenolpyruvate carboxylase (PEPCK) and glucose-6-phosphatase (G6Pase). In conclusion, the findings of this study demonstrate that FA improves the glucose and lipid homeostasis in HFD-induced obese mice probably via modulating the expression of lipogenic and gluconeogenic genes in liver tissues.

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A polyphenol rescues lipid induced insulin resistance in skeletal muscle cells and adipocytes

Cited by 28 publications

References 35 publications

PKCε as a novel promoter of skeletal muscle differentiation and regeneration

PKCε as a novel promoter of skeletal muscle differentiation and regeneration

Beneficial effects of metformin on muscle atrophy induced by obesity in rats

Ferulic acid improves lipid and glucose homeostasis in high‐fat diet‐induced obese mice

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