Zingiberene attenuates high fat diet–induced non-alcoholic fatty liver disease through suppression of lipogenesis and oxidative stress in rats

Sivaraj, Rajeshwari; Jaikumar, S; Sengottuvelu, S.

doi:10.1007/s00580-022-03321-9

Cited by 4 publications

(2 citation statements)

References 38 publications

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“…Lipid homeostasis is regulated by lipolysis and lipogenesis, which are strongly connected with the pathogenesis of obesity, IR, type 2 diabetes, and nonalcoholic fatty liver disease. [7][8][9] PPAR-γ plays an important role in adipose tissue differentiation and fat metabolism, which is extremely expressed in brown and white adipose tissue and is well thought-out as the master regulator of adipogenesis. 36 In addition, PPARγ promotes the discharge of free fatty acids from circulating lipoproteins and stimulates their uptake enhancing lipid storage.…”

Section: Discussionmentioning

confidence: 99%

“…Low-density lipoprotein cholesterol (LDL) levels could be lofty or moderately increased, although the number of LDL particles can be augmented. 6,7 On the other hand, lipid equilibrium is regulated by lipolysis and lipogenesis, which are strongly connected with obesity and nonalcoholic fatty liver disease, 8 IR, 9 and type 2 diabetes mellitus. 10 In addition, Meriga et al 11 reported that high-fat-diet (HFD) supplementation in rats leads to body weight gain, and biochemical changes occurred through modulation of key lipid metabolizing and obesogenic genes in particular major alterations in transcription factors like superior mRNA expression of peroxisome proliferator-activated receptor-gamma (PPAR-γ) in adipose tissue.…”

Section: Introductionmentioning

confidence: 99%

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Beta‐glucan suppresses high‐fat‐diet‐induced obesity by attenuating dyslipidemia and modulating obesogenic marker expressions in rats

Eraniappan

Balasubramaniyan

Uddandrao

et al. 2023

Fundamemntal Clinical Pharma

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The current study was designed to evaluate the therapeutic potential of beta-glucan (BG), which is a key bioactive compound predominantly present in mushrooms and cereals against high-fat-diet (HFD)-induced obesity, and to understand its mechanism of action. Obesity was induced in rats by supplementing the diet with HFD and BG (40 mg/kg body weight) for a period of 6 weeks. At the end of the experimental period, the body weight, as well as hyperglycemic, dyslipidemia, and obesogenic marker expressions, was assessed in the control group and in the experimental obese rats. Administration of BG to obese rats significantly reduced body weight gain and attenuated hyperglycemia, which was confirmed by the decreased blood glucose and insulin resistance. At the same time, BG mitigated dyslipidemia by altering expressions of peroxisome proliferator-activated receptor-gamma (PPAR-γ), sterol regulatory element-binding protein 1 (SREBP-1c), fatty acid synthase (FAS), 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, and fatty acid-binding protein-4 (Fab-4) in HFDinduced obese rats. In conclusion, this study revealed that BG is a potential candidate to ameliorate HFD-induced obesity by modulating obesogenic marker expressions, especially by regulating the master regulator PPAR-γ.

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