Abstract
Obesity is one of major health challenges in the industrial world. Although rice hull has been reported to show various bioactivities, no studies have evaluated its anti-obesity effect. We hope to demonstrate the anti-obesity effect of rice hull extract (RHE) and the underlying mechanism in high-fat diet (HFD)-induced obese mice and 3T3-L1 preadipocytes. Serum lipid profiles were determined by enzymatic methods. Histological analysis of liver and epididymis fat tissues was carried out with hematoxylin and eosin stain. The mRNA expression of adipogenic markers was analyzed with qRT-PCR and western blotting. Oral administration of RHE reduced body weight gain and fat accumulation in HFD-fed mice. RHE also reduced lipid accumulation by inhibiting the mRNA expression of adipogenic-related genes in HFD-fed obese mice and differentiated preadipocytes. The downregulation of adipogenesis by RHE was mediated through the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC). In addition, RHE induced the phosphorylation of c-Jun N-terminal kinases (JNK) and extracellular-signal-regulated kinases (ERK) in liver and epididymis adipose tissues of HFD-fed obese mice. Taken together, these findings indicate that RHE could inhibit the differentiation of adipose cell and prevent HFD-induced obesity, suggesting its potential in the prevention of obesity and metabolic syndrome and related-disorders.
Highlights
Obesity is a multifactorial chronic disease that is associated with a number of risks
high-fat diet (HFD)-induced obese animals and differentiated 3T3-L1 preadipocytes were used as models of adipogenesis and obesity to investigate the molecular mechanism of the anti-adipogenic properties of rice hull extract (RHE)
Our data showed that RHE enhanced the phosphorylation of extracellular-signal-regulated kinases (ERK) and Jun N-terminal kinases (JNK) (Figure 5), whereas both had no effect on p38 activation in liver tissue and epididymis adipose tissue of HFD-fed obese mice
Summary
Obesity is a multifactorial chronic disease that is associated with a number of risks. There are three known major transcription factors of adipogenesis: nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer binding protein-alpha (C/EBPα), and sterol regulatory element-binding transcription factor 1 (SREBP1). They are crucial in the intricate transcriptional cascade of adipocyte differentiation [6]. Glucocorticoids, and cAMP-elevating agents are regarded as adipogenic stimulators These stimulators induce the expression of some transcription factors, subsequently upregulating PPARγ. HFD-induced obese animals and differentiated 3T3-L1 preadipocytes were used as models of adipogenesis and obesity to investigate the molecular mechanism of the anti-adipogenic properties of RHE
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