Prevalence of obesity has steadily increased over the past three decades both in the United States and worldwide. Recent studies have shown the role of dietary polyphenols in the prevention of obesity and obesity-related chronic diseases. Here we evaluated the impact of commonly consumed polyphenols, including green tea catechins and epigallocatechin gallates, resveratrol, and curcumin, on obesity and obesity-related-inflammation. Cellular studies demonstrated that these dietary polyphenols reduce viability of adipocytes and proliferation of preadipocytes, suppress adipocyte differentiation and triglyceride accumulation, stimulate lipolysis and fatty acid β-oxidation, and reduce inflammation. Concomitantly, the polyphenols modulate signaling pathways including the AMP-activated protein kinase, peroxisome proliferator activated receptor γ, CCAAT/enhancer binding protein α, PPAR gamma activator 1-alpha, sirtuin 1, sterol regulatory element binding protein-1c, uncoupling proteins 1 and 2, and nuclear factor kappa B that regulate adipogenesis, antioxidant and anti-inflammatory responses. Animal studies strongly suggest that commonly consumed polyphenols described in this review have a pronounced effect on obesity as shown by lower body weight, fat mass, and triglycerides through enhancing energy expenditure and fat utilization, and modulating glucose hemostasis. Limited human studies have been conducted in this area, and are inconsistent about the anti-obesity impact of dietary polyphenols, probably due to the various study designs and lengths, variation among subjects (age, gender, ethnicity), chemical forms of the dietary polyphenols used and confounding factors such as other weight reducing agents. Future randomized controlled trials are warranted to reconcile the discrepancies between preclinical efficacies and inconclusive clinic outcomes of these polyphenols.
Green tea catechins are known to have hypocholesterolaemic effects in animals and human subjects. In the present study, we investigated the effects of green tea catechins on the mRNA level and promoter activity of hepatic cholesterol 7a-hydroxylase (CYP7A1), the rate-limiting enzyme in the conversion of cholesterol to bile acids, in human hepatoma cells. Real-time PCR assays showed that different catechins, (2)-epicatechin gallate (ECG), (2 )-epigallocatechin-3-gallate (EGCG), (2)-epigallocatechin (EGC) and (2)-epicatechin (EC), up regulated the CYP7A1 mRNA level by 5·5-, 4·2-, 2·9-and 1·9-fold, respectively, compared with the control. The 21312/þ 358 bp of the CYP7A1 promoter was subcloned into the pGL3 basic vector that includes luciferase as a reporter gene. ECG or EGCG significantly increased CYP7A1 promoter activity by 6·0-or 4·0-fold, respectively, compared with the control. Also, EGCG stimulated CYP7A1 at both mRNA level and promoter activity in a dosedependent manner. These results suggest that the expression of the CYP7A1 gene may be directly regulated by green tea catechins at the transcriptional level.
In this study, we investigated the lipolytic effects of eicosapentaenoic acid (EPA) in 3T3-L1 adipocytes. The differentiated 3T3-L1 adipocytes were treated in a serum-free medium with 300 lM of EPA for 3, 6, 12, and 24 h. In comparison with the control, intracellular lipid accumulation was significantly decreased by 24% at 24 h following the addition of EPA (P \ 0.05). Under the same experimental conditions, there was an increase of glycerol and free fatty acids (FFAs). The mRNA level of carnitine palmitoyltransferase I-a, a component of the fatty-acid shuttle system involved in the mitochondrial oxidation of long-chain fatty acids, was also significantly elevated by EPA (P \ 0.05). However, the expression of peroxisome proliferator-activated receptor-c and acetyl-CoA carboxylase (ACC), which are involved in adipogenesis, was significantly down-regulated by EPA (P \ 0.05). These results suggest that EPA may modulate lipid metabolism by stimulation of lipolysis, which was associated with induction of lipolytic gene expression and suppression of adipogenic gene expression in 3T3-L1 adipocytes.
Zn deficiency reduces food intake and growth rate in rodents. To determine the relationship between Zn deficiency and the regulation of food intake, we evaluated leptin gene expression in epididymal white adipose tissue (eWAT), and hypothalamic corticotropin-releasing hormone (hCRH) and hypothalamic neuropeptide Y (hNPY) of rats Zn-deficient only to show reduced food intake and growth rate but not food intake cycling. Growing male Sprague-Dawley rats (240 g) were randomly assigned to one of four dietary groups: Zn-adequate (ZA; 30 mg/kg diet), Zn-deficient (ZD; 3 mg/kg diet), pair-fed with ZD (PF; 30 mg/kg diet) and Zn-sufficient (ZS; 50 mg/kg diet) (n 8), and were fed for 3 weeks. Food intake and body weight were measured, as were blood mononuclear cells and pancreas Zn levels. eWAT leptin, hCRH and hNPY mRNA levels were determined. Food intake was decreased by about 10 % in ZD and PF rats compared to ZA and ZS rats. Growth and eWAT leptin mRNA levels were unaffected in PF rats but were significantly (P, 0·05) decreased in ZD rats. However, hNPY showed a tendency to increase, and hCRH significantly (P, 0·05) decreased, in both ZD and PF rats. These results suggest that while leptin gene expression may be directly affected by Zn, hNPY and hCRH are likely responding to reduced food intake caused by Zn deficiency.Zinc deficiency: Corticotrophin-releasing hormone: Leptin: Food intake: Growth Zn is an essential component of numerous enzymes and transcription factors and influences many biological processes including the control of food intake and growth 1,2 . Zn deficiency in experimental animals and in man causes anorexia, poor appetite, weight loss and growth retardation. Food intake is controlled by appetite and satiety centres in the central nervous system involving systemic hormonal and nervous feedback of fat reserves and food ingestion 3 . Leptin, a 16 kDa protein secreted primarily by white adipocytes, targets receptors in neurons of hypothalamic nuclei, informing the central nervous system about fat reserves and regulating the expression and signalling of orexigenic and anorexigenic neuropeptides 3 . Leptin negatively and positively regulates the release of neuropeptide Y (NPY) and corticotropinreleasing hormone (CRH), respectively, from the hypothalamic paraventricular nucleus 4 . NPY is a potent stimulator of appetite whereas CRH inhibits food intake, and so in starved animals, NPY expression is increased and CRH decreased due principally to decreased circulating leptin levels 4 .Zn may be a mediator of leptin production in human subjects 5,6 and rodents 7 -9 . Circulating leptin levels and white adipose tissue leptin mRNA levels are decreased in Zn deficiency 7,8 . Also, Zn supplementation of obese mice 10 and diabetic mice 11 increased circulating leptin levels. As would be expected, in acute Zn deficiency where food intake is reduced, body adipose tissue diminishes resulting in reduced leptin synthesis and secretion. Hypothalamic NPY mRNA and protein levels increase in Zn deficiency 12 , although the r...
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