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J Nutr Biochem. 2014 Jan;25(1):1-18. doi: 10.1016/j.jnutbio.2013.09.001.

Novel insights of dietary polyphenols and obesity.

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Department of Nutritional Sciences, Texas Tech University, Lubbock, TX 79409, USA.


The 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, especially 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 adenosine-monophosphate-activated protein kinase, peroxisome proliferator activated receptor γ, CCAAT/enhancer binding protein α, peroxisome proliferator activator receptor gamma activator 1-alpha, sirtuin 1, sterol regulatory element binding protein-1c, uncoupling proteins 1 and 2, and nuclear factor-κB 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 antiobesity 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.


ABCA1; ACAT; ACC; AGP; AMPK; ATGL; Animal; Antioxidants; Apo; BMI; BW; C/EBPα; CCAAT/enhancer binding protein α; CPT-1; CVD; Cell; DBP; Dietary polyphenols; EC; ECG; EGC; EGCG; FA; FABP4; FAS; FASN; FFA; FFM; FM; FOXO1; GPAT; GPX; GSSG; GTC; GTE; GTP; HDL-C; HF; HOMA-IR; HSL; Human; IFN; IGF-I; IL; LDL-C; LPL; LXR; MAPK; MCP-1; MDA; MMP; Molecular mechanism; NF-κB; Obesity; PAI-1; PDEs; PGC-1α; PON; PPARγ; RCT; ROS; SBP; SCD1; SIRT1; SOD; SREBP-1c; TBARS; TC; TG; TNF-α; UCP; aP2; acetyl-coenzyme A carboxylase; acyl-coenzyme A: cholesterol acyltransferase; adenosine-monophosphate-activated protein kinase; adenosine-triphosphate-binding cassette A1; adipocyte P2 protein, which is also known as aFABP, the adipocyte fatty acid binding protein or FAPB-4; adipose triglyceride lipase; aminoalkyl glucosaminide 4-phosphate; apolipoprotein; body mass index; body weight; cAMP; cardiovascular disease; carnitine palmitoyltransferase-1; cyclic adenosine monophosphate; diastolic blood pressure; epicatechin; epicatechin gallate; epigallocatechin; epigallocatechin gallate; fat mass; fat-free mass; fatty acid; fatty acid binding protein 4; fatty acid synthase; forkhead box protein O1; free fatty acid; glutathione disulfide; glutathione peroxidase; glycerol-3-phosphate acyltransferase; green tea catechin; green tea extracts; green tea polyphenols; high fat; high-density lipoprotein cholesterol; homeostasis model assessment of insulin resistance; hormone-sensitive lipase; insulin-like growth factor-I; interferon; interleukin; lipoprotein lipase; liver X receptor; low-density lipoprotein cholesterol; malondialdehyde; matrix metalloproteinase; mitogen-activated protein kinase; monocyte chemoattractant protein-1; nuclear factor-κB; paraoxonase; peroxisome proliferator activator receptor γ; peroxisome proliferator-activated receptor gamma coactivator 1-alpha; phosphodiesterases; plasminogen activator inhibitor type 1; randomized controlled trial; reactive oxygen species; sirtuin 1; stearoyl-CoA desaturase-1; sterol regulatory element-binding protein 1c; superoxide dismutase; systolic blood pressure; thiobarbituric acid reactive substances; total cholesterol; triglyceride; tumor necrosis factor-alpha; uncoupling protein

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