A mixture of citrus polymethoxyflavones, green tea polyphenols and lychee extracts attenuates adipogenesis in 3T3-L1 adipocytes and obesity-induced adipose inflammation in mice

• Published in: Food & function Vol. 1; no. 12; pp. 7667 - 7677
• Main Authors: Pan, Min-Hsiung, Li, Ming-Yi, Tsai, Mei-Ling, Pan, Chih-Yu, Badmaev, Vladimir, Ho, Chi-Tang, Lai, Ching-Shu
• Format: Journal Article
• Language: English
• Published: England Royal Society of Chemistry 11.12.2019
• Subjects: 3T3-L1 Cells; Adipocytes; Adipocytes - drug effects; Adipogenesis; Adipogenesis - drug effects; Adipose tissue; Adiposity - drug effects; AMP; AMP-activated protein kinase; AMP-Activated Protein Kinases - genetics; AMP-Activated Protein Kinases - immunology; Animals; Antibodies; Camellia sinensis - chemistry; CCAAT-Enhancer-Binding Protein-alpha - genetics; CCAAT-Enhancer-Binding Protein-alpha - immunology; CD163 antigen; Cell cycle; Citrus - chemistry; Cytokines; Differentiation; Flavones - administration & dosage; Fruit - chemistry; Green tea; High fat diet; Humans; Induced infiltration; Inflammation; Insulin; Interleukin 10; Interleukin 6; Kinases; Lipids; Litchi - chemistry; Macrophages; Male; Mice; Mice, Inbred C57BL; Monocyte chemoattractant protein; Monocyte chemoattractant protein 1; Monocytes; Obesity; Obesity - drug therapy; Obesity - genetics; Obesity - immunology; Obesity - physiopathology; p53 Protein; Plant Extracts - administration & dosage; Polyphenols; Polyphenols - administration & dosage; PPAR gamma - genetics; PPAR gamma - immunology; Pretreatment; Proteins; Tea; Western blotting
• ISSN: 2042-6496; 2042-650X
• DOI: 10.1039/c9fo02235j

Adipocyte-macrophage interaction in obesity can cause adipose tissue inflammation and contribute to insulin resistance. Here, we investigated the effect of SlimTrym®-a formulated product containing citrus polymethoxyflavones (PMFs), green tea extract, and lychee polyphenols-on 3T3-L1 adipocyte differentiation and obesity-induced inflammation. SlimTrym® inhibited mitotic clonal expansion (MCE) of 3T3-L1 adipocytes by inducing G1 cell cycle arrest via upregulation of p21 and p53. SlimTrym® attenuated adipogenic differentiation by downregulating adipogenic factors, such as CCAAT-enhancer-binding proteins (C/EBPs) and peroxisome proliferator-activated receptor γ (PPARγ), and upregulating AMP-activated protein kinase (AMPK). Pretreatment with compound C significantly reduced SlimTrym®-mediated suppression of lipid accumulation. SlimTrym® reduced the expression of pro-inflammatory cytokines, including monocyte chemoattractant protein 1 (MCP-1), interleukin (IL)-1β and IL-6, in co-cultured 3T3-L1 adipocytes and RAW264.7 macrophages. C57BL/6 mice administered with SlimTrym® for 16 weeks showed markedly reduced high-fat diet (HFD)-induced infiltration of monocytes/macrophages in adipose tissue; however, the level of M2 macrophage markers (CD163 and IL-10) was increased. Taken together, these findings indicate that SlimTrym® exerts both anti-adipogenic and anti-inflammatory effects, and can potentially treat obesity and adipose tissue inflammation. Adipocyte-macrophage interaction in obesity can cause adipose tissue inflammation and contribute to insulin resistance.