Effects of Genistein on Differentiation and Viability of Human Visceral Adipocytes

Abstract

Obesity can lead to pathological growth of adipocytes by inducing inflammation and oxidative stress. Genistein could be a potential candidate for the treatment of obesity due to its antioxidant properties. Specific kits were used to examine the effects of genistein vs adiponectin on human visceral pre-adipocytes differentiation, cell viability, mitochondrial membrane potential, and oxidative stress in pre-adipocytes and in white/brown adipocytes. Western Blot was performed to examine changes in protein activation/expression. Genistein increased human visceral pre-adipocytes differentiation and browning, and caused a dose-related improvement of cell viability and mitochondrial membrane potential. Similar effects were observed in brown adipocytes and in white adipocytes, although in white cells the increase of cell viability was inversely related to the dose. Moreover, genistein potentiated AMP-activated protein kinase (AMPK)/mitofusin2 activation/expression in pre-adipocytes and white/brown adipocytes and protected them from the effects of hydrogen peroxide. The effects caused by genistein were similar to those of adiponectin. The results obtained showed that genistein increases human visceral pre-adipocytes differentiation and browning, protected against oxidative stress in pre-adipocytes and white/brown adipocytes through mechanisms related to AMPK-signalling and the keeping of mitochondrial function.

Genistein Induces Adipogenic and Autophagic Effects in Rainbow Trout (Oncorhynchus mykiss) Adipose Tissue: In Vitro and In Vivo Models

“…Regarding in vivo assays, GE is generally considered hypolipidemic [19], but differences have been shown depending on its content in the diet. A reduction in adipose tissue mass has also been reported in several in vivo mice models with GE stimulating lipolysis and adipocytes apoptosis at the same time (reviewed in [14]), while in human visceral preadipocytes, GE has been demonstrated to promote adipogenesis [20]. In addition, high levels of dietary GE included in mice diets decreased hepatic fat accumulation by increasing fatty acid oxidation, and even a low dose of GE increased mitochondrial enzyme activity in mice with fatty liver and obesity induced by high-fat diets, although specific effects on adipose tissue were not mentioned in that study [21].…”

Flavonoids as antiobesity agents: A review

“…Genistein modulated the thermogenesis and mitochondrial function mechanisms by increasing browning in human visceral preadipocytes and white/brown adipocytes. These actions seem to occur through mechanisms involving the AMPK signaling pathways, which therefore ensure a normal mitochondrial function in the same manner as adiponectin 131 . Similarly, genistein promoted WAT browning by increasing UCP‐1, PRDM‐16, and PGC‐1α proteins in ovariectomized rats subjected to HFD 130 .…”

“…Mesenchymal stem cells (MSCs) from human adipose tissue [126] Decreases body fat accumulation Ovariectomized female cats [127] Increases fatty acid oxidation Increased activity of CPT-1; decreased plasma leptin HFD-obese C57BL/6J mice [128] Decreases adipogenesis; inhibits lipid accumulation; decreases the nonesterified fatty acid content Inhibited expression of FAS; suppressed expression of C/ EBP α 3T3-L1 adipocytes [129] Increases WAT browning; reduces adipogenesis Increased UCP-1, PRDM-16, PGC-1α, and CIDEA proteins; inhibited expression of SREBP-1c, ACC, and FAS HFD-ovariectomized female rats [130] Stimulates adipocyte differentiation; increases thermogenesis Increased AMPK-signaling; increased mitochondrial function Human preadipocytes [131] T A B L E 2 (Continued) Reduces plasma TC, TGs, and FFAs levels; decreases BW and visceral fat; accelerates fatty acid oxidation Induced carnitine O-octanoyltransferase HFD-obese C57BL/6J mice [135] Decreases food intake, BW, and fat pad weight…”

Precision Nutrition to Activate Thermogenesis as a Complementary Approach to Target Obesity and Associated-Metabolic-Disorders

“…Indeed, in the last years, there have been reported several plant-derived bioactive compounds with the capacity to activate and to augment thermogenesis. Therefore, the upregulation of several signaling pathways including UCP1, AMPK, PGC1α, Sirt1, PRDM16 and/or PPARs have been shown to increase the WAT browning [ 96 , 97 , 98 , 99 , 100 , 101 , 102 , 103 , 104 , 105 ].…”