Abstract
Obesity is a major health concern and is becoming an increasingly serious societal problem worldwide. The browning of white adipocytes has received considerable attention because of its potential protective effect against obesity-related metabolic disease. The gintonin-enriched fraction (GEF) is a non-saponin, glycolipoprotein component of ginseng that is known to have neuroprotective and anti-inflammatory effects. However, the anti-obesity and browning effects of GEF have not been explored to date. Therefore, we aimed to determine whether GEF has a preventive effect against obesity. We differentiated 3T3-L1 cells and mouse primary subcutaneous adipocytes for 8 days in the presence or absence of GEF, and then measured the expression of intermediates in signaling pathways that regulate triglyceride (TG) synthesis and browning by Western blotting and immunofluorescence analysis. We found that GEF reduced lipid accumulation by reducing the expression of pro-adipogenic and lipogenic factors, and increased lipolysis and thermogenesis, which may be mediated by an increase in the phosphorylation of protein kinase A. These findings suggest that GEF may induce fat metabolism and energy expenditure in white adipocytes and therefore may represent a potential treatment for obesity.
Highlights
Obesity is a major risk factor for type 2 diabetes, cardiovascular disease, hypertension, hyperlipidemia, and some forms of cancer [1]
uncoupling protein 1 (UCP1) expression is characteristic of the brown adipose tissue (BAT) phenotype, and its expression is stimulated by transcription factors, including PR domain-containing 16 (PRDM16) and peroxisome proliferator-activated receptor gamma co-activator 1 α (PGC1α) [6]
We first determined the effect of gintonin-enriched fraction (GEF) on fat metabolism in 3T3-L1s and primary subcutaneous adipocytes (SAT)
Summary
Obesity is a major risk factor for type 2 diabetes, cardiovascular disease, hypertension, hyperlipidemia, and some forms of cancer [1]. It is characterized by an enlargement of adipose tissue depots to store excess energy in the form of triglycerides (TGs). Numerous studies have investigated whether WAT-to-BAT transdifferentiation can be induced by treatment with chemical agents [4]. This “browning” of WAT is characterized by an increase in the expression of uncoupling protein 1 (UCP1) and mitochondrial expansion. The stimulation of adipocyte transdifferentiation in WAT could represent a therapeutic strategy for obesity and obesity-related metabolic disease
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