10‑Gingerol, a novel ginger compound, exhibits antiadipogenic effects without compromising cell viability in 3T3‑L1 cells

Obesity is defined as excessive fat accumulation that can be detrimental to health and currently affects a large part of the global population. Obesity arises from excessive energy intake along with a sedentary lifestyle and leads to adipocytes with aggravated hypertrophy. Strategies have been designed to prevent and treat obesity. Nutrigenomics may serve a role in prevention of obesity using bioactive compounds present in certain foods with anti‑obesogenic effects. Ginger (Zingiber officinale Roscoe) contains gingerols, key bioactive compounds that inhibit hypertrophy and hyperplasia of adipocytes. The present study aimed to evaluate the antiadipogenic activity of 10‑gingerol (10‑G) in the 3T3‑L1 cell line. Three study groups were formed: Negative (3T3‑L1 preadipocytes) and positive control (mature 3T3‑L1 adipocytes) and 10‑G (3T3‑L1 preadipocytes stimulated with 10‑G during adipogenic differentiation). Cell viability and lipid content were evaluated by MTT assay and Oil Red O staining, respectively. mRNA expression of CCAAT enhancer‑binding protein α (C/ebpα), peroxisome proliferator‑activated receptor γ (Pparγ), mechanistic target of rapamycin complex (Mtor), sterol regulatory element binding transcription factor 1 (Srebf1), acetyl‑coenzyme A carboxylase (Acaca), fatty acid binding protein 4 (Fabp4), and 18S rRNA (Rn18s), was quantified by quantitative PCR. The protein expression of C/EPBα was analyzed by western blot. In the 10‑G group, lipid content was decreased by 28.83% (P<0.0001) compared with the positive control; notably, cell viability was not affected (P=0.336). The mRNA expression in the 10‑G group was higher for C/ebpα (P<0.001) and lower for Acaca (P<0.001), Fabp4 (P<0.001), Mtor (P<0.0001) and Srebf1 (P<0.0001) compared with the positive control group, while gene expression of Pparγ did not present significant changes. The presence of 10‑G notably decreased C/EBPα protein levels in 3T3‑L1 adipocytes. In summary, the antiadipogenic effect of 10‑G during the differentiation of 3T3‑L1 cells into adipocytes may be explained by mRNA downregulation of adipogenic transcriptional factors and lipid metabolism‑associated genes.