Abstract
The development of metabolic complications associated with obesity has been correlated with a failure of white adipose tissue (WAT) to expand. Our group has previously reported that a 12-week administration of grape seed proanthocyanidin extract (GSPE) together with an obesogenic diet mitigated the development of cardiometabolic complications in rats. Using the same cohort of animals, we aim to elucidate whether the prevention of cardiometabolic complications by proanthocyanidins is produced by a healthier expansion of visceral WAT and/or an induction of the browning of WAT. For this, adipocyte size and number in retroperitoneal WAT (rWAT) were determined by histological analyses, and the gene expression levels of markers of adipogenesis, browning, and WAT functionality were quantified by RT-qPCR. The long-term administration of GSPE together with an obesogenic diet expanded rWAT via an increase in the adipocyte number and a preventive decrease in the adipocyte size in a dose-dependent manner. At the molecular level, GSPE seems to induce WAT adipogenesis through the upregulation of peroxisome proliferator-activated receptor (Pparγ) in a Sirtuin 1 (Sirt1)-dependent manner. In conclusion, the healthier visceral WAT expansion induced by proanthocyanidins supplementation may explain the improvement in the cardiometabolic risks associated with obesogenic diets.
Highlights
In obesity, fat is excessively accumulated in white adipose tissue (WAT) under conditions of energy surplus or reduced energy expenditure
That study reported that the daily administration of grape seed proanthocyanidin extract (GSPE) with the CAF diet did not prevent body weight (BW) gain during the 12 weeks of the experiment, with 200 mg GSPE/kg BW, a tendency to avoid the obesogenic diet-induced increase in BW was observed by the end of the experiment [13]
The results demonstrated that the administration of GSPE with the CAF diet mitigated the obesogenic diet-induced hypertension and dyslipidemia in rats without a clear dose effect
Summary
Fat is excessively accumulated in white adipose tissue (WAT) under conditions of energy surplus or reduced energy expenditure. The prevalence of obesity is increasing, and this is dangerous, since the risk for cardiovascular complications and type 2 diabetes among other diseases increases with obesity [1]. It seems that the total fat mass may not be the direct link between obesity and its associated diseases, since some obese individuals are relatively metabolically healthy [2]. The capacity of the WAT to expand to store the excess energy may prevent the development of metabolic complications in response to the surplus energy, since it may prevent the lipids from targeting other organs [3]. WAT can only expand up to a certain threshold, beyond which their capacity to store more fat is diminished, which is associated with metabolic complications [4]. Several of the obesity-related metabolic complications might be explained by WAT dysfunction as a consequence of an impaired capacity of the fat depots to store more energy [5]
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