Papel de genes adipogénicos y termogénicos en la resistencia o susceptibilidad al desarrollo de obesidad inducida por la dieta en rata

Abstract

The aim of the present work was to assess whether changes in adipose tissue gene expression related with adipogenesis and/or thermogenesis could be involved in the mechanism conferring susceptibility or resistance to develop obesity in high-fat fed outbreed rats. For this purpose, male Wistar rats were fed with standard laboratory diet (control group) or high fat diet. After 15 days, two groups of rats with significant differences on body weight gain in response to the high fat diet were characterized and identified as diet-induced obesity (DIO) and diet resistant (DR) rats. A significant increase in visceral white adipose tissue (WAT) PPARgamma and aP2 (p < 0.05) mRNA levels associated to a decrease in RARgamma expression (p < 0.05) was observed in DIO rats, suggesting an increase of adipogenesis. Furthermore, our data showed a marked increase in brown adipose tissue (BAT) of UCP1 mRNA in DIO animals (p < 0.01) (without affecting PGC-1alpha gene expression), whereas no changes were found in WAT UCP2 gene expression. All these data suggest that the variations found in the expression pattern of PPARgamma, aP2 and RARgamma by high-fat diet could be involved, at least in part, in the differences in body weight gain and adiposity observed between DR and DIO animals. The compensatory adaptations through the increase in energy expenditure by changes on the expression levels of UCP1 seem not to be enough to avoid the obesity onset in the DIO group.

Treatment with a SOD mimetic reduces visceral adiposity, adipocyte death, and adipose tissue inflammation in high fat‐fed mice

“…It is worth noting that MnTBAP caused a slight but significant increase in the average adipocyte diameter in NC-fed animals (Figure 4a, b). Next, we examined the effect of MnTBAP on adipogenesis and fat uptake in eWAT and found that consistent with prior reports (14, 15), HFD enhanced adipogenesis in eWAT as evidenced by the significant (p<0.05) increase in mRNA expression of key adipogenic genes such as PPARγ and aP2 (Figure 4c), an induction that was prevented with MnTBAP. Interestingly, these changes in adipogenesis were not observed in iWAT (Supplementary Figure 3), suggesting a depot-specific effects of HFD and MnTBAP.…”

Retinoic acid receptor γ is a therapeutically targetable driver of growth and survival in prostate cancer

“…49 The down-regulation of RARγ expression prior the onset of adipogenesis is an essential molecular signature of several in vitro pre-adipocyte differentiation models [48][49][50] while in vivo, an inverse correlation between RARγ expression and adiposity has been demonstrated. 48,65 Moreover, RARγ agonism inhibits the expression of the pro-adipogenic nuclear receptor PPARγ and thereby blocks the adipogenic signals emanating from this receptor. 46,51,66,67 Our observation that the addition of an RARγ agonist prior to adipogenesis induction blocks PPARγ-stimulated adipogenesis of LNCaP cells is consistent with these findings.…”

Adipose tissue stearoyl-CoA desaturase 1 index is increased and linoleic acid is decreased in obesity-prone rats fed a high-fat diet

“…Compared with their OR counterparts, OP rats show a more adverse metabolic risk profile as well as lower energy expenditure on a HFD [9,10], and a proadipogenic expression profile [11-13]. In addition, OP rats also have lower relative fat oxidation and fat oxidation enzyme expression [14-17].…”