High-fat diet induces emergence of brown-like adipocytes in white adipose tissue of spontaneously hypertensive rats

Abstract

Obesity has a profound adverse impact on health. In this study, we present evidence for high-fat diet (HFD)-induced emergence of brown-like adipocytes in white adipose tissue (WAT) of the spontaneously hypertensive rat (SHR). We studied adult males fed a HFD or normal diet (ND) for 12 weeks. At the end of the 12-week dietary intervention, HFD compared with ND rats showed significantly higher whole-body energy expenditure. HFD vs. ND rats also showed higher expression of genes involved in fatty acid oxidation, mitochondrial biogenesis and brown fat adipogenesis, as well as augmented mitochondrial mass in WAT but not in the liver or skeletal muscle. Consistent with the molecular changes, in HFD but not in ND rats, histological and immunohistochemistry-based analyses of WAT demonstrated the presence of small multilocular cells staining positively for uncoupling protein 1, indicating the emergence of brown-like adipocytes in WAT. Our results suggest that SHR may have the capacity to increase energy expenditure in response to a chronic HFD that may be linked to the emergence of brown-like adipocytes in WAT. Thus, the SHR may be an important genetic model to uncover novel mechanisms of resistance to dietary obesity.

Host genetics and diet composition interact to modulate gut microbiota and predisposition to metabolic syndrome in spontaneously hypertensive stroke‐prone rats

“…Apart from muscle, the up-regulation of b-3 AR in the brown fat and retroperitoneal fat suggests that b-3 AR signaling in these tissues may also contribute to the enhanced expenditure of the SHRSP, with the retroperitoneal adipose likely playing a minor role. In contrast to our findings with SHRSP, the SHR were reported to have lower food intake (89) and greater total heat production following chronic high-fat feeding (32). Thus, although the SHRSP were selectively bred from SHR for their hypertensive and stroke-prone characteristics (17)(18)(19), whether the underlying mechanisms of energy balance regulation diverged between the SHRSP and SHR remains to be investigated.…”

“…We previously reported that a high-fat and high-salt diet promotes hypertension, glucose intolerance, susceptibility to kidney damage, and early onset of stroke in SHRSP rats (31); however, the normotensive Wistar-Kyoto (WKY) control rats were not used to parse out whether the metabolic readouts are due to the diet caloric density per se. There is some evidence that HFD enhances energy expenditure (EE) and adipose browning with resistance to obesity in spontaneously hypertensive (SHR) rats, which are hypertensive but not inherently sensitive to spontaneous stroke (32). However, it is unknown whether sympathetic signaling is involved in the enhanced EE and whether the SHRSP rats show similar metabolic adaptations.…”

Grape pomace extract induced beige cells in white adipose tissue from rats and in 3T3-L1 adipocytes

“…In order to assess whether GPE could induce brown-like cells in eWAT we used a rat model of cardiovascular disease, the spontaneously hypertensive (SHR) and their control normotensive Wistar-Kyoto (WKY) rat strain fed a HFD. SHR rats present an exacerbation of the sympathetic nervous system [6,32,33], which makes them susceptible to the emergence of "beige" cells and a good model to study "browning" pathways. Overall, we observed that GPE promoted brown-like cell formation in WAT and diminished adipose dysfunction.…”

“…VEGF-R2 activation by VEGF-A may protect from diet-induced insulin resistance by decreasing adipose tissue inflammation through its effect on M2 anti-inflammatory macrophage recruitment. VEGF-A overexpression can also increase brown adipose tissue (BAT) thermogenesis and promote a "BAT-like" phenotype in WAT depots, increasing energy expenditure and therefore reducing obesity [5][6][7]. Furthermore, peroxisome proliferator-activated receptor- (PPARγ) is a central modulator of adipogenesis, enhancing insulin sensitivity and decreasing macrophage adipose infiltration [8,9].…”

Maternal Choline Intake Programs Hypothalamic Energy Regulation and Later‐Life Phenotype of Male Wistar Rat Offspring

“…All measurements were taken at room temperature (23 °C) and each animal was monitored for two consecutive 24 h periods, the first 24 h period was to allow the animals to acclimatize to the metabolic cages, and second period was used for data collection and analysis as described elsewhere. [ 33,34 ] Air flow rate through the chambers was adjusted to 2 L min −1 and an extracted outflow to 0.4 L min −1 . The input air for the chambers and the expired air were sequentially analyzed for CO 2 and O 2 with a gas analyzer every 13 min.…”