Influence of dietary macronutrient composition on adiposity and cellularity of different fat depots in Wistar rats

Boqué, Noemí; Campión, Javier; Paternain, Laura; García-Díaz, Diego F.; Galarraga, M.; Portillo, Marı́a P.; Milagro, Fermı́n I.; Ortiz‐de‐Solórzano, Carlos; Martínéz, J. Alfredo

doi:10.1007/bf03185934

Cited by 39 publications

(34 citation statements)

References 36 publications

(39 reference statements)

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“…The HFD-fed rats utilized in this work showed an obesity state [4] that correlated positively with the TSP-1 levels in blood, and with the mRNA expression of this protein in adipocytes from epididymal WAT, which is consistent with a previous report [41]. Interestingly, when the adipocytes were subjected to culture treatments, cells from HFD rats showed lower TSP-1 gene expression than controls, except when the adipocytes where cultured under…”

Section: Discussionsupporting

confidence: 90%

Glucose and insulin modify thrombospondin 1 expression and secretion in primary adipocytes from diet-induced obese rats

et al. 2011

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Thrombospondin 1 (TSP-1), an anti-angiogenic factor and TGF-β activity regulator, has been recently recognized as an adipokine that correlates with obesity, inflammation and insulin-resistance processes. In the present study, epididymal adipocytes of rats that were fed a chow (C) or a high fat diet (HFD) for 50 days, were isolated and incubated (24-72 h) in low (LG; 5.6 mM) or high (HG; 25 mM) glucose, in presence or absence of 1.6 nM insulin. Rats fed the HF diet showed an established obesity state. Serum TSP-1 levels and TSP-1 mRNA basal expression of adipocytes from HFD rats were higher than those from controls. Adipocytes from HFD animals presented an insulin-resistance state, as suggested by the lower insulin-stimulated glucose uptake as compared to controls. TSP-1 expression in culture was higher in adipocytes from obese animals at 24 h, but when the adipocytes were treated with HG, these expression levels dropped dramatically. Later at 72 h, TSP-1 expression was lower in adipocytes from HFD rats, and no effects of the other treatments were observed. Surprisingly, the secretion levels of this protein at 72 h were increased significantly by the HG treatment in both types of adipocytes, although they were even higher in adipocytes from obese animals. Finally, cell viability was significantly reduced by HG treatment in both types of adipocytes. In summary, TSP-1 expression/secretion was modulated in an in vitro model of insulinresistant adipocytes. The difference between expression and secretion patterns suggests a post-transcriptional regulation. The present study confirms that TPS-1 is closely associated with obesity-related mechanisms.

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Section: Discussionsupporting

confidence: 90%

Glucose and insulin modify thrombospondin 1 expression and secretion in primary adipocytes from diet-induced obese rats

et al. 2011

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“…In line with our data, a previous study of Wistar rats showed that adding fat to a high-sucrose diet reversed the increase in adipocyte number due to high-sucrose diet alone (7). It should also be noted that the low-fat group in our experiment gained more weight than anticipated, resulting in no significant difference between lowfat diet and continuous hypercaloric feeding in regard to total body mass.…”

Section: E221supporting

confidence: 91%

Weight cycling promotes fat gain and altered clock gene expression in adipose tissue in C57BL/6J mice

Dankel

Degerud

Borkowski

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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peated attempts to lose weight by temporary dieting may result in weight cycling, eventually further gain of body fat, and possible metabolic adaptation. We tested this with a controlled experiment in C57BL/6J mice subjected to four weight cycles (WC), continuous hypercaloric feeding (HF), or low-fat feeding (LF). To search for genes involved in an adaptive mechanism to former weight cycling and avoid acute effects of the last cycle, the last hypercaloric feeding period was prolonged by an additional 2 wk before euthanization. Total energy intake was identical in WC and HF. However, compared with HF, the WC mice gained significantly more total body mass and fat mass and showed increased levels of circulating leptin and lipids in liver. Both the HF and WC groups showed increased adipocyte size and insulin resistance. Despite these effects, we also observed an interesting maintenance of circulating adiponectin and free fatty acid levels after WC, whereas changes in these parameters were observed in HF mice. Global gene expression was analyzed by microarrays. Weight-cycled mice were characterized by a downregulation of several clock genes (Dbp, Tef, Per1, Per2, Per3, and Nr1d2) in adipose tissues, which was confirmed by quantitative PCR. In 3T3-L1 cells, we found reduced expression of Dbp and Tef early in adipogenic differentiation, which was mediated via cAMP-dependent signaling. Our data suggest that clock genes in adipose tissue may play a role in metabolic adaptation to weight cycling. caloric restriction; metabolism; clock genes; obesity; adipokines WEIGHT CYCLING RESULTING FROM INTERMITTENT OVEREATING and dieting represents a major challenge for many individuals (27,58,63) and may ultimately promote further expansion of adipose tissue (11,32,46,53,65). Evolutionary conserved molecular mechanisms allow fine-tuning of metabolic processes to environmental cues. Fat storage is a key evolutionary process conducive to survival in organisms ranging from the worm C. elegans to humans (41). The adipocyte, being the primary fat-storing cell, responds to changes in energy availability in part by releasing the peptide hormones leptin and adiponectin. These potent hormones exert local, central, and peripheral effects, coordinating the systemic response to fasting/refeeding cycles by modulating energy storage/expenditure, appetite, biological rhythms, and other functions. In adipose tissue, signals such as leptin may modulate the capacity for lipogenesis in response to weight fluctuations, predisposing to compensatory fat regain during subsequent energy surplus (28,29,59). Identification of novel genes associated with a history of weight cycling may provide novel molecular insight into the evolutionary adaptation to variable availability of energy.To our knowledge, there are no reports on the genome-wide transcriptional responses to weight cycling in adipose tissues. In rats, it has been shown previously that weight cycling increases feed efficiency (the weight gained relative to the amount of energy ingested) and resista...

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“…Fat areas were identifi ed, manually separated, and excised to avoid mixing white fat from different depots ( 10,11 ). Tissue blocks from all depots were labeled either for histology or for the analysis of cells in suspension.…”

Section: Animal Workmentioning

confidence: 99%

Adiposoft: automated software for the analysis of white adipose tissue cellularity in histological sections

Galarraga

Campión

Muñoz-Barrutia

et al. 2012

Journal of Lipid Research

305

227

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Influence of dietary macronutrient composition on adiposity and cellularity of different fat depots in Wistar rats

Cited by 39 publications

References 36 publications

Glucose and insulin modify thrombospondin 1 expression and secretion in primary adipocytes from diet-induced obese rats

Glucose and insulin modify thrombospondin 1 expression and secretion in primary adipocytes from diet-induced obese rats

Weight cycling promotes fat gain and altered clock gene expression in adipose tissue in C57BL/6J mice

Adiposoft: automated software for the analysis of white adipose tissue cellularity in histological sections

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