Adiponectin and Resistin Response in the Onset of Obesity in Male and Female Rats

Ribot, Joan; Rodríguez, Ana; Rodrı́guez, Enrique; Palou, Andreu

doi:10.1038/oby.2008.113

Cited by 61 publications

(51 citation statements)

References 41 publications

(80 reference statements)

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“…When adiponectin levels were corrected for body fat mass, a clear decrease is seen with higher age, with HFD-feeding, and in BFMI mice compared to B6. This supports the hypothesis of Ribot et al [26] state that adiponectin expression would depend on the composition of adipose tissue. While hyperplasia produces new adipocytes which might be associated with higher adiponectin expression, mainly adipocyte hypertrophy leads to reduced adiponectin levels.…”

Section: Discussionsupporting

confidence: 80%

“…This implies that the reproductive adipose tissue would be important for adiponectin serum levels in prolonged obesity. However, after short-term HFD-feeding of rats an altered adiponectin mRNA expression could not be found [26]. Different from other diet-induced obesity models [30], the weight of adipose tissue did not correlate with adiponectin serum levels in this study.…”

Section: Discussionmentioning

confidence: 41%

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Age and depot-specific adipokine responses to obesity in mice

Hantschel¹,

Wagener²,

Neuschl³

et al. 2012

Health

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Leptin and adiponectin are the most abundant adipokines that regulate energy homeostasis. Here, we report the changes of leptin and adiponectin in response to age and their depotspecific expression in lean and genetically obese mice. Fat deposition patterns, adipokine levels and their adipose-tissue depot-specific expression patterns were examined in both sexes of lean and obese mice on two different diets at four and 20 weeks. In obese mice, body fat mass was higher than in lean mice and was increased with age. Leptin levels correlated with body fat mass and therefore increased with age. Leptin levels were correlated higher with the weight of subcutaneous than with the weight of reproductive adipose tissue. Likewise, leptin mRNA levels in subcutaneous adipose tissue corresponded well with serum leptin levels. Adiponectin levels did not differ significantly between the ages and did not correlate with body fat mass or with either of the adipose-tissue depots, although obese mice had lower adiponectin levels than lean mice. Nevertheless, serum adiponectin levels showed a pattern of changes that was similar to that of the adiponectin transcript amounts in the reproductive adipose tissue. Our results confirm that serum leptin levels are regulated by the body fat mass, predominantly by the subcutaneous adipose tissue mass. Furthermore, our data provide evidence that serum adiponectin levels are influenced by other factors than body fat mass alone.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 41%

Age and depot-specific adipokine responses to obesity in mice

Hantschel¹,

Wagener²,

Neuschl³

et al. 2012

Health

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“…Plasma adiponectin levels normalized to adipose tissue weight As plasma adiponectin levels are determined not only by the function of adipose tissue but also by adipose tissue mass, 20 according to earlier reports on the pre-advanced stage of diet-induced obesity models, 21,22 plasma adiponectin levels were normalized by the weight of epididymal WAT. 22 The plasma adiponectin/WAT weight ratio was significantly decreased in the untreated OLETF rats down to 48% of the normal value LETO rats (Po0.05).…”

Section: Glucose Tolerancementioning

confidence: 99%

Effects of combined olmesartan and pravastatin on glucose intolerance and cardiovascular remodeling in a metabolic-syndrome model

et al. 2009

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Hypertension and dyslipidemia frequently coexist in patients with progressive insulin resistance and thus constitute metabolic syndrome. We sought to determine the merits of combining an angiotensin II receptor blocker and a 3-hydroxy-3-methylglutarylcoenzyme A reductase inhibitor in treating this pathological condition. Five-week-old Otsuka Long-Evans Tokushima Fatty rats, a model of metabolic syndrome, were untreated or treated with olmesartan 3 mg kg À1 per day, pravastatin 30 mg kg À1 per day or their combination for 25 weeks. Long-Evans Tokushima Otsuka rats served as normal controls. The antihypertensive effect of olmesartan and the lipid-lowering properties of pravastatin were both augmented by the combination. The oral glucose tolerance test revealed that only the combined treatment significantly reduced the area under the time-glucose curve, which was accompanied by augmented adiponectin messenger RNA expression in epididymal adipose tissue. Although the total cardiac endothelial nitric oxide synthetase (eNOS) content did not significantly differ among the groups, the combined treatment significantly increased the content of dihydrofolate reductase, a key eNOS coupler. Dihydroethidium staining of the aorta showed that the combination most significantly attenuated superoxide production. Moreover, Azan-Mallory staining revealed that the combination most significantly limited the perivascular fibrosis and wall thickening of intramyocardial coronary arteries. In conclusion, the combination of olmesartan and pravastatin augmented adiponectin expression in white adipose tissue and improved glucose tolerance in a rat model of metabolic syndrome, which was associated with more significant ameliorations of cardiovascular redox state and remodeling than those by treatments with either agent alone.

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“…It is worth noting that not all the components of the diet are equally eaten by the animals, as they usually have a preference for the compounds with a higher lipid content. 30 At the age of 6 months, rats from the control and cafeteria groups were submitted to three different feeding conditions (n ¼ 5 animals per group): ad libitum feeding, nocturnal 14 h fasting and 6 h re-feeding after a fasting of 14 h.…”

Section: Animalsmentioning

confidence: 99%

“…For this reason, we were interested in assessing adiponutrin and ATGL expression and nutritional regulation in adipose tissue using a rat diet-induced obesity model. To induce obesity, we selected cafeteria diet feeding; the cafeteria diet is a mixed, varied, palatable, hyperlipidic diet, extensively experienced and very useful as it mimics human obesity studies [25][26][27][28][29][30][31] because it induces voluntary hyperphagia, eliciting an increase of body weight and adipose mass in rats even after a short period of time. 32 Adipose tissue is distributed in different anatomical sites with different biological functions and metabolic activities, 33,34 and we have described important regional differences regarding adiponutrin and ATGL expression.…”

Section: Introductionmentioning

confidence: 99%

Diet-induced obesity affects expression of adiponutrin/PNPLA3 and adipose triglyceride lipase, two members of the same family

et al. 2011

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Background: Adiponutrin/PNPLA3 and adipose triglyceride lipase (ATGL) are proteins highly expressed in adipose tissue which have apparently different roles (lipogenic/lipolytic). Gene expression of both proteins and their nutritional regulation have been described to be altered in genetically obese animals. Methods: We studied adiponutrin and ATGL expression in 6-month-old rats made obese by cafeteria diet feeding, submitted to different feeding conditions (feeding/fasting/re-feeding), compared with normoweight animals. Adiponutrin and ATGL mRNA levels were determined in white adipose tissue depots (subcutaneous and visceral) and in interscapular brown adipose tissue, and ATGL protein levels in selected depots. In addition, basal adiponutrin and ATGL expression levels were compared between 6-and 3-month-old animals. Results: Obesity decreased adiponutrin and ATGL expression in different adipose depots. For adiponutrin, a tendency to lower mRNA levels was observed in the white adipose depots studied in obese animals, although the decrease was only significant in the subcutaneous depot. For ATGL, a generalized and significant lower expression was found in white and brown adipose tissue of cafeteria-obese rats. When considering nutritional regulation, according to a lipogenic role, adiponutrin mRNA expression decreased with fasting and was recovered by re-feeding in normoweight animals; this regulation was lost in obese rats. Expression of the lipolytic ATGL (mRNA and protein levels) was increased by fasting in normoweight animals in the mesenteric adipose depot, while no change was evident in obese rats. Moreover, adiponutrin and ATGL nutritional regulation was affected by age, and we report a downregulation of adiponutrin mRNA basal levels with age in internal adipose depots. Conclusions: Cafeteria diet-induced obesity and age alter adiponutrin and ATGL expression and their regulation by feeding conditions. These results reinforce the importance of a proper expression and regulation of both proteins for body weight maintenance and their role in energy metabolism.

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Adiponectin and Resistin Response in the Onset of Obesity in Male and Female Rats

Cited by 61 publications

References 41 publications

Age and depot-specific adipokine responses to obesity in mice

Age and depot-specific adipokine responses to obesity in mice

Effects of combined olmesartan and pravastatin on glucose intolerance and cardiovascular remodeling in a metabolic-syndrome model

Diet-induced obesity affects expression of adiponutrin/PNPLA3 and adipose triglyceride lipase, two members of the same family

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