Cloning and expression of porcine adiponectin, and its relationship to adiposity, lipogenesis and the acute phase response

Jacobi, SK; Ajuwon, KM; Weber, T. E.; Kuske, JL; Dyer, CJ; Spurlock, M. E.

doi:10.1677/joe.0.1820133

Cited by 57 publications

(40 citation statements)

References 34 publications

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“…Interestingly, polymorphism ϩ45T3 G showed a strong association with body adiposity in diabetic women. Such an association is consistent with the autocrine function of adiponectin in regulating fat accumulation at adipose tissue (26). However, given its silent nature, ϩ45T3 G more likely acts as a genetic marker for other unknown causal variants.…”

Section: Discussionsupporting

confidence: 68%

Adiponectin Genetic Variability, Plasma Adiponectin, and Cardiovascular Risk in Patients With Type 2 Diabetes

et al. 2006

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Adiponectin is an adipocyte-derived hormone that has shown anti-inflammatory and antiatherogenic effects. We assessed the associations of variants in the adiponectin gene (ADIPOQ) with circulating adiponectin levels and cardiovascular risk among women with type 2 diabetes. Of 989 diabetic women from the Nurses' Health Study, 285 developed cardiovascular disease (CVD) during follow-up through 2000. We genotyped five ADIPOQ polymorphisms in the CVD case and control subjects. A promoter polymorphism ؊11365C3 G was significantly associated with lower plasma adiponectin levels (P ‫؍‬ 0.004). The homozygotes of allele ؊4034C were significantly associated with ϳ60% increased cardiovascular risk (odds ratio 1.62 [95% CI 1.07-2.45]). Adjustment for age, BMI, and other covariates did not appreciably change the associations. In addition, a common haplotype possessing allele ؉276T (CAATT) was associated with a significantly lower CVD risk than the most common haplotype (CAATG) (0.70 [0.50 -0.98]). In our meta-analysis of 827 CVD case and 1,887 CVD-free control subjects, polymorphism ؉276G3 T was significantly associated with ϳ45% (20 -62%) decreased CVD risk under a recessive inheritance mode in diabetic patients. In conclusion, ADIPOQ promoter polymorphism ؊11365C3 G was associated with plasma adiponectin levels, whereas polymorphisms ؊4034A3 C and ؉276G3 T were associated with CVD risk in diabetic patients.

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Section: Discussionsupporting

confidence: 68%

Adiponectin Genetic Variability, Plasma Adiponectin, and Cardiovascular Risk in Patients With Type 2 Diabetes

et al. 2006

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“…It has been reported that LPS injection in mammals does not affect adiponectin expression in adipose tissue (Gomez-Ambrosi et al, 2004;Jacobi et al, 2004). In our experiment, the first response of adipose tissue was to increase the expression of adipoR1, which could indicate an increased mobilization of the lipid reserves to other tissues with immune function, such as spleen or head kidney.…”

Section: In Vivo Experimentsmentioning

confidence: 47%

Adiponectin effects and gene expression in rainbow trout: an in vivo and in vitro approach

Sanchez-Gurmaches

Cruz-García

Gutiérrez

et al. 2012

Journal of Experimental Biology

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SUMMARYHere we present the presence of adiponectin and adiponectin receptors [type 1 (adipoR1) and type 2 (adipoR2)] in rainbow trout (Oncorhynchus mykiss) tissues and cell cultures together with the response to different scenarios. In response to fasting, adiponectin expression was up-regulated in adipose tissue, while the expression of its receptors increased in white and red muscle. Insulin injection decreased adipoR1 expression in white and red muscles. We deduce that the adipoRs in trout muscle show opposite responses to increasing insulin plasma levels, which may maintain sensitivity to insulin in this tissue. Adiponectin expression was inhibited by the inflammatory effect of lipopolysaccharide (LPS) in adipose tissue and red muscle. Moreover, results indicate that LPS may lead to mobilization of fat reserves, increasing adipoR1 expression in adipose tissue. The effects of LPS could be mediated through tumour necrosis factor  (TNF), at least in red muscle. Insulin, growth hormone and TNF all diminished expression of adipoR2 in adipocytes and adipoR1 in myotubes, while insulin increased the expression of adipoR2 in the muscle cells. Adiponectin activates Akt in rainbow trout myotubes, which may lead to an increase in fatty acid uptake and oxidation. Overall, our results show that the adiponectin system responds differently to various physiological challenges and that it is hormonally controlled in vivo and in vitro. To the best of our knowledge, this is the first time this has been demonstrated in teleosts, and it may be a valuable contribution to our understanding of adipokines in fish.

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“…This study is the first to show adiponectin expression during bovine adipocytes differentiation. The major adiponectin transcript in bovine adipocytes is approximately 2.5kb and there are at least two additional transcripts, like swine and rat adiponectin genes [33][34][35], whereas mouse adipose tissue expresses a single transcript [33].…”

Section: Discussionmentioning

confidence: 99%

Inverse regulation of leptin mRNA expression by short- and long-chain fatty acids in cultured bovine adipocytes

Soliman

Kimura

Ahmed

et al. 2007

Domestic Animal Endocrinology

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Leptin is an adipose tissue-derived cytokine plays key roles in the regulation of food intake and energy expenditure. However, regulatory mechanisms of leptin gene expression are not fully elucidated in ruminants that utilize short-chain fatty acids (SCFA), known as volatile fatty acids, as principal energy sources. In this study, we determined effects of SCFA and long-chain fatty acids (LCFA) on leptin expression in bovine adipocytes. Bovine stromal vascular cells isolated from subcutaneous adipose tissue of Holstein cows were cultured to confluence and treated sequentially with dexamethasone and isobutylmethylxanthine for 2 days and insulin and troglitazone for 12 days to achieve full differentiation to adipocytes. The cells started to accumulate lipids 4 days after the onset of treatment, with increased mRNAs expression of leptin, as well as aP2, adiponectin, and PPAR-γ  Removal of fetal calf serum and reduction of glucose in the culture medium of differentiated adipocytes decreased leptin mRNA expression.Subsequent addition of acetate, butyrate, or propionate dose-dependently restored and rather increased leptin expression, while addition of LCFA suppressed it. The stimulatory effect of acetate was abolished by prior treatment of the cells with pertussis toxin and by addition of LCFA. Furthermore, cows fasted for 48h and fed thereafter, elaborate reduced and increased plasma leptin levels, respectively. Thus, these results suggest that plasma leptin levels in cows are inversely controlled at transcription by VFA and LCFA, and that the effects of SCFA possibly act through a G protein-coupled receptor for SCFA.

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Cloning and expression of porcine adiponectin, and its relationship to adiposity, lipogenesis and the acute phase response

Cited by 57 publications

References 34 publications

Adiponectin Genetic Variability, Plasma Adiponectin, and Cardiovascular Risk in Patients With Type 2 Diabetes

Adiponectin Genetic Variability, Plasma Adiponectin, and Cardiovascular Risk in Patients With Type 2 Diabetes

Adiponectin effects and gene expression in rainbow trout: an in vivo and in vitro approach

Inverse regulation of leptin mRNA expression by short- and long-chain fatty acids in cultured bovine adipocytes

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