Cloning, expression and chromosome localization of porcine adiponectin and adiponectin receptors genes

Dai, Menghong; Xia, Tao; Zhang, G.D.; Chen, X.D.; Gan, Li; Shi, Feng; Qiu, Hao; Peng, Yanjie; Zhou, Yang

doi:10.1016/j.domaniend.2005.06.006

Cited by 36 publications

(34 citation statements)

References 24 publications

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“…It acts through two receptors: Adipor1 and Adipor2 (Yamauchi et al 2003. Adiponectin receptors were localized in various peripheral tissues (Kharroubi et al 2003, Berner et al 2004, Ding et al 2004, Kadowaki & Yamauchi 2005, Pineiro et al 2005, Dai et al 2006, Kadowaki et al 2008. However, Adipor1 is more abundantly expressed in muscles while Adipor2 predominates in the liver (Yamauchi et al 2003).…”

Section: Introductionmentioning

confidence: 99%

Adiponectin receptors are expressed in hypothalamus and colocalized with proopiomelanocortin and neuropeptide Y in rodent arcuate neurons

Guillod-Maximin¹,

Roy²,

Vacher³

et al. 2008

Journal of Endocrinology

141

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Adiponectin is involved in the control of energy homeostasis in peripheral tissues through Adipor1 and Adipor2 receptors. An increasing amount of evidence suggests that this adipocytesecreted hormone may also act at the hypothalamic level to control energy homeostasis. In the present study, we observed the gene and protein expressions of Adipor1 and Adipor2 in rat hypothalamus using different approaches. By immunohistochemistry, Adipor1 expression was ubiquitous in the rat brain. By contrast, Adipor2 expression was more limited to specific brain areas such as hypothalamus, cortex, and hippocampus. In arcuate and paraventricular hypothalamic nuclei, Adipor1, and Adipor2 were expressed by neurons and astrocytes. Furthermore, using transgenic green fluorescent protein mice, we showed that Adipor1 and Adipor2 were present in proopiomelanocortin (POMC) and neuropeptide Y (NPY) neurons in the arcuate nucleus. Finally, adiponectin treatment by intracerebroventricular injection induced AMP-activated protein kinase (AMPK) phosphorylation in the rat hypothalamus. This was confirmed by in vitro studies using hypothalamic membrane fractions. In conclusion, Adipor1 and Adipor2 are both expressed by neurons (including POMC and NPY neurons) and astrocytes in the rat hypothalamic nuclei. Adiponectin is able to increase AMPK phosphorylation in the rat hypothalamus. These data reinforced a potential role of adiponectin and its hypothalamic receptors in the control of energy homeostasis.

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Section: Introductionmentioning

confidence: 99%

Adiponectin receptors are expressed in hypothalamus and colocalized with proopiomelanocortin and neuropeptide Y in rodent arcuate neurons

Guillod-Maximin¹,

Roy²,

Vacher³

et al. 2008

Journal of Endocrinology

141

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“…Serum adiponectin levels are inversely related to hepatic fat stores, whereas adiponectin is anti-inflammatory by opposing the synthesis and release of TNF-a from adipose tissues (Larter and Farrell, 2006;Masaki et al, 2004). Two hepatic adiponectin receptors (AdipoR1 and AdipoR2) are expressed at different levels in almost all tissues and species including porcine (Dai et al, 2006;Yamauchi et al, 2003) and regulate the phosphorylation and activation of adenosine monophosphate kinase (AMPK) and its effects on subsequent liver lipid metabolism (Kadowaki and Yamauchi, 2005). Low circulating adiponectin levels were associated with hepatic steatosis, whereas the administration of adiponectin promoted hepatic lipid oxidation and reduced lipid synthesis in ethanol-fed mice (Xu et al, 2003).…”

mentioning

confidence: 99%

S‐Adenosylmethionine Attenuates Hepatic Lipid Synthesis in Micropigs Fed Ethanol With a Folate‐Deficient Diet

Esfandiari

You

Villanueva

et al. 2007

Alcoholism Clin & Exp Res

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Background: To demonstrate a causative role of abnormal methionine metabolism in the pathogenesis of alcoholic steatosis, we measured the effects on hepatic lipid synthesis of supplementing ethanol and folate-deficient diets with S-adenosylmethionine (SAM), a metabolite that regulates methionine metabolism.Methods: Yucatan micropigs were fed folate-deficient diets as control, with ethanol at 40% of kcal, and with ethanol supplemented with SAM at 0.4 g/1,000 kcal for 14 weeks. Histopathology, triglyceride levels and transcripts, and protein levels of the regulatory signals of hepatic lipid synthesis were measured in terminal omental adipose and liver samples.Results: Feeding ethanol at 40% of kcal with folate-deficient diets for 14 weeks increased and supplemental SAM maintained control levels of liver and plasma triglyceride. Serum adiponectin, liver transcripts of adiponectin receptor-1 (AdipoR1), and phosphorylated adenosine monophosphate kinase-b (p-AMPKb) were each reduced by ethanol feeding and were sustained at normal levels by SAM supplementation of the ethanol diets. Ethanol feeding activated and SAM supplementation maintained control levels of ER stress-induced transcription factor sterol regulatory element-binding protein-1c (SREBP-1c) and its targeted transcripts of lipid synthesizing enzymes acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and glycerol-3-phosphate acyltransferase (GPAT).Conclusions: Ethanol feeding with a folate-deficient diet stimulates hepatic lipid synthesis by down-regulating adiponectin-mediated pathways of p-AMPK to increase the expression of nSREBP1c and its targeted lipogenic enzymes. Preventing abnormal hepatic methionine metabolism by supplementing ethanol diets with SAM reduces liver triglyceride levels by up-regulation of adiponectin-mediated pathways to decrease fatty acid and triglyceride synthesis. This study demonstrates that ethanol-induced hepatic lipid synthesis is mediated in part by abnormal methionine metabolism, and strengthens the concept that altered methionine metabolism plays an integral role in the pathogenesis of steatosis.

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“…Acrp30 has been partially characterized in the pig [13][14][15][16][17]. A correlation has been reported among serum levels of Acrp30, of its high-molecular weight oligomers and fat accumulation in the pig [14,16].…”

Section: Introductionmentioning

confidence: 94%

Tissue-specific downregulation of the adiponectin “system”: possible implications for fat accumulation tendency in the pig

Rosa

Monaco

Nigro

et al. 2013

Domestic Animal Endocrinology

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Cloning, expression and chromosome localization of porcine adiponectin and adiponectin receptors genes

Cited by 36 publications

References 24 publications

Adiponectin receptors are expressed in hypothalamus and colocalized with proopiomelanocortin and neuropeptide Y in rodent arcuate neurons

Adiponectin receptors are expressed in hypothalamus and colocalized with proopiomelanocortin and neuropeptide Y in rodent arcuate neurons

S‐Adenosylmethionine Attenuates Hepatic Lipid Synthesis in Micropigs Fed Ethanol With a Folate‐Deficient Diet

Tissue-specific downregulation of the adiponectin “system”: possible implications for fat accumulation tendency in the pig

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