Adiponectin receptor 1 overexpression reduces lipid accumulation and hypertrophy in the heart of diet-induced obese mice – possible involvement of oxidative stress and autophagy

Chou, I-Pin; Chiu, Yao-Pang; Ding, Shih‐Torng; Liu, Bing-Hsien; Lin, Yanfu; Chen, Ching‐Yi

doi:10.3109/07435800.2013.879165

Cited by 29 publications

(18 citation statements)

References 32 publications

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“…When adiponectin binds to its receptors (Adipor1/2), it activates adenosine 5`-monophosphate-activated protein kinase (AMPK), promoting glucose uptake by skeletal muscle via intracellular translocation of the glucose transpoter type 4 (GLUT4). Animal studies showed that Adipor1 transgene mice enabled mice to resist high fat/high sucrose diet-induced obesity while decreasing lipid accumulation [23]. We found that in mature F442A adipocytes, GH treatment increased the abundance or availability of adiponectin receptors, and increased adiponectin protein expression.…”

Section: Gh Modulates the Expression Of Genes Related To Lipolysis Inmentioning

confidence: 59%

The Effect of Growth Hormone on Lipid Accumulation or Maturation in Adipocytes

Zhang

Gao

et al. 2016

Cell Physiol Biochem

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Background: Adipogenesis of adipocytes includes two stages: initiation and maturation. Growth hormone (GH) secretion is decreased in obese subjects and GH levels are inversely correlated with abdominal fat mass. The effects of growth hormone (GH) on lipids accumulation or maturation of adipocytes remains elusive. Methods: In the present study, effect of GH on lipid accumulation in vitro and in vivo was examined. cDNA microarray, quantitative real time-PCR (qPCR) and western blotting was used to analyze the expression of genes related to adipocyte lipid accumulation or degradation in pre- or mature 3T3-F442A adipocytes treated with GH and in epididymal adipose tissue of C57BL/6 mice administrated with GH. Level of adiponectin in supernatants of cultured F442A adipocytes was determined by enzyme-linked immune-sorbent assay. Results: We found that in 3T3-F442A especially 6 days post initiation of adipogenesis, GH intervention resulted in decreased expression of adipocyte maturation regulators (C/EBPα, PPARγ) and prominent genes related to lipid synthesis such as FAS and FABP, while the expression of UCP1 was markedly enhanced. cDNA microarray analysis and qPCR showed that the expression of SOCS2 and Adipor2 was increased under GH-treatment in mature 3T3-F442A adipocytes. GH treatment increased the mRNA expression of adiponectin and UCP1 in mature adipocytes. The above results were confirmed by in vivo study. Conclusions: GH potentially negatively modulates the maturation and accumulation of lipid in adipocytes.

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Section: Gh Modulates the Expression Of Genes Related To Lipolysis Inmentioning

confidence: 59%

The Effect of Growth Hormone on Lipid Accumulation or Maturation in Adipocytes

Zhang

Gao

et al. 2016

Cell Physiol Biochem

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“…Since our first report of increased cardiac autophagy in the type 2 diabetic fructose-fed mouse (59), the experimental literature in this field has expanded considerably, but it is not yet possible to synthesize a comprehensive understanding. Relying on a variable selection of molecular tools, states of increased (4,12,49,50,59,61,78,93,102), unchanged (47,48,57,62), and decreased (6,23,28,29,73,82,101,103,104,110) basal cardiac autophagy activity have all been reported in diabetic/ insulin resistant contexts (see Table 1). These discrepancies are not necessarily attributable to the different models of diabetes, since contrasting findings have been observed within the same diabetic model [e.g., STZ-mouse: increased LC3BII (12) vs. decreased LC3BII (103)].…”

Section: )mentioning

confidence: 99%

Myocardial autophagic energy stress responses—macroautophagy, mitophagy, and glycophagy

Delbridge

Mellor

Taylor

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…AdipoR is cell autonomously required for GSC maintenance (Fig. 4), and overexpression of adiponectin receptors has been shown to enhance adiponectin signaling in mammals (Chou et al, 2014; Luo et al, 2013). We therefore wondered if increasing the expression of AdipoR in the germline might counteract the normal process of GSC loss over time.…”

Section: Resultsmentioning

confidence: 99%

Insulin-independent role of adiponectin receptor signaling in Drosophila germline stem cell maintenance

Laws¹,

Sampson²,

Drummond‐Barbosa

2015

Developmental Biology

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Adipocytes have a key endocrine role, mediated in large part by secreted protein hormones termed adipokines. The adipokine adiponectin is well known for its role in sensitizing peripheral tissues to insulin, and several lines of evidence suggest that adiponectin might also modulate stem cells/precursors. It remains unclear, however, how adiponectin signaling controls stem cells and whether this role is secondary to its insulin-sensitizing effects or distinct. Drosophila adipocytes also function as an endocrine organ and, although no obvious adiponectin homolog has been identified, Drosophila AdipoR encodes a well-conserved homolog of mammalian adiponectin receptors. Here, we generate a null AdipoR allele and use clonal analysis to demonstrate an intrinsic requirement for AdipoR in germline stem cell (GSC) maintenance in the Drosophila ovary. AdipoR null GSCs are not fully responsive to bone morphogenetic protein ligands from the niche and have a slight reduction of E-cadherin at the GSC-niche junction. Conversely, germline-specific overexpression of AdipoR inhibits natural GSC loss, suggesting that reduction in adiponectin signaling might contribute to the normal decline in GSC numbers observed over time in wild-type females. Surprisingly, AdipoR is not required for insulin sensitization of the germline, leading us to speculate that insulin sensitization is a more recently acquired function than stem cell regulation in the evolutionary history of adiponectin signaling. Our findings establish Drosophila female GSCs as a new system for future studies addressing the molecular mechanisms whereby adiponectin receptor signaling modulates stem cell fate.

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Adiponectin receptor 1 overexpression reduces lipid accumulation and hypertrophy in the heart of diet-induced obese mice – possible involvement of oxidative stress and autophagy

Abstract: The AdipoR1 transgene enabled mice to resist diet-induced obesity while decreasing lipid accumulation, oxidative stress and autophagic damage. These effects might contribute to the improvement of heart functions in diet-induced obese mice.

Cited by 29 publications

References 32 publications

The Effect of Growth Hormone on Lipid Accumulation or Maturation in Adipocytes

The Effect of Growth Hormone on Lipid Accumulation or Maturation in Adipocytes

Myocardial autophagic energy stress responses—macroautophagy, mitophagy, and glycophagy

Insulin-independent role of adiponectin receptor signaling in Drosophila germline stem cell maintenance

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