FABP4 reversed the regulation of leptin on mitochondrial fatty acid oxidation in mice adipocytes

Gan, Lu; Liu, Zhenjiang; Cao, Weina; Zhang, Zhenzhen; Sun, Cheng

doi:10.1038/srep13588

Cited by 56 publications

(51 citation statements)

References 37 publications

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“…In brief, adipose tissues was homogenized in sucrose/Tris/EDTA buffer, and incubated for 60 min in the reaction mixture which contained [1- 14 C] palmitic acid and measured for trapped CO 2 . For in vivo study of palmitate oxidation to CO 2 , we used the modified method from Sebastián and our pervious study5556. For the trapped radioactive CO 2 measurement, a parafilm-sealed system was used.…”

Section: Methodsmentioning

confidence: 99%

α-MSH and Foxc2 promote fatty acid oxidation through C/EBPβ negative transcription in mice adipose tissue

Gan

Liu

Chen

et al. 2016

Sci Rep

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Alpha melanocyte stimulating hormone (α-MSH) and Forkhead box C2 protein (Foxc2) enhance lipolysis in multiple tissues. However, their relationship in adipose fatty acid oxidation (FAO) remains unclear. Here, we demonstrated that α-MSH and Foxc2 increased palmitate oxidation to CO2 in white (WAT) and brown adipose tissue (BAT). C/EBPβ expression was reduced by α-MSH and Foxc2. FFA level was elevated by α-MSH and pc-Foxc2 treatment along with increased FAO in white and brown adipocytes. The expression of FAO key enzymes, medium-chain acyl-CoA dehydrogenase (MCAD) and long-chain acyl-CoA dehydrogenase (LCAD) were increased in α-MSH and pc-Foxc2 group. Combination of α-MSH and Foxc2 treatment synergistically promoted FAO through increasing the activity of CPT-1 and phosphorylation of ACC. We found C/EBPβ bind to MC5R and Foxc2 promoter regions and inhibited FAO. cAMP level was increased by α-MSH and Foxc2 individually treated or combined treatment. Furthermore, cAMP/PKA pathway-specific inhibitor (H89) blocked the FAO, despite in α-MSH and Foxc2 both added group. While forskolin, the cAMP agonist, promoted FAO and enhanced the effect of α-MSH and Foxc2. Collectively, α-MSH and Foxc2 mutual promote FAO in WAT and BAT via cAMP/PKA signal pathway. And C/EBPβ as a transcription suppressor inhibits α-MSH and Foxc2 expression and FAO.

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Section: Methodsmentioning

confidence: 99%

α-MSH and Foxc2 promote fatty acid oxidation through C/EBPβ negative transcription in mice adipose tissue

Gan

Liu

Chen

et al. 2016

Sci Rep

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“…FABP4, identified as a cytosolic protein, is strongly up-regulated during differentiation of preadipocytes into adipocytes [21, 38]. Here, we first determined that Hoxa5 acts as a transcriptional activator of the key adipogenic factor-Fabp4.…”

Section: Discussionmentioning

confidence: 99%

“…The X-treme GENE HP Reagent (Roche, Switzerland) was used in plasmids transfection. The transfection procedure was as described in our previous reports in detail [21]. …”

Section: Methodsmentioning

confidence: 99%

Hoxa5 Promotes Adipose Differentiation via Increasing DNA Methylation Level and Inhibiting PKA/HSL Signal Pathway in Mice

Cao

Luo

Saeed

et al. 2018

Cell Physiol Biochem

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Background/Aims: Impaired adipogenesis may be the underlying cause in the development of obesity and type II diabetes. Mechanistically, the family of Homeobox transcription factors is implicated in the regulation of adipocyte fate. Hoxa5 is highly expressed in adipocytes, and its mRNA expression is decreased during differentiation. However, the function of Hoxa5 in adipose tissue has been poorly understood. The aim of this study is to unveil the role of Hoxa5 on adipocyte differentiation and its underlying mechanisms. Methods: Quantitative real-time PCR (qPCR) and western blot were performed to determine Hoxa5 expression in primary adipocytes and in adipose tissues from mice. Lipid accumulation was evaluated by bodipy staining. Dual luciferase assay was applied to explore the transcription factor of Hoxa5 and the transcriptional target gene modulated by Hoxa5. All measurements were performed at least for three times at least. Results: A significant reduction of Hoxa5 expression was observed in adipose tissue of High Fat Diet (HFD) induced obesity mice. We determined Hoxa5 increased adipocytes differentiation and mitochondrial biogenesis in adipocytes in vitro. CEBPβ was determined a transcription factor of Hoxa5 and inhibited methylation level of Hoxa5 by combining on the promoter of Hoxa5. Importantly, we found Fabp4, a known positive regulator of adipocytes differentiation, was transcriptional activation by Hoxa5. In addition, Hoxa5 promotes adipocytes differentiation by inhibiting PKA/HSL pathway. Conclusion: Our study demonstrated the promoting role of Hoxa5 in adipocytes differentiation and therefore bringing a new therapeutic mean to the treatment of obesity and type II diabetes.

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“…It has been reported that knockout mice with null Fabp4 expression had an increase of EAT mass [42]. Moreover, the fatty acids solubility could trigger other routes that are related with the Lep role [43].…”

Section: Discussionmentioning

confidence: 99%

Amaranth Protein Improves Lipid Profile and Insulin Resistance in a Diet-induced Obese Mice Model

Escobedo-Moratilla¹,

Velarde‐Salcedo²,

Magaña-Hernández³

et al. 2017

JFNR

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Amaranth has been claimed as functional food, but its function on obesity-related disorder is not fully known. The aim of this study was to analyse the effect of amaranth protein intake on blood lipids profile and insulin resistance in diet-induced obese mice. The effect of soybean protein was also analysed for comparative purposes. C57BL-6 mice were fed for eight weeks with regular or high fat diet. Amaranth or soybean protein isolates (10 mg/kg) were supplied via oral administration. Changes in body weight, adipose tissue, total cholesterol, triglycerides, insulin, a glucose tolerance test, as well as the expression of lipid metabolism-related genes were measured. Our results have shown that amaranth protein induces a decrease in plasma insulin in mice fed with a regular diet, whereas a decrease in triglycerides was observed in mice fed with high fat diet. Furthermore, down-regulation of Tnf-α and Res, suggested the inhibition of inflammation state. The present study demonstrates that amaranth protein, but not soybean protein, improves the obese mice health, and the hormonal modulation (Lep, Fasn, Lpl) could lead to new mechanism of action by which amaranth consumption exerts its beneficial health effect.

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FABP4 reversed the regulation of leptin on mitochondrial fatty acid oxidation in mice adipocytes

Cited by 56 publications

References 37 publications

α-MSH and Foxc2 promote fatty acid oxidation through C/EBPβ negative transcription in mice adipose tissue

α-MSH and Foxc2 promote fatty acid oxidation through C/EBPβ negative transcription in mice adipose tissue

Hoxa5 Promotes Adipose Differentiation via Increasing DNA Methylation Level and Inhibiting PKA/HSL Signal Pathway in Mice

Amaranth Protein Improves Lipid Profile and Insulin Resistance in a Diet-induced Obese Mice Model

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