Palmitic acid interferes with energy metabolism balance by adversely switching the SIRT1-CD36-fatty acid pathway to the PKC zeta-GLUT4-glucose pathway in cardiomyoblasts

Chen, Yeh Peng; Tsai, Chia Wen; Shen, Chia Yao; Day, Cecilia Hsuan; Yeh, Yu Lan; Chen, Ray Jade; Ho, Tsung Jung; Padma, Viswanadha Vijaya; Kuo, Wei Wen; Huang, Chih Yang

doi:10.1016/j.jnutbio.2016.01.007

Cited by 27 publications

(29 citation statements)

References 34 publications

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“…From our previous finding (Chen et al, ) and from this study it is very significant that palmitic acid‐induced energy metabolism switches from CD36 to GLUT4 and decreased CD36 protein expression. Therefore, we used MG132‐proteasomal inhibitor to confirm this data.…”

Section: Resultssupporting

confidence: 66%

“…Activation of apoptosis in cardiomyocytes by saturated palmitic acids contributes to cardiac dysfunction in diabetic cardiomyopathy (Ying, Zhu, Liang, Ma, & Li, ). Similarly, in our recent study PA have been found to induce lipotoxicity in H9c2 cells and adversely switched the energy source from the CD36 pathway to the GLUT4 pathway (Chen et al, ). High‐density lipoprotein (HDL) has been reported to have cardioprotective properties (Frias, Lang, Gerber‐Wicht, & James, ); however, its role in palmitate‐induced lipotoxicity remains unclear.…”

Section: Discussionsupporting

confidence: 53%

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High density lipoprotein (HDL) reverses palmitic acid induced energy metabolism imbalance by switching CD36 and GLUT4 signaling pathways in cardiomyocyte

Velmurugan

Day

et al. 2017

Journal Cellular Physiology

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In our previous study palmitic acid (PA) induced lipotoxicity and switches energy metabolism from CD36 to GLUT4 in H9c2 cells. Low level of high density lipoprotein (HDL) is an independent risk factor for cardiac hypertrophy. Therefore, we in the present study investigated whether HDL can reverse PA induced lipotoxicity in H9c2 cardiomyoblast cells. In this study, we treated H9c2 cells with PA to create a hyperlipidemia model in vitro and analyzed for CD36 and GLUT4 metabolic pathway proteins. CD36 metabolic pathway proteins (phospho-AMPK, SIRT1, PGC1α, PPARα, CPT1β, and CD36) were decreased by high PA (150 and 200 μg/μl) concentration. Interestingly, expression of GLUT4 metabolic pathway proteins (p-PI3K and pAKT) were increased at low concentration (50 μg/μl) and decreased at high PA concentration. Whereas, phospho-PKCζ, GLUT4 and PDH proteins expression was increased in a dose dependent manner. PA treated H9c2 cells were treated with HDL and analyzed for cell viability. Results showed that HDL treatment induced cell proliferation efficiency in PA treated cells. In addition, HDL reversed the metabolic effects of PA: CD36 translocation was increased and reduced GLUT4 translocation, but HDL treatment significantly increased CD36 metabolic pathway proteins and reduced GLUT4 pathway proteins. Rat neonatal cardiomyocytes showed similar results. In conclusion, HDL reversed palmatic acid-induced lipotoxicity and energy metabolism imbalance in H9c2 cardiomyoblast cells and in neonatal rat cardiomyocyte cells.

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Section: Resultssupporting

confidence: 66%

Section: Discussionsupporting

confidence: 53%

High density lipoprotein (HDL) reverses palmitic acid induced energy metabolism imbalance by switching CD36 and GLUT4 signaling pathways in cardiomyocyte

Velmurugan

Day

et al. 2017

Journal Cellular Physiology

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“…Palmitic acid and high-fat diets cause lipotoxicity in vivo and in vitro and adversely switch the energy source from the CD36 pathway to the GLUT4 pathway [12]. Recently, a review by Maréchal et al has emphasized that growth hormone releasing peptides (GHRP) are a potent inducer of PPAR through activation of CD36 [7], thereby regulating essential aspects of lipid and energy metabolism [30].…”

Section: Nifedipine Upregulated the Expression Of Cd36 Proteins Relatmentioning

confidence: 99%

“…To understand whether the cholesterol accumulating effect of nifedipine was due to stimulation of the de novo biosynthetic pathway or merely because of translocation, we further explored the effect of nifedipine on the de novo biosynthetic pathway of cholesterol. 12 Nifedipine stimulated the production of the enzyme acetyl CoA synthase (ACS) (p < 0.05 at 7.5 M; p < 0.01 at 15 M and 30 M compared to controls) (Fig 4a), acetyl CoA carboxylase (ACC) to 128.5% and 144.4% of the control values at 15 M and 30 M doses (p < 0.05) (Fig 4b), and long chain fatty acyl elongase (ACSL1) (p < 0.01 at all concentrations) (Fig 4c), but simultaneously inhibited fatty acid synthase (FAS) (Fig 4d), and p-ACC (p < 0.01) because of inhibitory phosphorylation of ACC (Fig 4b). Two pathways of butyrate synthesis by fatty acid synthetase have been identified [31].…”

Section: Nifedipine Upregulated the Expression Of Cd36 Proteins Relatmentioning

confidence: 99%

“…SREBP-1c, regulated by the insulin and AMPK signaling pathways, was found to play a role in nonalcoholic fatty liver disease [11]. In addition, lipin plays an important role in lipid metabolic homeostasis [12]. Lipin-1 has been shown to act as a key mediator of the effects of mTORC1 on SREBP-dependent fatty acid and cholesterol biosynthesis [13].…”

Section: Introductionmentioning

confidence: 99%

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Nifedipine Modulated Renal Lipogenesis via AMPK-SREBP Transcriptional Pathways

Lin

Chen

et al. 2018

Preprint

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The hypothesis being tested Lipid accumulation in renal cells has been implicated in the pathogenesis of obesity-related kidney disease, and lipotoxicity occurring in kidney can be considered to be a surrogate marker for renal failure or renal fibrosis. Nifedipine-induced lipotoxicity in kidney has never been cited, although a few literature had shown that Nifedipine inhibited lipogenesis via activation of the LKB1-AMPK pathway. Previously, we had recognized in our laboratory some events that seemingly were associated with lipogenesis affected by administration of Nifedipine.

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GPRC6A is a key mediator of palmitic acid regulation of lipid synthesis in bovine mammary epithelial cells

Jin

Zhen

Wang

et al. 2022

Cell Biology International

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Fatty acids (FAs) can promote lipid synthesis in the mammary gland via stimulating lipogenic gene expression, but the underlying molecular mechanism is still not fully understood. Here, we showed the dose‐dependent effects of palmitic acid (PA) on lipid synthesis in primary bovine mammary epithelial cells (BMECs) and explored the corresponding molecular mechanism. BMECs were treated with PA (0, 50, 100, 150, and 200 μM), and the 100 μM treatment had the best stimulatory effect on lipid synthesis and expression and maturation of sterol regulatory element‐binding protein 1c (SREBP‐1c) in cells. Inhibition of phosphatidylinositol 3‐kinase (PI3K) almost totally blocked the stimulation of PA on SREBP‐1c expression, whereas protein kinase Cα (PKCα) knockdown only partially decreased the stimulation of PA on SREBP‐1c expression but abolished the stimulation of PA on its maturation. Knockdown of GPR120 did not change the stimulation of PA on the SREBP‐1c signaling. G protein‐coupled receptor family C group 6 member A (GPRC6A) knockdown almost totally blocked the stimulation of FA on PI3K and PKCα phosphorylation as well as SREBP‐1c expression and maturation. Furthermore, PA dose‐dependently promoted GPRC6A expression and plasma membrane localization. Together, these above results reveal that GPRC6A is a key mediator of PA signaling to lipid synthesis in BMECs via the PI3K/PKCα–SREBP‐1c pathways.

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Palmitic acid interferes with energy metabolism balance by adversely switching the SIRT1-CD36-fatty acid pathway to the PKC zeta-GLUT4-glucose pathway in cardiomyoblasts

Cited by 27 publications

References 34 publications

High density lipoprotein (HDL) reverses palmitic acid induced energy metabolism imbalance by switching CD36 and GLUT4 signaling pathways in cardiomyocyte

High density lipoprotein (HDL) reverses palmitic acid induced energy metabolism imbalance by switching CD36 and GLUT4 signaling pathways in cardiomyocyte

Nifedipine Modulated Renal Lipogenesis via AMPK-SREBP Transcriptional Pathways

GPRC6A is a key mediator of palmitic acid regulation of lipid synthesis in bovine mammary epithelial cells

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