AMPK-mediated increase in myocardial long-chain fatty acid uptake critically depends on sarcolemmal CD36

Habets, Daphna D. J.; Coumans, Will A.; Voshol, Peter J.; Boer, Marion A. M. den; Febbraio, Maria; Bonen, Arend; Glatz, Jan F. C.; Luiken, Joost J. F. P.

doi:10.1016/j.bbrc.2007.01.141

Cited by 132 publications

(118 citation statements)

References 23 publications

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“…The present study documents that FABPpm, FAT/CD36, FATP1, and FATP4 all exhibit fatty acid transport capacities in skeletal muscle. This concurs with studies in FABPpm-overexpressing muscle, in which fatty acid transport was increased (28), and with studies in FAT/CD36 null (23) and FATP1 null mice (51), in which fatty acid transport was reduced. Unlike some studies in cultured cells, in which FATP4 appears not to be located at the plasma membrane and/or has no fatty acid transport role per se (19,20), we and others find that FATP4 is present at the plasma membrane in rat (present study) (11) and human skeletal muscle (12).…”

Section: Relationship Between Fatty Acid Transporters and Indices Of supporting

confidence: 90%

“…This approach has been used previously in our laboratory (26 -28) to overexpress selected proteins. A key feature in the present study is that we overexpressed each fatty acid transporter independently without altering the expression of the other fatty acid transporters, thereby avoiding the compensatory responses that have been observed in animals in which a fatty acid transporter has been ablated (23,24). We also show that the inde- (Fig.…”

Section: Relationship Between Fatty Acid Transporters and Indices Of mentioning

confidence: 71%

“…Assessment of fatty acid transporter effectiveness, in vivo, cannot be determined in knock-out animals, since compensatory responses in some fatty acid transporters (FATP1 and -4) occur when another fatty acid transporter (FAT/CD36) has been ablated (23,24). Thus, the relative effectiveness of selected fatty acid transporters on fatty acid transport in vivo remains unknown.…”

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confidence: 99%

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Greater Transport Efficiencies of the Membrane Fatty Acid Transporters FAT/CD36 and FATP4 Compared with FABPpm and FATP1 and Differential Effects on Fatty Acid Esterification and Oxidation in Rat Skeletal Muscle

Nickerson

Alkhateeb

Benton

et al. 2009

Journal of Biological Chemistry

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168

144

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In selected mammalian tissues, long chain fatty acid transporters (FABPpm, FAT/CD36, FATP1, and FATP4) are co-expressed. There is controversy as to whether they all function as membrane-bound transporters and whether they channel fatty acids to oxidation and/or esterification. Among skeletal muscles, the protein expression of FABPpm, FAT/CD36, and FATP4, but not FATP1, correlated highly with the capacities for oxidative metabolism (r > 0.94), fatty acid oxidation (r > 0.88), and triacylglycerol esterification (r > 0.87). We overexpressed independently FABPpm, FAT/CD36, FATP1, and FATP4, within a normal physiologic range, in rat skeletal muscle, to determine the effects on fatty acid transport and metabolism. Independent overexpression of each fatty acid transporter occurred without altering either the expression or plasmalemmal content of other fatty acid transporters. All transporters increased fatty acid transport, but FAT/CD36 and FATP4 were 2.3-and 1.7-fold more effective than FABPpm and FATP1, respectively. Fatty acid transporters failed to alter the rates of fatty acid esterification into triacylglycerols. In contrast, all transporters increased the rates of long chain fatty acid oxidation, but the effects of FABPpm and FAT/CD36 were 3-fold greater than for FATP1 and FATP4. Thus, fatty acid transporters exhibit different capacities for fatty acid transport and metabolism. In vivo, FAT/CD36 and FATP4 are the most effective fatty acid transporters, whereas FABPpm and FAT/CD36 are key for stimulating fatty acid oxidation.

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Section: Relationship Between Fatty Acid Transporters and Indices Of supporting

confidence: 90%

Section: Relationship Between Fatty Acid Transporters and Indices Of mentioning

confidence: 71%

mentioning

confidence: 99%

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Greater Transport Efficiencies of the Membrane Fatty Acid Transporters FAT/CD36 and FATP4 Compared with FABPpm and FATP1 and Differential Effects on Fatty Acid Esterification and Oxidation in Rat Skeletal Muscle

Nickerson

Alkhateeb

Benton

et al. 2009

Journal of Biological Chemistry

Self Cite

168

144

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“…ACC is a classic AMPK target and phosphorylation inhibits the action of ACC to synthesize malonyl-CoA, a potent inhibitor of CPT-1, the rate-limiting step for mitochondrial fatty acid oxidation (27). AMPK is also known to activate glucose uptake and glycolysis (28) as well as fatty acid uptake (29) in the heart. These effects of Ucn2 to promote cardiac metabolism further elucidate its pharmacologic The recovery of LV contractile function in these hearts after ischemia determined by the product of LV developed pressure (LVDP) and heart rate (HR).…”

Section: Discussionmentioning

confidence: 99%

Urocortin 2 autocrine/paracrine and pharmacologic effects to activate AMP-activated protein kinase in the heart

Qi²,

Cheng

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Urocortin 2 (Ucn2), a peptide of the corticotropin-releasing factor (CRF) family, binds with high affinity to type 2 CRF receptors (CRFR2) on cardiomyocytes and confers protection against ischemia/reperfusion. The mechanisms by which the Ucn2-CRFR2 axis mitigates against ischemia/reperfusion injury remain incompletely delineated. Activation of AMP-activated protein kinase (AMPK) also limits cardiac damage during ischemia/reperfusion. AMPK is classically activated by alterations in cellular energetics; however, hormones, cytokines, and additional autocrine/paracrine factors also modulate its activity. We examined the effects of both the endogenous cardiac Ucn2 autocrine/paracrine pathway and Ucn2 treatment on AMPK regulation. Ucn2 treatment increased AMPK activation and downstream acetyl-CoA carboxylase phosphorylation and glucose uptake in isolated heart muscles. These actions were blocked by the CRFR2 antagonist anti-sauvagine-30 and by a PKCe translocation-inhibitor peptide (eV1-2). Hypoxia-induced AMPK activation was also blunted in heart muscles by preincubation with either anti-sauvagine-30, a neutralizing anti-Ucn2 antibody, or eV1-2. Treatment with Ucn2 in vivo augmented ischemic AMPK activation and reduced myocardial injury and cardiac contractile dysfunction after regional ischemia/reperfusion in mice. Ucn2 also directly activated AMPK in ex vivo-perfused mouse hearts and diminished injury and contractile dysfunction during ischemia/reperfusion. Thus, both Ucn2 treatment and the endogenous cardiac Ucn2 autocrine/paracrine pathway activate AMPK signaling pathway, via a PKCe-dependent mechanism, defining a Ucn2-CRFR2-PKCe-AMPK pathway that mitigates against ischemia/reperfusion injury. metabolism | cardiac function

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“…That causes to reduce malonyl-coA level which results in the decrease of FA transportation and oxidation in mitochondria and ultimately decreases the toxicity in cells. In addition, AMPK is also an activator for expression of fatty acid transport proteins, FAT/CD36 and plasma membrane fatty acid-binding protein (FABPpm), in a time dependent and dose dependent, which were not overexpressed when the AMPK phosphorylation was blocked [41,53,54]. Thus, AMPK is an essential 'master regulator' of the metabolism of sugar and FA for the normal functioning of heart.…”

Section: Amp Activated Protein Kinasementioning

confidence: 99%

Lipid-induced cardiovascular diseases

Manandhar¹,

Ju²,

Choi³

et al. 2017

J Cardiol Cardiovasc Med

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Cardiovascular diseases are the leading cause of death worldwide. There are many evidences that the dysfunctioning lipotoxicity is the one of major factors of cardiovascular diseases such as, atherosclerosis, hypertension, and coronary heart disease. Obesity and diabetes increase circulating lipids that are likely with more generation of toxic intermediates, which leading to the complications associated with cardiovascular diseases. Indeed, lipotoxicity is a metabolic syndrome caused by abnormal lipid accumulation, which leads to cellular dysfunction and necrosis. Here we review the factors that induced pathogenesis of cardiovascular diseases by lipid accumulation and the mechanisms underlying the lipotoxicity.

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AMPK-mediated increase in myocardial long-chain fatty acid uptake critically depends on sarcolemmal CD36

Cited by 132 publications

References 23 publications

Greater Transport Efficiencies of the Membrane Fatty Acid Transporters FAT/CD36 and FATP4 Compared with FABPpm and FATP1 and Differential Effects on Fatty Acid Esterification and Oxidation in Rat Skeletal Muscle

Greater Transport Efficiencies of the Membrane Fatty Acid Transporters FAT/CD36 and FATP4 Compared with FABPpm and FATP1 and Differential Effects on Fatty Acid Esterification and Oxidation in Rat Skeletal Muscle

Urocortin 2 autocrine/paracrine and pharmacologic effects to activate AMP-activated protein kinase in the heart

Lipid-induced cardiovascular diseases

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