CD36 regulates substrates utilisation in brown adipose tissue of spontaneously hypertensive rats: In vitro study
Jazyk angličtina Země Spojené státy americké Médium electronic-ecollection
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
37053180
PubMed Central
PMC10101526
DOI
10.1371/journal.pone.0283276
PII: PONE-D-22-29497
Knihovny.cz E-zdroje
- MeSH
- antigeny CD36 * genetika metabolismus MeSH
- glukosa metabolismus MeSH
- GSK3B metabolismus MeSH
- hnědá tuková tkáň * metabolismus MeSH
- krysa rodu Rattus MeSH
- mastné kyseliny metabolismus MeSH
- palmitany metabolismus MeSH
- potkani inbrední SHR MeSH
- potkani transgenní MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antigeny CD36 * MeSH
- glukosa MeSH
- GSK3B MeSH
- mastné kyseliny MeSH
- palmitany MeSH
Thermogenesis in brown adipose tissue (BAT) uses intracellular triglycerides, circulating free fatty acids and glucose as the main substrates. The objective of the current study was to analyse the role of CD36 fatty acid translocase in regulation of glucose and fatty acid utilisation in BAT. BAT isolated from spontaneously hypertensive rat (SHR) with mutant Cd36 gene and SHR-Cd36 transgenic rats with wild type variant was incubated in media containing labeled glucose and palmitate to measure substrate incorporation and oxidation. SHR-Cd36 versus SHR rats showed significantly increased glucose incorporation into intracellular lipids associated with reduced glycogen synthase kinase 3β (GSK-3β) protein expression and phosphorylation and increased oxidation of exogenous palmitate. It can be concluded that CD36 enhances glucose transport for lipogenesis in BAT by suppressing GSK-3β and promotes direct palmitate oxidation.
Department of Physiology Faculty of Science Charles University Prague Czech Republic
Institute for Clinical and Experimental Medicine Prague Czech Republic
Institute of Physiology Czech Academy of Sciences Prague Czech Republic
Zobrazit více v PubMed
Bartelt A, Bruns OT, Reimer R, Hohenberg H, Ittrich H, Peldschus K, et al.. Brown adipose tissue activity controls triglyceride clearance. Nat Med. 2011;17: 200–205. doi: 10.1038/nm.2297 PubMed DOI
Vijgen GH, Bouvy ND, Teule GJ, Brans B, Schrauwen P, van Marken Lichtenbelt WD. Brown adipose tissue in morbidly obese subjects. PLoS One. 2011;6: e17247. doi: 10.1371/journal.pone.0017247 PubMed DOI PMC
Virtanen KA. The rediscovery of BAT in adult humans using imaging. Best Pract Res Clin Endocrinol Metab. 2016;30: 471–477. doi: 10.1016/j.beem.2016.09.001 PubMed DOI
Pravenec M, Zídek V, Mlejnek P, Landa V, Mlejnek P, Šilhavý J, et al.. Systems analysis of brown adipose tissue function in recombinant inbred rats. Physiol Genomics. 2018;50: 52–66. PubMed PMC
Glazier AM, Scott J, Aitman TJ. Molecular basis of the Cd36 chromosomal deletion underlying SHR defects in insulin action and fatty acid metabolism. Mamm Genome. 2002;13: 108–113. doi: 10.1007/s00335-001-2132-9 PubMed DOI
Aitman TJ, Gotoda T, Evans AL, Imrie H, Heath KE, Trembling PM, et al.. (1997) Quantitative trait loci for cellular defects in glucose and fatty acid metabolism in hypertensive rats. Nat Genet. 1997;16: 197–201. PubMed
Aitman TJ, Glazier AM, Wallace CA, Cooper LD, Norsworthy PJ, Wahid FN, et al.. Identification of Cd36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats. Nat Genet. 1999;21: 76–83. doi: 10.1038/5013 PubMed DOI
Pravenec M, Zídek V, Šimáková M, Křen V, Křenová D, Horký K, et al.. Genetics of Cd36 and the clustering of multiple cardiovascular risk factors in spontaneous hypertension. J Clin Invest. 1999; 103: 1651–1657. doi: 10.1172/JCI6691 PubMed DOI PMC
Pravenec M, Landa V, Zídek V, Musilová A, Křen V, Kazdová L, et al.. Transgenic rescue of defective Cd36 ameliorates insulin resistance in spontaneously hypertensive rats. Nat Genet. 2001;27: 156–158. doi: 10.1038/84777 PubMed DOI
Pravenec M, Churchill PC, Churchill MC, Viklický O, Kazdová L, Aitman TJ, et al.. Identification of renal Cd36 as a determinant of blood pressure and risk for hypertension. Nat Genet. 2008;40: 952–954. doi: 10.1038/ng.164 PubMed DOI
Hankir MK, Klingenspor M. Brown adipocyte glucose metabolism: a heated subject. EMBO Rep. 2018;19: e46404. doi: 10.15252/embr.201846404 PubMed DOI PMC
Labbé SM, Caron A, Bakan I, Laplante M, Carpentier AC, Lecomte R, et al.. In vivo measurement of energy substrate contribution to cold-induced brown adipose tissue thermogenesis. FASEB J. 2015;29: 2046–2058. doi: 10.1096/fj.14-266247 PubMed DOI
Putri M, Syamsunarno MR, Iso T, Yamaguchi A, Hanaoka H, Sunaga H, et al..(2015) CD36 is indispensable for thermogenesis under conditions of fasting and cold stress. Biochem Biophys Res Commun. 2015;457: 520–525. PubMed PMC
Trnovská J, Šilhavý J, Kuda O, Landa V, Zídek V, Mlejnek P, et al.. Salsalate ameliorates metabolic disturbances by reducing inflammation in spontaneously hypertensive rats expressing human C-reactive protein and by activating brown adipose tissue in nontransgenic controls. PLoS One. 2017;12: e0179063. doi: 10.1371/journal.pone.0179063 PubMed DOI PMC
Novotný J, Bourová L, Kolář F, Svoboda P. Membrane-bound and cytosolic forms of heterotrimeric G proteins in young and adult rat myocardium: influence of neonatal hypo- and hyperthyroidism. J Cell Biochem. 2001;82: 215–224. doi: 10.1002/jcb.1157 PubMed DOI
Hajri T, Han XX, Bonen A, Abumrad NA. Defective fatty acid uptake modulates insulin responsiveness and metabolic responses to diet in CD36-null mice. J Clin Invest. 2002;109: 1381–1389. doi: 10.1172/JCI14596 PubMed DOI PMC
Goudriaan JR, Dahlmans VE, Teusink B, Ouwens DM, Febbraio M, Maassen JA, et al.. CD36 deficiency increases insulin sensitivity in muscle, but induces insulin resistance in the liver in mice. J Lipid Res. 2003;44: 2270–2277. doi: 10.1194/jlr.M300143-JLR200 PubMed DOI
Son N-H, Basu D, Samovski D, Pietka TA, Peche VS, Willecke F, et al.. Endothelial cell CD36 optimizes tissue fatty acid uptake. J Clin Invest. 2018;128: 4329–4342. doi: 10.1172/JCI99315 PubMed DOI PMC
Samovski D, Dhule P, Pietka T, Jacome-Sosa M, Penrose E, Son NH, et al.. Regulation of insulin receptor pathway and glucose metabolism by CD36 signaling. Diabetes. 2018;67: 1272–1284. doi: 10.2337/db17-1226 PubMed DOI PMC
Yang P, Zeng H, Tan W, Luo X, Zheng E, Zhao L, et al.. Loss of CD36 impairs hepatic insulin signaling by enhancing the interaction of PTP1B with IR. FASEB J. 2020;34: 5658–5672. doi: 10.1096/fj.201902777RR PubMed DOI
Eldar-Finkelman H, Krebs EG. Phosphorylation of insulin receptor substrate 1 by glycogen synthase kinase 3 impairs insulin action. Proc Natl Acad Sci USA. 1997;94: 9660–9664. doi: 10.1073/pnas.94.18.9660 PubMed DOI PMC
Sun S, Tan P, Huang X, Kong C, Ren F, Su X. Ubiquitinated CD36 sustains insulin-stimulated Akt activation by stabilizing insulin receptor substrate 1 in myotubes. J Biol Chem. 2018;293: 2383–2394. doi: 10.1074/jbc.M117.811471 PubMed DOI PMC
Markussen LK, Winther S, Wicksteed B, Hansen JB. GSK3 is a negative regulator of the thermogenic program in brown adipocytes. Sci Rep. 2018;8: 3469. doi: 10.1038/s41598-018-21795-y PubMed DOI PMC
Irshad Z, Dimitri F, Christian M, Zammit VA. Diacylglycerol acyltransferase 2 links glucose utilization to fatty acid oxidation in the brown adipocytes. J Lipid Res. 2017;58: 15–30. doi: 10.1194/jlr.M068197 PubMed DOI PMC
Ma SW, Foster DO. Uptake of glucose and release of fatty acids and glycerol by rat brown adipose tissue in vivo. Can J Physiol Pharmacol. 1986;64: 609–614. doi: 10.1139/y86-101 PubMed DOI
Ouellet V, Labbe SM, Blondin DP, Phoenix S, Guérin B, Haman F, et al.. Brown adipose tissue oxidative metabolism contributes to energy expenditure during acute cold exposure in humans. J Clin Invest. 2012;122: 545–552. doi: 10.1172/JCI60433 PubMed DOI PMC
Shin H, Ma Y, Chanturiya T, Cao Q, Wang Y, Kadegowda AKG, et al.. Lipolysis in brown adipocytes is not essential for cold-induced thermogenesis in mice. Cell Metab. 2017;26: 764–777. doi: 10.1016/j.cmet.2017.09.002 PubMed DOI PMC
Cao Y. Angiogenesis and vascular functions in modulation of obesity, adipose metabolism, and insulin sensitivity. Cell Metab. 2013;18: 478–489. doi: 10.1016/j.cmet.2013.08.008 PubMed DOI
Dawson DW, Pearce SFA, Zhong R, Silverstein RL, Frazier WA, Bouck NP. CD36 mediates the inhibitory effects of thrombospondin-1 on endothelial cells. J Cell Biol. 1997;138: 707–717. PubMed PMC