受体 CD36 将一个与风险相关的等位基因与肥胖和代谢紊乱联系起来。
Receptor CD36 links a risk-associated allele to obesity and metabolic disorders.
机构信息
From the Department of Pathology and Laboratory Medicine and
From the Department of Pathology and Laboratory Medicine and.
出版信息
J Biol Chem. 2018 Aug 24;293(34):13349-13350. doi: 10.1074/jbc.H118.004818.
Abstract
Mice harboring a particular allele of the human brain-derived neurotropic factor (BDNF mice) develop extreme obesity and insulin resistance when fed a high-fat diet. The underlying mechanisms of this genetic risk factor for obesity are unclear. In the current issue of JBC, Yang report that pharmacological inhibition of integral membrane protein CD36 significantly reduces body weight gain and improves glucose tolerance in BDNF mice. Targeting CD36 may therefore be a promising strategy to improve metabolic dysfunctions and normalize risk factors in obese individuals.
摘要
当喂食高脂肪饮食时，携带人类脑源性神经营养因子（BDNF）特定等位基因的小鼠会发展出极度肥胖和胰岛素抵抗。这种肥胖遗传风险因素的潜在机制尚不清楚。在本期 JBC 中，Yang 报告称，整膜蛋白 CD36 的药理学抑制可显著减少 BDNF 小鼠的体重增加并改善葡萄糖耐量。因此，靶向 CD36 可能是改善代谢功能障碍和使肥胖个体的危险因素正常化的有前途的策略。
相似文献
1
Receptor CD36 links a risk-associated allele to obesity and metabolic disorders.受体 CD36 将一个与风险相关的等位基因与肥胖和代谢紊乱联系起来。
J Biol Chem. 2018 Aug 24;293(34):13349-13350. doi: 10.1074/jbc.H118.004818.
2
Inhibition of the CD36 receptor reduces visceral fat accumulation and improves insulin resistance in obese mice carrying the BDNF- variant.抑制 CD36 受体可减少携带 BDNF-变体的肥胖小鼠内脏脂肪堆积并改善胰岛素抵抗。
J Biol Chem. 2018 Aug 24;293(34):13338-13348. doi: 10.1074/jbc.RA118.002405. Epub 2018 Jun 18.
3
Reversal of behavioral and metabolic abnormalities, and insulin resistance syndrome, by dietary restriction in mice deficient in brain-derived neurotrophic factor.脑源性神经营养因子缺乏小鼠通过饮食限制逆转行为和代谢异常以及胰岛素抵抗综合征。
Endocrinology. 2003 Jun;144(6):2446-53. doi: 10.1210/en.2002-0113.
4
Hepatic Overexpression of CD36 Improves Glycogen Homeostasis and Attenuates High-Fat Diet-Induced Hepatic Steatosis and Insulin Resistance.CD36在肝脏中的过表达改善糖原稳态并减轻高脂饮食诱导的肝脂肪变性和胰岛素抵抗。
Mol Cell Biol. 2016 Oct 13;36(21):2715-2727. doi: 10.1128/MCB.00138-16. Print 2016 Nov 1.
5
Acute exercise induced BDNF-TrkB signalling is intact in the prefrontal cortex of obese, glucose-intolerant male mice.急性运动诱导的脑源性神经营养因子-TrkB 信号在肥胖、葡萄糖不耐受雄性小鼠的前额叶皮层中完整。
Appl Physiol Nutr Metab. 2018 Oct;43(10):1083-1089. doi: 10.1139/apnm-2018-0108. Epub 2018 May 4.
6
Metabolic challenges reveal impaired fatty acid metabolism and translocation of FAT/CD36 but not FABPpm in obese Zucker rat muscle.代谢挑战揭示肥胖 Zucker 大鼠肌肉中脂肪酸代谢受损以及 FAT/CD36 而非 FABPpm 的转运受损。
Am J Physiol Endocrinol Metab. 2007 Aug;293(2):E566-75. doi: 10.1152/ajpendo.00106.2007. Epub 2007 May 22.
7
Palmitate aggravates proteinuria-induced cell death and inflammation via CD36-inflammasome axis in the proximal tubular cells of obese mice.棕榈酸通过肥胖小鼠近端肾小管细胞中的 CD36-炎症小体轴加剧蛋白尿诱导的细胞死亡和炎症。
Am J Physiol Renal Physiol. 2018 Dec 1;315(6):F1720-F1731. doi: 10.1152/ajprenal.00536.2017. Epub 2018 Sep 19.
8
Role of FAT/CD36 in fatty acid sensing, energy, and glucose homeostasis regulation in DIO and DR rats.在 DIO 和 DR 大鼠中，FAT/CD36 在脂肪酸感应、能量和葡萄糖稳态调节中的作用。
Am J Physiol Regul Integr Comp Physiol. 2015 Feb 1;308(3):R188-98. doi: 10.1152/ajpregu.00367.2014. Epub 2014 Dec 4.
9
d-Allulose supplementation normalized the body weight and fat-pad mass in diet-induced obese mice via the regulation of lipid metabolism under isocaloric fed condition.在等热量喂养条件下，补充d-阿洛酮糖通过调节脂质代谢使饮食诱导的肥胖小鼠的体重和脂肪垫质量恢复正常。
Mol Nutr Food Res. 2016 Jul;60(7):1695-706. doi: 10.1002/mnfr.201500771. Epub 2016 Apr 24.
10
RS 10767664 gene variant in Brain Derived Neurotrophic Factor (BDNF) affect metabolic changes and insulin resistance after a standard hypocaloric diet.脑源性神经营养因子（BDNF）中的 RS 10767664 基因变异会影响标准低热量饮食后的代谢变化和胰岛素抵抗。
J Diabetes Complications. 2018 Feb;32(2):216-220. doi: 10.1016/j.jdiacomp.2017.10.005. Epub 2017 Oct 14.
引用本文的文献
1
The efferocytosis process in aging: Supporting evidence, mechanisms, and therapeutic prospects for age-related diseases.衰老过程中的胞葬作用：支持证据、机制及与年龄相关疾病的治疗前景
J Adv Res. 2025 Mar;69:31-49. doi: 10.1016/j.jare.2024.03.008. Epub 2024 Mar 17.
2
CD36 aggravates podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy in lupus nephritis.CD36 通过激活 NLRP3 炎症小体和抑制自噬加重狼疮肾炎足细胞损伤。
Cell Death Dis. 2022 Aug 23;13(8):729. doi: 10.1038/s41419-022-05179-9.
3
Current Status and Future Perspectives on Therapeutic Potential of Apigenin: Focus on Metabolic-Syndrome-Dependent Organ Dysfunction.芹菜素治疗潜力的现状与未来展望：聚焦于代谢综合征相关器官功能障碍
Antioxidants (Basel). 2021 Oct 19;10(10):1643. doi: 10.3390/antiox10101643.
4
CD36 Signal Transduction in Metabolic Diseases: Novel Insights and Therapeutic Targeting.CD36 在代谢性疾病中的信号转导：新的见解和治疗靶点。
Cells. 2021 Jul 20;10(7):1833. doi: 10.3390/cells10071833.
5
Effects of Long-Term Endurance Exercise and Lithium Treatment on Neuroprotective Factors in Hippocampus of Obese Rats.长期耐力运动和锂处理对肥胖大鼠海马神经保护因子的影响。
Int J Environ Res Public Health. 2020 May 10;17(9):3317. doi: 10.3390/ijerph17093317.
6
The clearance of dead cells by efferocytosis.细胞凋亡细胞的清除作用。
Nat Rev Mol Cell Biol. 2020 Jul;21(7):398-414. doi: 10.1038/s41580-020-0232-1. Epub 2020 Apr 6.
7
The Aryl Hydrocarbon Receptor (AhR) Mediates the Counter-Regulatory Effects of Pelargonidins in Models of Inflammation and Metabolic Dysfunctions.芳基烃受体（AhR）介导锦葵素在炎症和代谢功能障碍模型中的抗调控作用。
Nutrients. 2019 Aug 7;11(8):1820. doi: 10.3390/nu11081820.
本文引用的文献
1
Inhibition of the CD36 receptor reduces visceral fat accumulation and improves insulin resistance in obese mice carrying the BDNF- variant.抑制 CD36 受体可减少携带 BDNF-变体的肥胖小鼠内脏脂肪堆积并改善胰岛素抵抗。
J Biol Chem. 2018 Aug 24;293(34):13338-13348. doi: 10.1074/jbc.RA118.002405. Epub 2018 Jun 18.
2
Neurotrophic factor control of satiety and body weight.神经营养因子对饱腹感和体重的控制。
Nat Rev Neurosci. 2016 May;17(5):282-92. doi: 10.1038/nrn.2016.24. Epub 2016 Apr 7.
3
Fatty acid transporter CD36 mediates hypothalamic effect of fatty acids on food intake in rats.脂肪酸转运蛋白 CD36 介导了脂肪酸对大鼠摄食的下丘脑效应。
PLoS One. 2013 Sep 6;8(9):e74021. doi: 10.1371/journal.pone.0074021. eCollection 2013.
4
From obesity genetics to the future of personalized obesity therapy.从肥胖遗传学到个性化肥胖治疗的未来。
Nat Rev Endocrinol. 2013 Jul;9(7):402-13. doi: 10.1038/nrendo.2013.57. Epub 2013 Mar 26.
5
Salvianolic acid B inhibits macrophage uptake of modified low density lipoprotein (mLDL) in a scavenger receptor CD36-dependent manner.丹酚酸 B 通过清道夫受体 CD36 依赖性途径抑制巨噬细胞摄取修饰的低密度脂蛋白（mLDL）。
Atherosclerosis. 2012 Jul;223(1):152-9. doi: 10.1016/j.atherosclerosis.2012.05.006. Epub 2012 May 15.
6
Brain-derived neurotrophic factor, food intake regulation, and obesity.脑源性神经营养因子、摄食调节与肥胖。
Arch Med Res. 2011 Aug;42(6):482-94. doi: 10.1016/j.arcmed.2011.09.005. Epub 2011 Sep 22.
7
A CD36-dependent pathway enhances macrophage and adipose tissue inflammation and impairs insulin signalling.一条依赖CD36的信号通路会加剧巨噬细胞和脂肪组织的炎症反应，并损害胰岛素信号传导。
Cardiovasc Res. 2011 Feb 15;89(3):604-13. doi: 10.1093/cvr/cvq360. Epub 2010 Nov 18.
8
Soluble CD36 (sCD36) clusters with markers of insulin resistance, and high sCD36 is associated with increased type 2 diabetes risk.可溶性 CD36（sCD36）与胰岛素抵抗的标志物聚集在一起，高 sCD36 与 2 型糖尿病风险增加相关。
J Clin Endocrinol Metab. 2010 Apr;95(4):1939-46. doi: 10.1210/jc.2009-2002. Epub 2010 Feb 5.
9
The BDNF val66met polymorphism affects activity-dependent secretion of BDNF and human memory and hippocampal function.脑源性神经营养因子（BDNF）缬氨酸66位甲硫氨酸多态性影响BDNF的活性依赖性分泌以及人类记忆和海马功能。
Cell. 2003 Jan 24;112(2):257-69. doi: 10.1016/s0092-8674(03)00035-7.
10
Obesity and insulin resistance.肥胖与胰岛素抵抗。
J Clin Invest. 2000 Aug;106(4):473-81. doi: 10.1172/JCI10842.
Zotero 插件