[1]蒋芬 肖新华.线粒体衍生肽MOTS-c与代谢性疾病[J].国际内分泌代谢杂志,2020,40(01):52-54.[doi:10.3760/cma.j.issn.1673-4157.2020.01.012]
 Jiang Fen,Xiao Xinhua.Mitochondrial-derived peptide MOTS-c and metabolic diseases[J].International Journal of Endocrinology and Metabolism,2020,40(01):52-54.[doi:10.3760/cma.j.issn.1673-4157.2020.01.012]
点击复制

线粒体衍生肽MOTS-c与代谢性疾病()
分享到:

《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
40
期数:
2020年01期
页码:
52-54
栏目:
基础研究
出版日期:
2020-01-20

文章信息/Info

Title:
Mitochondrial-derived peptide MOTS-c and metabolic diseases
作者:
蒋芬 肖新华
南华大学附属第一医院内分泌代谢科,衡阳 421001
Author(s):
Jiang Fen Xiao Xinhua
Department of Metabolism and Endocrinology, The First Affiliated Hospital of University of South China, Hengyang 421001, China
关键词:
代谢性疾病 线粒体衍生肽 MOTS-c
Keywords:
Metabolic disease Mitochondrial-derived peptide MOTS-c
DOI:
10.3760/cma.j.issn.1673-4157.2020.01.012
摘要:
MOTS-c是线粒体衍生肽家族成员之一,可促进脂肪酸氧化、促进白色脂肪棕色化、提高葡萄糖利用率、改善胰岛素抵抗、促进成骨、抑制破骨。它与肥胖、2型糖尿病、非酒精性脂肪性肝病和代谢性骨病密切相关。尽管MOTS-c在啮齿类动物中有较多研究,但其对人的影响尚不明确。从病理生理学的角度分析MOTS-c,有望使其成为治疗一系列代谢性疾病的新靶点。
Abstract:
MOTS-c is one of the mitochondrial-derived peptide. MOTS-c can promote fatty acid oxidation, promote white fat browning, enhance glucose utilization, improve insulin resistance, promote osteogenesis and inhibit osteoclast. It is closely related to obesity, diabetes, non-alcoholic fatty liver disease and metabolic osteopathy.Although MOTS-c has been studied more in rodents, its impact on human is still unclear. From the perspective of pathophysiology, MOTS-c is expected to be a nvoel target for the treatment of metabolic diseases.

参考文献/References:

[1] Lee C,Zeng J,Drew BG,et al.The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance[J]. Cell Metab,2015,21(3):443-454.DOI:10.1016/j.cmet.2015.02.009.
[2] Ramanjaneya M,Bettahi I,Jerobin J,et al.Mitochondrial-derived peptides are down regulated in diabetes subjects[J].Front Endocrinol(Lausanne),2019,10:331.DOI:10.3389/fendo.2019.00331.
[3] Mangalhara KC,Shadel GS.A mitochondrial-derived peptide exercises the nuclear option[J].Cell Metab,2018,28(3):330-331.DOI:10.1016/j.cmet.2018.08.017.
[4] Kim KH,Son JM,Benayoun BA,et al.The mitochondrial-encoded peptide MOTS-c translocates to the nucleus to regulate nuclear gene expression in response to metabolic stress[J].Cell Metab,2018,28(3):516-524.e7.DOI:10.1016/j.cmet.2018.06.008.
[5] Quirós PM,Mottis A,Auwerx J.Mitonuclear communication in homeostasis and stress[J].Nat Rev Mol Cell Biol,2016,17(4):213-226.DOI:10.1038/nrm.2016.23.
[6] Du C,Zhang C,Wu W,et al.Circulating MOTS-c levels are decreased in obese male children and adolescents and associatedwith insulin resistance[J].Pediatr Diabetes,2018,[Epub ahead of print].DOI:10.1111/pedi.12685.
[7] Chondronikola M,Volpi E,Børsheim E,et al.Brown adipose tissue activation is linked to distinct systemic effects on lipid metabolism in humans[J].Cell Metab,2016,23(6):1200-1206.DOI:10.1016/j.cmet.2016.04.029.
[8] Lu H,Wei M,Zhai Y,et al.MOTS-c peptide regulates adipose homeostasis to prevent ovariectomy-induced metabolic dysfunction[J].J Mol Med(Berl),2019,97(4):473-485.DOI:10.1007/s00109-018-01738-w.
[9] 魏明.MOTS-c对OVX小鼠脂代谢异常和骨丢失的保护效能与机制研究[D].西安:第四军医大学,2016.
[10] Lu H,Tang S,Xue C,et al.Mitochondrial-derived peptide MOTS-c increases adipose thermogenic activation to promote cold adaptation[J].Int J Mol Sci,2019,20(10):pii: E2456. DOI:10.3390/ijms20102456.
[11] Kim SJ,Miller B,Mehta HH,et al.The mitochondrial-derived peptide MOTS-c is a regulator of plasma metabolites and enhances insulin sensitivity[J].Physiol Rep,2019,7(13):e14171.DOI:10.14814/phy2.14171.
[12] Cataldo LR,Fernández-Verdejo R,Santos JL,et al.Plasma MOTS-c levels are associated with insulin sensitivity in lean but not in obese individuals[J].J Investig Med,2018,66(6):1019-1022.DOI:10.1136/jim-2017-000681.
[13] Hu BT,Chen WZ.MOTS-c improves osteoporosis by promoting osteogenic differentiation of bone marrow mesenchymal stem cells via TGF-β/Smad pathway[J].Eur Rev Med Pharmacol Sci,2018,22(21):7156-7163.DOI:10.26355/eurrev_201811_16247.
[14] Che N,Qiu W,Wang JK,et al.MOTS-c improves osteoporosis by promoting the synthesis of type Ⅰ collagen in osteoblasts via TGF-β/SMAD signaling pathway[J].Eur Rev Med Pharmacol Sci,2019,23(8):3183-3189.DOI:10.26355/eurrev_201904_17676.
[15] Ming W,Lu G,Xin S,et al.Mitochondrial related peptide MOTS-c suppresses ovariectomy-induced bone loss via AMPK activation[J].Biochem Biophys Res Commun,2016,476(4):412-419.DOI:10.1016/j.bbrc.2016.05.135.
[16] Yan Z,Zhu S,Wang H,et al.MOTS-c inhibits osteolysis in the mouse calvaria by affecting osteocyte-osteoclast crosstalk and inhibiting inflammation[J].Pharmacol Res,2019,147:104381.DOI:10.1016/j.phrs.2019.104381.
[17] Lee C,Kim KH,Cohen P.MOTS-c:a novel mitochondrial-derived peptide regulating muscle and fat metabolism[J].Free Radic Biol Med,2016,100:182-187.DOI:10.1016/j.freeradbiomed.2016.05.015.

相似文献/References:

[1]叶婷婷,董艳.表观遗传学在子代代谢性疾病发生中的作用[J].国际内分泌代谢杂志,2014,(01):60.[doi:10.3760/cma.j.issn.1673-4157.2014.01.017]
 Ye Tingting,Dong Yan.Role of epigenetics in the development of metabolic diseases in offsprings[J].International Journal of Endocrinology and Metabolism,2014,(01):60.[doi:10.3760/cma.j.issn.1673-4157.2014.01.017]
[2]林天烨,方文军.肠道菌群与代谢性疾病的关系[J].国际内分泌代谢杂志,2014,(04):277.[doi:10.3760/cma.j.issn.1673-4157.2014.04.018]
 Lin Tianye*,Fang Wenjun..Relationship between microbiota and metabolic diseases[J].International Journal of Endocrinology and Metabolism,2014,(01):277.[doi:10.3760/cma.j.issn.1673-4157.2014.04.018]
[3]龚珏,邱菊.高脂饮食造成的肠道免疫失衡与代谢性疾病的关系研究进展[J].国际内分泌代谢杂志,2021,41(04):304.[doi:10.3760/cma.j.cn121383-20210511-05015]
 Gong Jue,Qiu Ju..Progress and perspective: the effect of disturbed intestinal homeostasis induced by high-fat-diet on metabolic diseases[J].International Journal of Endocrinology and Metabolism,2021,41(01):304.[doi:10.3760/cma.j.cn121383-20210511-05015]

备注/Memo

备注/Memo:
通信作者:肖新华, Email:xinhua0102@163.com
基金项目:国家自然科学基金(81870595)
Corresponding author: Xiao Xinhua, Email:xinhua0102@163.com
Fund program:National Natural Science Foundation of China(81870595)
更新日期/Last Update: 2020-01-20