[1]章卫平,史亚男,陈玉霞.肠道:调控糖脂代谢稳态的前哨与枢纽[J].国际内分泌代谢杂志,2021,41(04):286-289.[doi:10.3760/cma.j.cn121383-20210513-05023]
 Zhang Weiping,Shi Yanan,Chen Yuxia..Intestinal tract:a sentry hub for maintaining glucose and lipid homeostasis[J].International Journal of Endocrinology and Metabolism,2021,41(04):286-289.[doi:10.3760/cma.j.cn121383-20210513-05023]
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肠道:调控糖脂代谢稳态的前哨与枢纽()
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
41
期数:
2021年04期
页码:
286-289
栏目:
述评
出版日期:
2021-07-20

文章信息/Info

Title:
Intestinal tract:a sentry hub for maintaining glucose and lipid homeostasis
作者:
章卫平12史亚男1陈玉霞2
1天津医科大学朱宪彝纪念医院、天津市内分泌研究所、国家卫生健康委激素与发育重点实验室、天津市代谢性疾病重点实验室 300134; 2海军军医大学病理生理学教研室,上海 200433
Author(s):
Zhang Weiping12 Shi Yanan1 Chen Yuxia2.
1NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin 300134, China; 2Department of Pathophysiology, Naval Medical University, Shanghai 200433, China
关键词:
肠道 肠道微生物 糖代谢稳态 脂代谢稳态 代谢调节
Keywords:
intestine intestinal microorganism glucose homeostasis lipid homeostasis metabolic regulation
DOI:
10.3760/cma.j.cn121383-20210513-05023
摘要:
肠道是消化、吸收各种膳食营养素的重要场所,也是调节机体糖脂代谢稳态的主要器官。肠道可感受各种不同的营养信号,与脑、肝脏等代谢器官相互作用,形成复杂而又精细的糖脂代谢时空调控网络,发挥调节糖脂代谢稳态的“前哨”与“枢纽”作用。该领域的研究进展已成功转化为临床干预糖脂代谢紊乱的有效手段。本文将就该领域的基础理论和转化应用研究进展进行述评,并对该领域的未来研究热点提出展望。
Abstract:
The intestine is a primary organ for digestion and absorption of dietary nutrients. It also plays a pivotal role in regulating glucose and lipid metabolic homeostasis. Intestinal tract is able to sense various luminal nutrients, consequently triggers crosstalk with various metabolic tissues including brain and liver. This complex and delicate spatiotemporal network formed by inter-tissue crosstalk is considered crucial for maintaining glucose and lipid homeostasis, in which the intestine acts as a sentry hub. These significant outcomes have been clinically transformed as metabolic disease intervention. In this article, we prospected the promising research direction in future based on reviewing current outcomes of both basic research and transformation application in this hot field.

参考文献/References:

[1] Merino B,Fernández-Díaz CM,Cózar-Castellano I,et al.Intestinal fructose and glucose metabolism in health and disease[J].Nutrients,2019,12(1):94.DOI:10.3390/nu12010094.
[2] Jang C,Hui S,Lu W,et al.The small intestine converts dietary fructose into glucose and organic acids[J].Cell Metab,2018,27(2):351-361e3.DOI:10.1016/j.cmet.2017.12.016.
[3] 张晶,李昊,师建辉,等.果糖与代谢性疾病[J].中国病理生理杂志,2020,36(4):163-168.DOI:10.3969/j.issn.1000-4718.2020-04-022.
[4] Shi YN,Liu YJ,Xie Z,et al.Fructose and metabolic diseases:too much to be good [J].Chin Med J(Engl),2021,134(11):1276-1285.DOI:10.1097/CM9.0000000000001545.
[5] Kim M,Astapova II,Flier SN,et al.Intestinal,but not hepatic,ChREBP is required for fructose tolerance[J].JCI Insight,2017,2(24):e96703.DOI:10.1172/jci.insight.96703.
[6] Ko CW,Qu J,Black DD,et al.Regulation of intestinal lipid metabolism:current concepts and relevance to disease[J].Nat Rev Gastroenterol Hepatol,2020,17(3):169-183.DOI:10.1038/s41575-019-0250-7.
[7] Davies JP,Levy B,Ioannou YA.Evidence for a Niemann-pick C(NPC)gene family:identification and characterization of NPC1L1[J].Genomics,2000,65(2):137-145.DOI:10.1006/geno.2000.6151.
[8] Li PS,Fu ZY,Zhang YY,et al.The clathrin adaptor Numb regulates intestinal cholesterol absorption through dynamic interaction with NPC1L1[J].Nat Med,2014,20(1):80-86.DOI:10.1038/nm.3417.
[9] Ge L,Qi W,Wang LJ,et al.Flotillins play an essential role in Niemann-Pick C1-like 1-mediated cholesterol uptake[J].Proc Natl Acad Sci U S A,2011,108(2):551-556.DOI:10.1073/pnas.1014434108.
[10] Zhang YY,Fu ZY,Wei J,et al.A LIMA1 variant promotes low plasma LDL cholesterol and decreases intestinal cholesterol absorption[J].Science,2018,360(6393):1087-1092.DOI:10.1126/science.aao6575.
[11] Ge L,Wang J,Qi W,et al.The cholesterol absorption inhibitor ezetimibe acts by blocking the sterol-induced internalization of NPC1L1[J].Cell Metab,2008,7(6):508-519.DOI:10.1016/j.cmet.2008.04.001.
[12] Johnson TA,Pfeffer SR.Ezetimibe-sensitive cholesterol uptake by NPC1L1 protein does not require endocytosis[J].Mol Biol Cell,2016,27(11):1845-1852.DOI:10.1091/mbc.E16-03-0154.
[13] Worthington JJ,Reimann F,Gribble FM.Enteroendocrine cells-sensory sentinels of the intestinal environment and orchestrators of mucosal immunity[J].Mucosal Immunol,2018,11(1):3-20.DOI:10.1038/mi.2017.73.
[14] Haber AL,Biton M,Rogel N,et al.A single-cell survey of the small intestinal epithelium[J].Nature,2017,551(7680):333-339.DOI:10.1038/nature24489.
[15] Gehart H,HVE Johan,Hamer K,et al.Identification of enteroendocrine regulators by real-time single-cell differentiation mapping[J].Cell,2019,176(5):1158-1173.e16.DOI:10.1016/j.cell.2018.12.029.
[16] Baggio LL,Drucker DJ.Glucagon-like peptide-1 receptor co-agonists for treating metabolic disease[J].Mol Metab,2021,46:101090.DOI:10.1016/j.molmet.2020.101090.
[17] Fria JP,Nauck MA,Van J,et al.Efficacy and safety of LY3298176,a novel dual GIP and GLP-1 receptor agonist,in patients with type 2 diabetes:a randomised,placebo-controlled and active comparator-controlled phase 2 trial[J].Lancet,2018,392(10160):2180-2193.DOI:10.1016/S0140-6736(18)32260-8.
[18] Gribble FM,Reimann F.Enteroendocrine cells:chemosensors in the intestinal epithelium[J].Annu Rev Physiol,2016,78:277-299.DOI:10.1146/annurev-physiol-021115-105439.
[19] Zhou L,Yang H,Okoro EU,et al.Up-regulation of cholesterol absorption is a mechanism for cholecystokinin-induced hypercholesterolemia[J].J Biol Chem,2014,289(19):12989-12999.DOI:10.1074/jbc.M113.534388.
[20] Wang PY,Caspi L,Lam CK,et al.Upper intestinal lipids trigger a gut-brain-liver axis to regulate glucose production[J].Nature,2008,452(7190):1012-1016.DOI:10.1038/nature06852.
[21] Cheung GW,Kokorovic A,Lam CK,et al.Intestinal cholecystokinin controls glucose production through a neuronal network[J].Cell Metab,2009,10(2):99-109.DOI:10.1016/j.cmet.2009.07.005.
[22] Zheng X,Chen T,Jiang R,et al.Hyocholic acid species improve glucose homeostasis through a distinct TGR5 and FXR signaling mechanism[J].Cell Metab,2021,33(4):791-803 e7.DOI:10.1016/j.cmet.2020.11.017.
[23] Carabotti M,Scirocco A,Maselli MA,et al.The gut-brain axis:interactions between enteric microbiota,central and enteric nervous systems[J].Ann Gastroenterol,2015,28(2):203-209.DOI:10.37212/jcnos.610103.
[24] Duca FA,Bauer PV,Hamr SC,et al.Glucoregulatory relevance of small intestinal nutrient sensing in physiology,bariatric surgery,and pharmacology[J].Cell Metab,2015,22(3):367-380.DOI:10.1016/j.cmet.2015.07.003.
[25] Rastelli M,Cani PD,Knauf C.The gut microbiome influences host endocrine functions[J].Endocr Rev,2019,40(5):1271-1284.DOI:10.1210/er.2018-00280.
[26] Koh A,Molinaro A,Ståhlman M,et al.Microbially produced imidazole propionate impairs insulin signaling through mTORC1[J].Cell,2018,175(4):947-961.e17.DOI:10.1016/j.cell.2018.09.055.
[27] Fan Y,Pedersen O.Gut microbiota in human metabolic health and disease[J].Nat Rev Microbiol,2021,19(1):55-71.DOI:10.1038/s41579-020-0433-9.
[28] de Groot P,Nikolic T,Pellegrini S,et al.Faecal microbiota transplantation halts progression of human new-onset type 1 diabetes in a randomised controlled trial[J].Gut,2021,70(1):92-105.DOI:10.1136/gutjnl-2020-322630.
[29] Vrieze A,Van Nood E,Holleman F,et al.Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome[J].Gastroenterology,2012,143(4):913-916 e7.DOI:10.1053/j.gastro.2012.06.031.
[30] Kootte RS,Levin E,Salojärvi J,et al.Improvement of insulin sensitivity after lean donor feces in metabolic syndrome is driven by baseline intestinal microbiota composition[J].Cell Metab,2017,26(4):611-619.e6.DOI:10.1016/j.cmet.2017.09.008.

备注/Memo

备注/Memo:
基金项目:国家重点研发计划(2019YFA0802500); 国家自然科学基金重大研究计划重点项目(91857203)

通信作者:章卫平,Email:zhangwp@tmu.edu.cn
更新日期/Last Update: 1900-01-01