M. M. Soundarapandian, Maria L. Nieves, R. Pasquier, Ulrika Bergstrom, M. Atkinson, B. Tyrberg
{"title":"β -细胞质量稳态的遗传调控","authors":"M. M. Soundarapandian, Maria L. Nieves, R. Pasquier, Ulrika Bergstrom, M. Atkinson, B. Tyrberg","doi":"10.2174/1874216501004010011","DOIUrl":null,"url":null,"abstract":"Control of -cell function and mass is tightly linked to glucose homeostasis. Failing -cells inevitably lead to diabetes. Recently, several contradictory studies have been published arguing against or in favor of various mechanisms controlling -cell mass regulation. Here we review the literature on control of adult -cell mass and aim to reconcile thereby the contradictions. We discuss the role of � -cell proliferation and neogenesis, both in mice and man. We also discuss the influence of genetic predisposition on -cell mass control. We conclude that -cell generation in the adult human and mouse likely depends on many paths to assure sufficient numbers of -cells at any given time, thereby balancing mechanisms for negative regulation of -cell numbers. A simple model with only one pathway does not fit the current literature.","PeriodicalId":88751,"journal":{"name":"The open endocrinology journal","volume":"4 1","pages":"11-22"},"PeriodicalIF":0.0000,"publicationDate":"2010-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Genetic Control of β -Cell Mass Homeostasis\",\"authors\":\"M. M. Soundarapandian, Maria L. Nieves, R. Pasquier, Ulrika Bergstrom, M. Atkinson, B. Tyrberg\",\"doi\":\"10.2174/1874216501004010011\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Control of -cell function and mass is tightly linked to glucose homeostasis. Failing -cells inevitably lead to diabetes. Recently, several contradictory studies have been published arguing against or in favor of various mechanisms controlling -cell mass regulation. Here we review the literature on control of adult -cell mass and aim to reconcile thereby the contradictions. We discuss the role of � -cell proliferation and neogenesis, both in mice and man. We also discuss the influence of genetic predisposition on -cell mass control. We conclude that -cell generation in the adult human and mouse likely depends on many paths to assure sufficient numbers of -cells at any given time, thereby balancing mechanisms for negative regulation of -cell numbers. A simple model with only one pathway does not fit the current literature.\",\"PeriodicalId\":88751,\"journal\":{\"name\":\"The open endocrinology journal\",\"volume\":\"4 1\",\"pages\":\"11-22\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2010-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The open endocrinology journal\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2174/1874216501004010011\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The open endocrinology journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1874216501004010011","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Control of -cell function and mass is tightly linked to glucose homeostasis. Failing -cells inevitably lead to diabetes. Recently, several contradictory studies have been published arguing against or in favor of various mechanisms controlling -cell mass regulation. Here we review the literature on control of adult -cell mass and aim to reconcile thereby the contradictions. We discuss the role of � -cell proliferation and neogenesis, both in mice and man. We also discuss the influence of genetic predisposition on -cell mass control. We conclude that -cell generation in the adult human and mouse likely depends on many paths to assure sufficient numbers of -cells at any given time, thereby balancing mechanisms for negative regulation of -cell numbers. A simple model with only one pathway does not fit the current literature.