{"title":"Human Adipose Tissue Metabolism in Obesity.","authors":"Shuhao Lin, Michael D Jensen","doi":"10.7570/jomes25025","DOIUrl":null,"url":null,"abstract":"<p><p>The scientific understanding of adipose tissue has advanced tremendously during the past decade. Once thought to be an inert fat storage organ, we now know that adipose tissue serves important functions in energy balance and endocrinology, as well as playing a central role in the development of metabolic diseases. Adipose tissue lipid storage and lipolysis are tightly controlled by hormones, such as insulin, in response to the body's energy needs. Adipose insulin sensitivity can be measured <i>in vivo</i> in humans using isotopic fatty acid tracers and the insulin clamp technique. These data allow investigators to calculate the plasma insulin concentration that results in a 50% suppression of lipolysis. In obesity, insulin's action on adipose tissue lipolysis is clearly impaired, resulting in excess free fatty acids in circulation, which can lead to metabolic dysfunction. However, the cause of this impairment is unclear. The chronic, low-grade adipose tissue inflammation seen in obesity was thought to be the cause of adipose tissue insulin resistance. In this review, we discuss the structure of adipose tissue, how normal and abnormal adipose tissue metabolism contributes to metabolic diseases, and how inflammation might or might not play a role in adipose tissue insulin resistance.</p>","PeriodicalId":45386,"journal":{"name":"Journal of Obesity & Metabolic Syndrome","volume":" ","pages":""},"PeriodicalIF":4.7000,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Obesity & Metabolic Syndrome","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.7570/jomes25025","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 0
Abstract
The scientific understanding of adipose tissue has advanced tremendously during the past decade. Once thought to be an inert fat storage organ, we now know that adipose tissue serves important functions in energy balance and endocrinology, as well as playing a central role in the development of metabolic diseases. Adipose tissue lipid storage and lipolysis are tightly controlled by hormones, such as insulin, in response to the body's energy needs. Adipose insulin sensitivity can be measured in vivo in humans using isotopic fatty acid tracers and the insulin clamp technique. These data allow investigators to calculate the plasma insulin concentration that results in a 50% suppression of lipolysis. In obesity, insulin's action on adipose tissue lipolysis is clearly impaired, resulting in excess free fatty acids in circulation, which can lead to metabolic dysfunction. However, the cause of this impairment is unclear. The chronic, low-grade adipose tissue inflammation seen in obesity was thought to be the cause of adipose tissue insulin resistance. In this review, we discuss the structure of adipose tissue, how normal and abnormal adipose tissue metabolism contributes to metabolic diseases, and how inflammation might or might not play a role in adipose tissue insulin resistance.
期刊介绍:
The journal was launched in 1992 and diverse studies on obesity have been published under the title of Journal of Korean Society for the Study of Obesity until 2004. Since 2017, volume 26, the title is now the Journal of Obesity & Metabolic Syndrome (pISSN 2508-6235, eISSN 2508-7576). The journal is published quarterly on March 30th, June 30th, September 30th and December 30th. The official title of the journal is now "Journal of Obesity & Metabolic Syndrome" and the abbreviated title is "J Obes Metab Syndr". Index words from medical subject headings (MeSH) list of Index Medicus are included in each article to facilitate article search. Some or all of the articles of this journal are included in the index of PubMed, PubMed Central, Scopus, Embase, DOAJ, Ebsco, KCI, KoreaMed, KoMCI, Science Central, Crossref Metadata Search, Google Scholar, and Emerging Sources Citation Index (ESCI).