Mouse models of lipodystrophy and their significance in understanding fat regulation

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Adipose tissue plays a critical role in human metabolic health. This is most dramatically illustrated by the severe metabolic disease that occurs in syndromes of lipodystrophy where individuals fail to develop or maintain appropriate adipose tissue mass. The most severe form of this disorder is congenital generalized lipodystrophy (CGL). Individuals with CGL have a striking paucity of adipose tissue and typically display severe metabolic disease with insulin resistance and dyslipidemia. Understanding of the metabolic consequences of lipodystrophies and their underlying molecular mechanisms will provide new information regarding the development and function of human adipose tissue. Mouse models of these conditions offer key resources to investigate this in vivo. Adipocyte dysfunction is believed to underlie the development of metabolic disease in obesity. Hence, understanding how one might beneficially manipulate adipose tissue by studying genes whose disruption causes lipodystrophy is likely to suggest novel means to improve metabolic health in common obesity.

Original languageEnglish
Pages (from-to)53-96
Number of pages44
JournalCurrent topics in developmental biology
Volume109
Early online date16 Jun 2014
DOIs
Publication statusPublished - 2014

Fingerprint

Lipodystrophy
Adipose Tissue
Fats
Metabolic Diseases
Congenital Generalized Lipodystrophy
Obesity
Health
Human Development
Dyslipidemias
Adipocytes
Insulin Resistance
Genes

Keywords

  • lipodystrophy
  • BSCL
  • CGL
  • FPLD
  • adipocytes
  • adipogenesis
  • lipids
  • obesity
  • metabolic disease

Cite this

@article{cd7e75b988e64c989d6df0958d13c2f1,
title = "Mouse models of lipodystrophy and their significance in understanding fat regulation",
abstract = "Adipose tissue plays a critical role in human metabolic health. This is most dramatically illustrated by the severe metabolic disease that occurs in syndromes of lipodystrophy where individuals fail to develop or maintain appropriate adipose tissue mass. The most severe form of this disorder is congenital generalized lipodystrophy (CGL). Individuals with CGL have a striking paucity of adipose tissue and typically display severe metabolic disease with insulin resistance and dyslipidemia. Understanding of the metabolic consequences of lipodystrophies and their underlying molecular mechanisms will provide new information regarding the development and function of human adipose tissue. Mouse models of these conditions offer key resources to investigate this in vivo. Adipocyte dysfunction is believed to underlie the development of metabolic disease in obesity. Hence, understanding how one might beneficially manipulate adipose tissue by studying genes whose disruption causes lipodystrophy is likely to suggest novel means to improve metabolic health in common obesity.",
keywords = "lipodystrophy, BSCL, CGL, FPLD, adipocytes, adipogenesis, lipids, obesity, metabolic disease",
author = "Rochford, {Justin J}",
note = "{\circledC} 2014 Elsevier Inc. All rights reserved.",
year = "2014",
doi = "10.1016/B978-0-12-397920-9.00005-6",
language = "English",
volume = "109",
pages = "53--96",
journal = "Current topics in developmental biology",
issn = "1557-8933",
publisher = "Academic Press Inc.",

}

TY - JOUR

T1 - Mouse models of lipodystrophy and their significance in understanding fat regulation

AU - Rochford, Justin J

N1 - © 2014 Elsevier Inc. All rights reserved.

PY - 2014

Y1 - 2014

N2 - Adipose tissue plays a critical role in human metabolic health. This is most dramatically illustrated by the severe metabolic disease that occurs in syndromes of lipodystrophy where individuals fail to develop or maintain appropriate adipose tissue mass. The most severe form of this disorder is congenital generalized lipodystrophy (CGL). Individuals with CGL have a striking paucity of adipose tissue and typically display severe metabolic disease with insulin resistance and dyslipidemia. Understanding of the metabolic consequences of lipodystrophies and their underlying molecular mechanisms will provide new information regarding the development and function of human adipose tissue. Mouse models of these conditions offer key resources to investigate this in vivo. Adipocyte dysfunction is believed to underlie the development of metabolic disease in obesity. Hence, understanding how one might beneficially manipulate adipose tissue by studying genes whose disruption causes lipodystrophy is likely to suggest novel means to improve metabolic health in common obesity.

AB - Adipose tissue plays a critical role in human metabolic health. This is most dramatically illustrated by the severe metabolic disease that occurs in syndromes of lipodystrophy where individuals fail to develop or maintain appropriate adipose tissue mass. The most severe form of this disorder is congenital generalized lipodystrophy (CGL). Individuals with CGL have a striking paucity of adipose tissue and typically display severe metabolic disease with insulin resistance and dyslipidemia. Understanding of the metabolic consequences of lipodystrophies and their underlying molecular mechanisms will provide new information regarding the development and function of human adipose tissue. Mouse models of these conditions offer key resources to investigate this in vivo. Adipocyte dysfunction is believed to underlie the development of metabolic disease in obesity. Hence, understanding how one might beneficially manipulate adipose tissue by studying genes whose disruption causes lipodystrophy is likely to suggest novel means to improve metabolic health in common obesity.

KW - lipodystrophy

KW - BSCL

KW - CGL

KW - FPLD

KW - adipocytes

KW - adipogenesis

KW - lipids

KW - obesity

KW - metabolic disease

U2 - 10.1016/B978-0-12-397920-9.00005-6

DO - 10.1016/B978-0-12-397920-9.00005-6

M3 - Article

VL - 109

SP - 53

EP - 96

JO - Current topics in developmental biology

JF - Current topics in developmental biology

SN - 1557-8933

ER -