Molecular mechanisms controlling human adipose tissue development

insights from monogenic lipodystrophies

Justin J. Rochford*

*Corresponding author for this work

Research output: Contribution to journalLiterature review

17 Citations (Scopus)

Abstract

Appropriately functioning adipose tissue is essential for human health, a fact most clearly illustrated by individuals with lipodystrophy, who have impaired adipose development and often suffer severe metabolic disease as a result. Humans with obesity display a similar array of metabolic problems. This reflects failures in fat tissue function in obesity, which results in consequences similar to those seen when insufficient adipose tissue is present. Thus a better understanding of the molecules that regulate the development of fat tissue is likely to aid the generation of novel therapeutic strategies for the treatment of all disorders of altered fat mass. Single gene disruptions causing lipodystrophy can give unique insights into the importance of the proteins they encode in human adipose tissue development. Moreover, the mechanisms via which they cause lipodystrophy can reveal new molecules and pathways important for adipose tissue development and function as well as confirming the importance of molecules identified from studies of cellular and animal models.

Original languageEnglish
Article numbere24
Number of pages20
JournalExpert Reviews in Molecular Medicine
Volume12
DOIs
Publication statusPublished - 2 Aug 2010

Keywords

  • seip congenital lipodystrophy
  • AKT/protein-kinase-B
  • familial partial lipodystrophy
  • lipid-droplet formation
  • fat-specific protein-27
  • phosphoenolpyruvate carboxykinase gene
  • isoform-specific regulation
  • acid acyltransferase-beta
  • causes insulin-resistance
  • diet-induced obesity

Cite this

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title = "Molecular mechanisms controlling human adipose tissue development: insights from monogenic lipodystrophies",
abstract = "Appropriately functioning adipose tissue is essential for human health, a fact most clearly illustrated by individuals with lipodystrophy, who have impaired adipose development and often suffer severe metabolic disease as a result. Humans with obesity display a similar array of metabolic problems. This reflects failures in fat tissue function in obesity, which results in consequences similar to those seen when insufficient adipose tissue is present. Thus a better understanding of the molecules that regulate the development of fat tissue is likely to aid the generation of novel therapeutic strategies for the treatment of all disorders of altered fat mass. Single gene disruptions causing lipodystrophy can give unique insights into the importance of the proteins they encode in human adipose tissue development. Moreover, the mechanisms via which they cause lipodystrophy can reveal new molecules and pathways important for adipose tissue development and function as well as confirming the importance of molecules identified from studies of cellular and animal models.",
keywords = "seip congenital lipodystrophy, AKT/protein-kinase-B, familial partial lipodystrophy, lipid-droplet formation, fat-specific protein-27, phosphoenolpyruvate carboxykinase gene, isoform-specific regulation, acid acyltransferase-beta, causes insulin-resistance, diet-induced obesity",
author = "Rochford, {Justin J.}",
year = "2010",
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language = "English",
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journal = "Expert Reviews in Molecular Medicine",
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publisher = "Cambridge University Press",

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TY - JOUR

T1 - Molecular mechanisms controlling human adipose tissue development

T2 - insights from monogenic lipodystrophies

AU - Rochford, Justin J.

PY - 2010/8/2

Y1 - 2010/8/2

N2 - Appropriately functioning adipose tissue is essential for human health, a fact most clearly illustrated by individuals with lipodystrophy, who have impaired adipose development and often suffer severe metabolic disease as a result. Humans with obesity display a similar array of metabolic problems. This reflects failures in fat tissue function in obesity, which results in consequences similar to those seen when insufficient adipose tissue is present. Thus a better understanding of the molecules that regulate the development of fat tissue is likely to aid the generation of novel therapeutic strategies for the treatment of all disorders of altered fat mass. Single gene disruptions causing lipodystrophy can give unique insights into the importance of the proteins they encode in human adipose tissue development. Moreover, the mechanisms via which they cause lipodystrophy can reveal new molecules and pathways important for adipose tissue development and function as well as confirming the importance of molecules identified from studies of cellular and animal models.

AB - Appropriately functioning adipose tissue is essential for human health, a fact most clearly illustrated by individuals with lipodystrophy, who have impaired adipose development and often suffer severe metabolic disease as a result. Humans with obesity display a similar array of metabolic problems. This reflects failures in fat tissue function in obesity, which results in consequences similar to those seen when insufficient adipose tissue is present. Thus a better understanding of the molecules that regulate the development of fat tissue is likely to aid the generation of novel therapeutic strategies for the treatment of all disorders of altered fat mass. Single gene disruptions causing lipodystrophy can give unique insights into the importance of the proteins they encode in human adipose tissue development. Moreover, the mechanisms via which they cause lipodystrophy can reveal new molecules and pathways important for adipose tissue development and function as well as confirming the importance of molecules identified from studies of cellular and animal models.

KW - seip congenital lipodystrophy

KW - AKT/protein-kinase-B

KW - familial partial lipodystrophy

KW - lipid-droplet formation

KW - fat-specific protein-27

KW - phosphoenolpyruvate carboxykinase gene

KW - isoform-specific regulation

KW - acid acyltransferase-beta

KW - causes insulin-resistance

KW - diet-induced obesity

U2 - 10.1017/S1462399410001547

DO - 10.1017/S1462399410001547

M3 - Literature review

VL - 12

JO - Expert Reviews in Molecular Medicine

JF - Expert Reviews in Molecular Medicine

SN - 1462-3994

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