Review Series 10.1172/JCI129190

What lipodystrophies teach us about the metabolic syndrome

Jake P. Mann and David B. Savage

Metabolic Research Laboratories, Wellcome Trust–MRC Institute of Metabolic Science, University of Cambridge, Cambridge, United Kingdom.

Address correspondence to: David B. Savage, Metabolic Research Laboratories, Level 4, Institute of Metabolic Science, Box 289, Addenbrooke’s Hospital, Cambridge, United Kingdom CB2 0QQ. Phone: 44.1223.767923; Email: dbs23@cam.ac.uk.

Find articles by Mann, J. in: JCI | PubMed | Google Scholar |

Metabolic Research Laboratories, Wellcome Trust–MRC Institute of Metabolic Science, University of Cambridge, Cambridge, United Kingdom.

Address correspondence to: David B. Savage, Metabolic Research Laboratories, Level 4, Institute of Metabolic Science, Box 289, Addenbrooke’s Hospital, Cambridge, United Kingdom CB2 0QQ. Phone: 44.1223.767923; Email: dbs23@cam.ac.uk.

Find articles by Savage, D. in: JCI | PubMed | Google Scholar |

First published August 5, 2019 - More info

Published in Volume 129, Issue 10 on October 1, 2019
J Clin Invest. 2019;129(10):4009–4021. https://doi.org/10.1172/JCI129190.
© 2019 American Society for Clinical Investigation
First published August 5, 2019 - Version history

Lipodystrophies are the result of a range of inherited and acquired causes, but all are characterized by perturbations in white adipose tissue function and, in many instances, its mass or distribution. Though patients are often nonobese, they typically manifest a severe form of the metabolic syndrome, highlighting the importance of white fat in the “safe” storage of surplus energy. Understanding the molecular pathophysiology of congenital lipodystrophies has yielded useful insights into the biology of adipocytes and informed therapeutic strategies. More recently, genome-wide association studies focused on insulin resistance have linked common variants to genes implicated in adipose biology and suggested that subtle forms of lipodystrophy contribute to cardiometabolic disease risk at a population level. These observations underpin the use of aligned treatment strategies in insulin-resistant obese and lipodystrophic patients, the major goal being to alleviate the energetic burden on adipose tissue.

Preview pages

Reset
Page preview
4010 Page 4009 Back

Continue reading with a subscription.

A subscription is required for you to read this article in full. If you are a subscriber, you may sign in to continue reading.

Already subscribed?

Click here to sign into your account.

Don't have a subscription?

Please select one of the subscription options, which includes a low-cost option just for this article.

At an institution or library?

If you are at an institution or library and believe you should have access, please check with your librarian or administrator (more information).

Problems?

Please try these troubleshooting tips.

  • Purchase this article
  • $10
  • Purchasing this article will give you full access for the calendar year.
  • Purchase article
  • Purchase Site Pass
  • $25
  • This will give you access to every article on the site for 24 hours.
  • Order site pass
  • Online subscription
  • $95
  • Individual online subscriptions give you full online access for the calendar year.
  • Individual online subscriptions ordered from September 1st on will receive access for the remainder of current year as well as for the full following year subscription term.
  • Order Online
  • Print subscription
  • $830
  • Individual print subscriptions give you the print journal and full online access for the year.
  • Print + Online
  • JCI This Month subscription
  • $125
  • JCI This Month is a 16- to 20-page overview of the articles published each month
  • Subscribing to JCI This Month also gives subscribers full online access for the calendar year.
  • *Price outside U.S. and Canada: $225.
  • JCI This Month + Online
Advertisement