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Recent advances in understanding lipodystrophy: A focus on lipodystrophy-associated cardiovascular disease and potential effects of leptin therapy on cardiovascular function.

*Corresponding author for this work
  • University of Pittsburgh
    ,
  • Medical College of Georgia
    ,
Scholary Output:
Contribution to journal
Review article
Peer-review

Open access

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

Lipodystrophy is a disease characterized by a partial or total absence of adipose tissue leading to severe metabolic derangements including marked insulin resistance, type 2 diabetes, hypertriglyceridemia, and steatohepatitis. Lipodystrophy is also a source of major cardiovascular disorders which, in addition to hepatic failure and infection, contribute to a significant reduction in life expectancy. Metreleptin, the synthetic analog of the adipocyte-derived hormone leptin and current therapy of choice for patients with lipodystrophy, successfully improves metabolic function. However, while leptin has been associated with hypertension, vascular diseases, and inflammation in the context of obesity, it remains unknown whether its daily administration could further impair cardiovascular function in patients with lipodystrophy. The goal of this short review is to describe the cardiovascular phenotype of patients with lipodystrophy, speculate on the etiology of the disorders, and discuss how the use of murine models of lipodystrophy could be beneficial to address the question of the contribution of leptin to lipodystrophy-associated cardiovascular disease.

Publication Information

Output type

Scholary Output:
Contribution to journal
Review article
Peer-review

Original language

English (US)

Article number

1756

Journal (Volume, Issue Number)

F1000Research (Volume 8)

Publication milestones

  • Published - 10/16/2019

Publication status

Published - 10/16/2019

ISSN

2046-1402

Publication IDs

  • Scopus: 85074162403
  • PubMed: 31656583

Publication metrics

Metrics

Scopus
citations
Fractional count
1
Fractional count
0.33
Fractional count
2
Fractional count
0.67
Fractional count
1
Fractional count
1
SciVal
Author count
3
SciVal
Paper percentile
33

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Mentions
3
Captures
49
Citation count
20

Funding Details

This work was supported by an Established Investigator Award from the American Heart Association (19EIA34760167, to EB), a K99/R00 (1K99HL140139-01A1 and 4R00HL140139-03 to TBN) and R01s (1R01HL130301-01; 1R01HL147639-01A1 to EB) from the National Heart, Lung, and Blood Institute (NHLBI)
FundersFunding numbers
NHLBI
R01HL130301
AHA
4R00HL140139-03, 1R01HL147639-01A1, 1K99HL140139-01A1, 19EIA34760167, 1R01HL130301-01