Evidence map›Paper›PMID 34223895›Full record

ArticleThe Journal of clinical endocrinology and metabolism2021

Leptin Attenuates Cardiac Hypertrophy in Patients With Generalized Lipodystrophy.

My-Le Nguyen, Vandana Sachdev, Thomas R Burklow, Wen Li, Megan Startzell, Sungyoung Auh, Rebecca J Brown

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
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  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Approach to the Patient With Lipodystrophy.The Journal of clinical endocrinology and metabolism · 2022
    Article
  9. Article
  10. Review
  11. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

My-Le NguyenNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Vandana SachdevNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Thomas R BurklowNIH Clinical Center, National Institutes of Health, Bethesda, MD 20892, USA.
Wen LiNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Megan StartzellNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Sungyoung AuhNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Rebecca J BrownNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-2589-7382
National Institutes of Health · USNational Institutes of Health Clinical Center · US

Funding

Clinical utility of leptin therapy in syndromic forms of insulin resistance.ZIADK047052 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI BROWN, REBECCA · 2009 to 2025
$5.5M
Intramural NIH HHSNHLBI NIH HHSNIDDK NIH HHS
6 · The paper itself

Abstract

contextLipodystrophy syndromes are rare disorders of deficient adipose tissue, low leptin, and severe metabolic disease, affecting all adipose depots (generalized lipodystrophy, GLD) or only some (partial lipodystrophy, PLD). Left ventricular (LV) hypertrophy is common (especially in GLD); mechanisms may include hyperglycemia, dyslipidemia, or hyperinsulinemia.

objectiveDetermine effects of recombinant leptin (metreleptin) on cardiac structure and function in lipodystrophy.

methodsOpen-label treatment study of 38 subjects (18 GLD, 20 PLD) at the National Institutes of Health before and after 1 (N = 27), and 3 to 5 years (N = 23) of metreleptin. Outcomes were echocardiograms, blood pressure (BP), triglycerides, A1c, and homeostasis model assessment of insulin resistance.

resultsIn GLD, metreleptin lowered triglycerides (median [interquartile range] 740 [403-1239], 138 [88-196], 211 [136-558] mg/dL at baseline, 1 year, 3-5 years, P < .0001), A1c (9.5 ± 3.0, 6.5 ± 1.6, 6.5 ± 1.9%, P < .001), and HOMA-IR (34.1 [15.2-43.5], 8.7 [2.4-16.0], 8.9 [2.1-16.4], P < .001). Only HOMA-IR improved in PLD (P < .01). Systolic BP decreased in GLD but not PLD. Metreleptin improved cardiac parameters in patients with GLD, including reduced posterior wall thickness (9.8 ± 1.7, 9.1 ± 1.3, 8.3 ± 1.7 mm, P < .01), and LV mass (140.7 ± 45.9, 128.7 ± 37.9, 110.9 ± 29.1 g, P < .01), and increased septal e' velocity (8.6 ± 1.7, 10.0 ± 2.1, 10.7 ± 2.4 cm/s, P < .01). Changes remained significant after adjustment for BP. In GLD, multivariate models suggested that reduced posterior wall thickness and LV mass index correlated with reduced triglycerides and increased septal e' velocity correlated with reduced A1c. No changes in echocardiographic parameters were seen in PLD.

conclusionMetreleptin attenuated cardiac hypertrophy and improved septal e' velocity in GLD, which may be mediated by reduced lipotoxicity and glucose toxicity. The applicability of these findings to leptin-sufficient populations remains to be determined.

Indexed as

AdolescentAdultBlood PressureCardiomegalyEchocardiographyFemaleGlycated HemoglobinHumansHypertrophy, Left VentricularInsulin ResistanceLeptinLipodystrophyLipodystrophy, Congenital GeneralizedMaleMiddle AgedNational Institutes of Health (U.S.)Glycated HemoglobinLeptinmetreleptinTriglyceridescardiomyopathyleft ventricular hypertrophyLeptinlipodystrophy

Identifiers

PMID34223895
PMCPMC8530723
OpenAlexW3179143298

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.