Evidence mapPaperPMID 21079616Full record

ReviewNature reviews. Endocrinology2011

Lipodystrophy: pathophysiology and advances in treatment.

Christina G Fiorenza, Sharon H Chou, Christos S Mantzoros

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

121 citing papers in PubMed, 255 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Severe Insulin Resistance Syndromes: Clinical Spectrum and Management.International journal of molecular sciences · 2025
    Review
  10. Bone marrow adipocytes: key players in vascular niches, aging, and disease.Frontiers in cell and developmental biology · 2025
    Review
  11. Review
  12. Review
  13. Article
  14. Navigating Lipodystrophy: Insights from Laminopathies and Beyond.International journal of molecular sciences · 2024
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

61 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Christina G FiorenzaDivision of Endocrinology, Diabetes & Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.
Sharon H Chou
Christos S Mantzoros
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

Role of Leptin in the Neuroendocrine Response to FastingR01DK058785 · BETH ISRAEL DEACONESS MEDICAL CENTER · 2001 to 2004
$2.0M
Role of Leptin in the Neuroendocrine Response to FastingR56DK058785 · BETH ISRAEL DEACONESS MEDICAL CENTER · 2005 to 2005
$85k
NIA NIH HHS AG-032030NIA NIH HHS R01 AG032030NIDDK NIH HHS DK-081913NIDDK NIH HHS DK-58785NIDDK NIH HHS DK-79929NIDDK NIH HHS K24 DK081913NIDDK NIH HHS R01 DK058785NIDDK NIH HHS R01 DK079929NIDDK NIH HHS R56 DK058785
6 · The paper itself

Abstract

Lipodystrophy is a medical condition characterized by complete or partial loss of adipose tissue. Not infrequently, lipodystrophy occurs in combination with pathological accumulation of adipose tissue at distinct anatomical sites. Patients with lipodystrophy exhibit numerous metabolic complications, which indicate the importance of adipose tissue as an active endocrine organ. Not only the total amount but also the appropriate distribution of adipose tissue depots contribute to the metabolic state. Genetic and molecular research has improved our understanding of the mechanisms underlying lipodystrophy. Circulating levels of hormones secreted by the adipose tissue, such as leptin and adiponectin, are greatly reduced in distinct subpopulations of patients with lipodystrophy. This finding rationalizes the use of these adipokines or of agents that increase their circulating levels, such as peroxisome proliferator-activated receptor γ (PPARγ) agonists, for therapeutic purposes. Other novel therapeutic approaches, including the use of growth hormone and growth-hormone-releasing factors, are also being studied as potential additions to the therapeutic armamentarium. New insights gained from research and clinical trials could potentially revolutionize the management of this difficult-to-treat condition.

Indexed as

AdiponectinAdipose TissueHumansLeptinLipodystrophyPPAR gammaAdiponectinLeptinPPAR gamma

Identifiers

PMID21079616
PMCPMC3150735
OpenAlexW2020803051

What Socratic holds

Textmetadata
LicenceTDM
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.