Evidence map›Paper›PMID 23757408›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2013

Thrombospondin-1 regulates adiposity and metabolic dysfunction in diet-induced obesity enhancing adipose inflammation and stimulating adipocyte proliferation.

Ping Kong, Carlos Gonzalez-Quesada, Na Li, Michele Cavalera, Dong-Wook Lee, Nikolaos G Frangogiannis

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Cardio-Vascular Extracellular Matrix: The Unmet Enigma.International journal of molecular sciences · 2026
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7 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

6 authors at 2 institutions in 1 country.

Ping KongThe Wilf Family Cardiovascular Research Institute, Department of Medicine Cardiology Albert Einstein College of Medicine, Bronx, New York, USA.
Carlos Gonzalez-Quesada
Na Li
Michele Cavalera
Dong-Wook Lee
Nikolaos G Frangogiannis
Albert Einstein College of Medicine · USBaylor College of Medicine · US

Funding

Chemokines in Healing Myocardial InfarctsR01HL076246 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI Nikolaos G Frangogiannis · 2005 to 2026
$9.5M
Resolution of Inflammation in healing Myocardial InfarctsR01HL085440 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI FRANGOGIANNIS, NIKOLAOS G · 2008 to 2025
$8.5M
NHLBI NIH HHS R01 HL076246NHLBI NIH HHS R01 HL085440NHLBI NIH HHS R01 HL-76246NHLBI NIH HHS R01 HL-85440
6 · The paper itself

Abstract

As a typical matricellular protein, thrombospondin (TSP)-1, binds to the structural matrix and regulates cellular behavior by modulating growth factor and cytokine signaling. Obesity and diabetes are associated with marked upregulation of TSP-1 in adipose tissue. We hypothesized that endogenous TSP-1 may play an important role in the pathogenesis of diet-induced obesity and metabolic dysfunction. Accordingly, we examined the effects of TSP-1 gene disruption on weight gain, adiposity, and adipose tissue inflammation in mice receiving a high-fat diet (HFD: 60% fat, 20% carbohydrate) or a high-carbohydrate low-fat diet (HCLFD: 10% fat, 70% carbohydrate). HFD mice had significantly higher TSP-1 expression in perigonadal adipose tissue; TSP-1 was predominantly localized in the adipose interstitium. TSP-1 loss attenuated weight gain and fat accumulation in HFD and HCLFD groups. Compared with corresponding wild-type animals, TSP-1-null mice had decreased insulin levels but exhibited elevated free fatty acid and triglyceride levels, suggesting impaired fatty acid uptake. TSP-1 loss did not affect adipocyte size and had no effect on adipose vascular density. However, TSP-1-null mice exhibited attenuated tumor necrosis factor-α mRNA expression and reduced macrophage infiltration, suggesting a role for TSP-1 in mediating obesity-associated inflammation. In vitro, TSP-1 enhanced proliferation of 3T3-L1 preadipocytes but did not modulate inflammatory cytokine and chemokine synthesis. In conclusion, TSP-1 upregulation contributes to weight gain, adipose growth, and the pathogenesis of metabolic dysfunction. The effects of TSP-1 may involve stimulation of adipocyte proliferation, activation of inflammatory signaling, and facilitated fatty acid uptake by adipocytes.

Indexed as

Diet3T3 CellsAdipocytesAdipose TissueAdiposityAnimalsCalorimetry, IndirectCell ProliferationDiet, High-FatGene ExpressionImmunohistochemistryInflammationInsulinInsulin ResistanceMiceMice, Inbred C57BLInsulinThrombospondin 1adipocyteinflammationmacrophagematricellular proteinsobesity

Identifiers

PMID23757408
PMCPMC3742854
OpenAlexW2122346650

What OpenQuestion 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 OpenQuestion graph.