Evidence map›Paper›PMID 22326219›Full record

ArticleCell metabolism2012

Altered mitochondrial function and metabolic inflexibility associated with loss of caveolin-1.

Ingrid Wernstedt Asterholm, Dorothy I Mundy, Jian Weng, Richard G W Anderson, Philipp E Scherer

Abstract read
In one paragraph

Article in Cell metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed
–field-weighted citation impact
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

108 citing papers in PubMed.

  1. Trial
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  9. Serotonin Influences Insulin Secretion in Rat Insulinoma INS-1E Cells.International journal of molecular sciences · 2024
    Article
  10. Review
  11. Article
  12. Article
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  14. Review
  15. Article
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48 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

5 authors.

Ingrid Wernstedt AsterholmTouchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8549, USA.
Dorothy I Mundy
Jian Weng
Richard G W Anderson
Philipp E Scherer

Funding

TRANSCRIPTIONAL REGULATION OF LDL RECEPTOR PROMOTERP01HL020948 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI GOLDSTEIN, JOSEPH L · 1985 to 2021
$103.1M
Novel Mechanisms Regulating the Adipocyte-Brain-Hepatocyte AxisP01DK088761 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI SCHERER, PHILIPP E · 2010 to 2019
$17.4M
Adiponectin, A Protein Secreted From Adipose TissueR01DK055758 · NIDDK · YESHIVA UNIVERSITY · PI SCHERER, PHILIPP E · 2000 to 2024
$10.9M
FUNCTION OF CAVEOLAE IN POTOCYTOSIS AND CELL SIGNALINGR01GM052016 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI MICHAELY, PETER A. · 1995 to 2010
$4.9M
Stromal Contributions of Adipocytes in Breast CancerR01CA112023 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI SCHERER, PHILIPP E · 2005 to 2009
$1.5M
Dissecting Adipose Depot-Selective Regulation of Gene ProgramsRC1DK086629 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI SCHERER, PHILIPP E · 2009 to 2010
$1000k
NCI NIH HHS R01 CA112023NCI NIH HHS R01-CA112023NHLBI NIH HHS HL 20948NHLBI NIH HHS P01 HL020948NIDDK NIH HHS P01 DK088761NIDDK NIH HHS P01DK088761-01NIDDK NIH HHS R01 DK055758NIDDK NIH HHS R01-DK55758NIDDK NIH HHS RC1 DK086629NIGMS NIH HHS GM 52016NIGMS NIH HHS R01 GM052016
6 · The paper itself

Abstract

Caveolin-1 is a major structural component of raft structures within the plasma membrane and has been implicated as a regulator of cellular signal transduction with prominent expression in adipocytes. Here, we embarked on a comprehensive characterization of the metabolic pathways dysregulated in caveolin-1 null mice. We found that these mice display decreased circulating levels of total and high molecular weight adiponectin and a reduced ability to change substrate use in response to feeding/fasting conditions. Caveolin-1 null mice are extremely lean but retain muscle mass despite lipodystrophy and massive metabolic dysfunction. Hepatic gluconeogenesis is chronically elevated, while hepatic steatosis is reduced. Our data suggest that the complex phenotype of the caveolin-1 null mouse is caused by altered metabolic and mitochondrial function in adipose tissue with a subsequent compensatory response driven mostly by the liver. This mouse model highlights the central contributions of adipose tissue for system-wide preservation of metabolic flexibility.

Indexed as

AdiponectinAdipose TissueAnimalsCaveolin 1Fatty Acids, NonesterifiedFatty LiverGluconeogenesisHistological TechniquesLiverMetabolic Networks and PathwaysMiceMitochondriaTomography, X-Ray ComputedAdiponectinCaveolin 1Fatty Acids, Nonesterified

Identifiers

PMID22326219
PMCPMC3278712

What OpenQuestion holds

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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.