Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
March 19, 2010Arteriosclerosis Thrombosis and Vascular BiologyOpen Access

Lack of Association Between Adiponectin Levels and Atherosclerosis in Mice

View Full Paper
Ask AI
Bookmark
Share

Why the study?

Does genetic manipulation of adiponectin levels prevent atherosclerotic plaque formation in Ldlr(-/-) and Apoe(-/-) mouse models?

Population

Adiponectin knockout mice (Adn) or mice with chronically elevated adiponectin levels (Adn) crossed into…

Comparison

Genetic knockout or overexpression of adiponectin vs Control mice with normal adiponectin levels

Design

Preclinical

Authors

ANAndrea R. NawrockiJohnson & Johnson (United States)SHSusanna M. HofmannHelmholtz Zentrum MünchenDTDaniel TeupserLMU Klinikum

Discussion

Loading...

Member takes

Implication

Adiponectin modulation does not affect plaque in these mouse models; leaves open its causal role in human atherosclerosis.

Key Points

  • To determine whether circulating adiponectin levels play a direct causal role in protecting against the development and progression of atherosclerotic lesions.
  • Crossed adiponectin knockout mice (Adn-/-) and adiponectin-overexpressing transgenic mice (Adn(Tg)) with low-density lipoprotein receptor-null (Ldlr-/-) and apolipoprotein E-null (Apoe-/-) mouse models.
  • Assessed aortic root plaque volume, total aortic cholesterol accumulation, and plaque morphology under multiple dietary regimens.
  • Circulating adiponectin concentrations failed to correlate with the suppression or progression of atherogenic processes.
  • Aortic root plaque volume, aortic cholesterol accumulation, and overall plaque morphology were not altered by either genetic deletion or transgenic elevation of adiponectin.

Structured PICO

Does genetic manipulation of adiponectin levels prevent atherosclerotic plaque formation in Ldlr(-/-) and Apoe(-/-) mouse models?

P
Population
Adiponectin knockout mice (Adn(-/-)) or mice with chronically elevated adiponectin levels (Adn(Tg)) crossed into low-density lipoprotein receptor-null (Ldlr(-/-)) and apoliprotein E-null (Apoe(-/-)) mouse models
I
Intervention
Genetic knockout or overexpression of adiponectin
C
Comparator
Control mice with normal adiponectin levels (implied)
O
Outcome
Atherosclerotic plaque formation (plaque volume in the aortic root, cholesterol accumulation in the aorta, and plaque morphology)surrogate

In preclinical mouse models, genetic gain- or loss-of-function of adiponectin had no direct impact on atherosclerotic plaque formation, suggesting a lack of causation despite human associations.

Cite This Study

Nawrocki et al. (2010) studied this question.

synapsesocial.com/papers/6a929581ab121d91d03ab203https://doi.org/10.1161/atvbaha.109.195826
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Disruption of Adiponectin Causes Insulin Resistance and Neointimal Formation2002 · 1,216 citations
  2. 2Hypercholesterolemia in low density lipoprotein receptor knockout mice and its reversal by adenovirus-mediated gene delivery.1993 · 1,658 citations
  3. 3Effect of Rosiglitazone on the Risk of Myocardial Infarction and Death from Cardiovascular Causes2007 · 4,693 citations
  4. 4Thiazolidinediones, peripheral oedema and congestive heart failure: what is the evidence?2005 · 78 citations
  5. 5Genetic Influences of Adiponectin on Insulin Resistance, Type 2 Diabetes, and Cardiovascular Disease2007 · 279 citations