Level C· Early human research exploring benefitsProspective StudyEurope PMCOpen access

Resistin in rodents and humans

Park HK., Ahima RS.

Prospective Study on Type 2 Diabetes, Cardiovascular Disease, Stroke Research, Chronic Inflammation, published in Diabetes Metab J (2013) — summary generated from the PubMed abstract.

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Level C· Early human research exploring benefitsEvidence level of this study

Early human evidence such as case series or small samples is exploring possible benefits.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Prospective Study
Journal
Diabetes Metab J (2013)
Reported sample size
—
Source database
Europe PMC
PMID
24404511
PMCID
PMC3881324
DOI
10.4093/dmj.2013.37.6.404
Citations
122

Abstract (original English)

Obesity is characterized by excess accumulation of lipids in adipose tissue and other organs, and chronic inflammation associated with insulin resistance and an increased risk of type 2 diabetes. Obesity, type 2 diabetes, and cardiovascular diseases are major health concerns. Resistin was first discovered as an adipose-secreted hormone (adipokine) linked to obesity and insulin resistance in rodents. Adipocyte-derived resistin is increased in obese rodents and strongly related to insulin resistance. However, in contrast to rodents, resistin is expressed and secreted from macrophages in humans and is increased in inflammatory conditions. Some studies have also suggested an association between increased resistin levels and insulin resistance, diabetes and cardiovascular disease. Genetic studies have provided additional evidence for a role of resistin in insulin resistance and inflammation. Resistin appears to mediate the pathogenesis of atherosclerosis by promoting endothelial dysfunction, vascular smooth muscle cell proliferation, arterial inflammation, and formation of foam cells. Indeed, resistin is predictive of atherosclerosis and poor clinical outcomes in patients with coronary artery disease and ischemic stroke. There is also growing evidence that elevated resistin is associated with the development of heart failure. This review will focus on the biology of resistin in rode

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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