Format

Send to

Choose Destination
Clin Chim Acta. 2015 Jan 1;438:46-54. doi: 10.1016/j.cca.2014.07.043. Epub 2014 Aug 13.

Resistin: insulin resistance to malignancy.

Author information

1
Department of Pediatrics, Dr. Peset University Hospital, Valencia 46017, Spain; Department of Pediatrics, Obstetrics and Gynecology, University of Valencia, Valencia 46010, Spain. Electronic address: pilar.codoner@uv.es.
2
Department of Biochemistry and Molecular Biology, University of Valencia, Valencia 46010, Spain.

Abstract

Adipose tissue is recognized as an endocrine organ that secretes bioactive substances known as adipokines. Excess adipose tissue and adipose tissue dysfunction lead to dysregulated adipokine production that can contribute to the development of obesity-related co-morbidities. Among the various adipokines, resistin, which was initially considered as a determinant of the emergence of insulin resistance in obesity, has appeared as an important link between obesity and inflammatory processes. Several experimental and clinical studies have suggested an association between increased resistin levels and severe conditions associated with obesity such as cardiovascular disease and malignancies. In this review, we present the growing body of evidence that human resistin is an inflammatory biomarker and potential mediator of obesity-associated diseases. A common pathway seems to involve the combined alteration of immune and inflammatory processes that favor metabolic disturbances, atherosclerosis and carcinogenesis. The mode of action and the signaling pathways utilized by resistin in its interactions with target cells could involve oxidative and nitrosative stress. Therefore, resistin could function as a key molecule in the complications of obesity development and could potentially be used as a diagnostic and prognostic marker.

KEYWORDS:

Adipocytokines; Atherosclerosis; Cancer; Inflammation; Obesity; Resistin

PMID:
25128719
DOI:
10.1016/j.cca.2014.07.043
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center