Impact of the Adipokine Adiponectin and the Hepatokine Fetuin-A on the Development of Type 2 Diabetes: Prospective Cohort- and Cross-Sectional Phenotyping StudiesReport as inadecuate




Impact of the Adipokine Adiponectin and the Hepatokine Fetuin-A on the Development of Type 2 Diabetes: Prospective Cohort- and Cross-Sectional Phenotyping Studies - Download this document for free, or read online. Document in PDF available to download.

Background

Among adipokines and hepatokines, adiponectin and fetuin-A were consistently found to predict the incidence of type 2 diabetes, both by regulating insulin sensitivity.

Objective

To determine to what extent circulating adiponectin and fetuin-A are independently associated with incident type 2 diabetes in humans, and the major mechanisms involved.

Methods

Relationships with incident diabetes were tested in two cohort studies: within the European Prospective Investigation into Cancer and Nutrition EPIC-Potsdam study 628 cases and the Nurses- Health Study NHS; 470 cases. Relationships with body fat compartments, insulin sensitivity and insulin secretion were studied in the Tübingen Lifestyle Intervention Program TULIP; N = 358.

Results

Circulating adiponectin and fetuin-A, independently of several confounders and of each other, associated with risk of diabetes in EPIC-Potsdam RR for 1 SD: adiponectin: 0.45 95% CI 0.37–0.54, fetuin-A: 1.18 1.05–1.32 and the NHS 0.51 0.42–0.62, 1.35 1.16–1.58. Obesity measures considerably attenuated the association of adiponectin, but not of fetuin-A. Subjects with low adiponectin and concomitantly high fetuin-A had the highest risk. Whereas both proteins were independently both p<1.8×10−7 associated with insulin sensitivity, circulating fetuin-A r = −0.37, p = 0.0004, but not adiponectin, associated with insulin secretion in subjects with impaired glucose tolerance.

Conclusions

We provide novel information that adiponectin and fetuin-A independently of each other associate with the diabetes risk. Furthermore, we suggest that they are involved in the development of type 2 diabetes via different mechanisms, possibly by mediating effects of their source tissues, expanded adipose tissue and nonalcoholic fatty liver.



Author: Norbert Stefan , Qi Sun, Andreas Fritsche, Jürgen Machann, Fritz Schick, Felicia Gerst, Charlotte Jeppesen, Hans-Georg Joost, Fr

Source: http://plos.srce.hr/



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