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Exp Clin Endocrinol Diabetes 2014; 122(2): 126-134
DOI: 10.1055/s-0033-1363262
Article
© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Short-term Regulation of Visfatin Release in vivo by Oral Lipid Ingestion and in vitro by Fatty Acid Stimulation

T. Karrasch
1   Department of Internal Medicine III, Giessen University Hospital, Germany
,
S. Leszczak
2   Department of Internal Medicine I, Regensburg University Hospital, Germany
,
M. Bala
2   Department of Internal Medicine I, Regensburg University Hospital, Germany
,
I. Ober
2   Department of Internal Medicine I, Regensburg University Hospital, Germany
,
J. Martin
2   Department of Internal Medicine I, Regensburg University Hospital, Germany
,
A. Schmid
2   Department of Internal Medicine I, Regensburg University Hospital, Germany
,
A. Kopp
2   Department of Internal Medicine I, Regensburg University Hospital, Germany
,
A. Schaffler
1   Department of Internal Medicine III, Giessen University Hospital, Germany
› Author Affiliations
Further Information

Publication History

received 23 August 2013
first decision 21 October 2013

accepted 29 November 2013

Publication Date:
19 February 2014 (online)

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Abstract

Background:

Visfatin represents a new adipokine secreted by visceral adipose tissue and possibly regulating insulin sensitivity. Data on the regulation of visfatin are sparse and contradictory. Our study investigates the regulation of serum visfatin concentrations in healthy and non-diabetic subjects in response to the ingestion of a newly developed oral lipid solution (OLI) in vivo. Furthermore, the effects of a broad spectrum of fatty acids on adipocytic visfatin release were investigated in vitro.

Material and Methods:

100 (42 male and 58 female) healthy volunteers were included in the study. Anthropometric and laboratory parameters (lipoproteins, glucose, insulin, C-peptide) were measured after an overnight fast at 0 h and 2 h, 4 h, and 6 h after OLI. 3T3-L1 preadipocytes were differentiated into mature adipocytes and stimulated with increasing doses of 10 different fatty acids, and the release of visfatin into the supernatants was measured by ELISA.

Results:

Serum triglycerides significantly rose after OLI. This was accompanied by a significant decrease of glucose, insulin and C-peptide. Serum visfatin levels significantly decreased after OLI. Fasting visfatin levels were negatively correlated with fasting glucose levels. Of the 5 saturated fatty acids tested, only palmitic acid exerted significant effects by strongly downregulating visfatin release by about 66%. The mono-unsaturated fatty acids palmitoleic acid and oleic acid exerted opposite effects decreasing/increasing visfatin release, respectively. Both of the poly-unsaturated fatty acids linoleic acid and arachidonic acid decreased visfatin release.

Conclusions:

Oral lipid ingestion is a physiological regulator of systemic visfatin release. Fatty acids differentially regulate visfatin release in vitro.

Key words

visfatin - oral lipid load test - adipose tissue - adipokine - fatty acid
 

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