Exp Clin Endocrinol Diabetes 2014; 122 - P004
DOI: 10.1055/s-0034-1372021

Short-term regulation of visfatin release in vivo by oral lipid ingestion and in vitro by fatty acid stimulation

A Schmid 1, T Karrasch 1, S Leszczak 2, M Bala 2, I Ober 2, J Martin 2, A Kopp 2, A Schäffler 1
  • 1Gießen University Hospital, Gießen, Germany
  • 2University Hospital, Regensburg, Germany

Background: Visfatin represents a new adipokine secreted by visceral adipose tissue with a possible impact on systemic insulin sensitivity. Data on the regulation of visfatin are sparse and contradictory. Our study investigates the short-term regulation of serum visfatin concentrations in healthy, non-diabetic subjects in response to 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 was investigated in vitro.

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

Results: A significant rise of serum triglycerides at 2h, 4h, and 6h after OLI was observed, accompanied by a significant decrease of glucose, insulin and C-peptide. Fasting visfatin levels were negatively correlated with fasting glucose levels. Serum visfatin levels significantly decreased after OLI. Of five saturated fatty acids tested, only palmitic acid exerted significant effects by strongly downregulating visfatin release by about 66% (p = 0.004). The mono-unsaturated fatty acids palmitoleic acid and oleic acid exerted opposite effects with the former decreasing and the latter increasing visfatin release (p = 0.002 for both). Both of the poly-unsaturated fatty acids linoleic acid (p = 0.004) and arachidonic acid (p = 0.002) decreased visfatin release. Eicosapentaenoic acid had no effects on visfatin release.

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