Regulation of visfatin release in vivo by using an oral lipid solution completely free of proteins and carbohydrates

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 649-677-Adipocyte Biology
Basic
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-659
Stefanie Leszczak, Irene Ober, Margarita Bala and Andreas Schaeffler*
University of Regensburg, Regensburg, Germany
Background:

Visfatin represents a cytokine-enzyme expressed in and secreted by visceral adipose tissue. Visfatin is a pro-inflammatory adipokine and plays a role in the regulation of insulin secretion and carbohydrate metabolism. It is currently unclear whether or not visfatin is regulated in short-term by ingestion of an oral lipid load. Moreover, systematic data on serum concentrations in humans and their variations concerning age, gender and body mass index (BMI) are sparse.

Methods:

100 healthy volunteers (n=42 males and n=58 females) were enrolled in the study. 66 were lean (BMI < 25 kg/m2) and 34 were overweight/obese (BMI > 25 kg/m2). Basic anthropometric (waist-hip-ratio, skin fold thickness) and laboratory parameters such as C-reactive protein, plasma glucose, insulin, C-peptide, and lipoproteins were measured after an overnight fast and at 2,4 and 6h after ingestion of an oral lipid load. Visfatin serum levels were measured by ELISA. The novelty of this study is the fact that the used lipid load used was completely free of carbohydrates and proteins (pure triglyceride and plant oil solution). This designed solution was freshly mixed (160 ml; 758.1 kcal; 75 g vegetable fat as triglycerides, 9.2 g fatty acids as pure vegetable oils). Exclusion criteria were: pregnancy, acute or chronic infection, any underlying disease or medication. The study was approved by the local ethical committee.

Results:

As expected, triglycerides increased significantly at 2h and 4h whereas LDL, HDL and total cholesterol remained unchanged. Surprisingly, there was a significant and reversible decrease of glucose at 2h, whereas insulin showed a significant decrease from up to 6h. Serum visfatin concentrations were negatively correlated to fasting glucose levels and positively to waist-hip-ratio but not to BMI. Visfatin concentrations significantly decreased following the oral lipid load in both genders. Serum visfatin concentrations showed a broad interindividual range varying from 0.2 to 49.1 ng/ml.

Summary and conclusions:

This is the largest study available on the impact of fat ingestion on visfatin regulation in healthy probands and the only study investigating the isolated effect of nutritional fat by using a solution completely free of proteins and carbohydrates. Visfatin seems to represent an adipokine that can be regulated in short-term after ingestion of nutritional fat. Surprisingly, fat ingestion resulted in an decrease of glucose and insulin concentrations. This effect might be caused by a decrease of visfatin. Thus, visfatin might represent a visceral fat-derived mediator that cross-regulates carbohydrate and lipid metabolism.

Nothing to Disclose: SL, IO, MB, AS

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm