Karrasch T, Leszczak S, Bala M, Ober I, Martin J, Schmid A, Kopp A, Schaffler A
Department of Internal Medicine III, Giessen University Hospital, Germany.
Department of Internal Medicine I, Regensburg University Hospital, Germany.
Exp Clin Endocrinol Diabetes. 2014 Feb;122(2):126-34. doi: 10.1055/s-0033-1363262. Epub 2014 Feb 19.
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.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.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.Oral lipid ingestion is a physiological regulator of systemic visfatin release. Fatty acids differentially regulate visfatin release in vitro.
内脂素是一种由内脏脂肪组织分泌的新型脂肪因子，可能对胰岛素敏感性具有调节作用。关于内脂素调节的相关数据稀少且相互矛盾。我们的研究在体内调查了健康非糖尿病受试者摄入新研发的口服脂质溶液（OLI）后血清内脂素浓度的调节情况。此外，还在体外研究了多种脂肪酸对脂肪细胞内脂素释放的影响。100名（42名男性和58名女性）健康志愿者参与了该研究。在禁食过夜后0小时以及摄入OLI后2小时、4小时和6小时测量人体测量学和实验室参数（脂蛋白、葡萄糖、胰岛素、C肽）。将3T3-L1前脂肪细胞分化为成熟脂肪细胞，并用递增剂量的10种不同脂肪酸进行刺激，通过酶联免疫吸附测定法测量内脂素释放到上清液中的量。摄入OLI后血清甘油三酯显著升高。与此同时，葡萄糖、胰岛素和C肽显著降低。摄入OLI后血清内脂素水平显著下降。空腹内脂素水平与空腹血糖水平呈负相关。在所测试的5种饱和脂肪酸中，只有棕榈酸通过强烈下调内脂素释放约66%发挥了显著作用。单不饱和脂肪酸棕榈油酸和油酸分别产生了相反的作用，即降低/增加内脂素释放。两种多不饱和脂肪酸亚油酸和花生四烯酸均降低了内脂素释放。口服脂质摄入是全身内脂素释放的一种生理调节因素。脂肪酸在体外对内脂素释放具有不同的调节作用。
