垂体腺苷酸环化酶激活肽38抑制脂联素的释放。

PACAP 38 inhibits adiponectin release.

作者信息

Bik Wojciech, Wolinska-Witort Ewa, Baranowska-Bik Agnieszka, Martynska Lidia, Chmielowska Magdalena, Baranowska Boguslawa

机构信息

Neuroendocrinology Department, Medical Centre of Postgraduate Education, Warsaw, Poland.

出版信息

Neuro Endocrinol Lett. 2007 Apr;28(2):166-9.

PMID:17435668

Abstract

BACKGROUND

Pituitary adenylate cyclase activating peptide (PACAP 38) is a neuropeptide with anti-inflammatory activity. Vasoactive intestinal peptide (VIP)/PACAP receptors are found in immune cells, endocrine glands and also in adipose tissue. Adiponectin is an adipocyte-derived protein hormone which possesses anti-inflammatory, antidiabetic and antiatherogenic properties. The aim of this study was to examine the influence of PACAP 38 on adiponectin release in basal conditions and during lipopolysaccharide (LPS)-induced acute inflammation.

METHODS

Male Wistar-Kyoto rats were divided into four groups which received intraperitoneal injections of 0.9% NaCl, LPS, PACAP 38 or LPS+PACAP 38, respectively. Serum adiponectin concentrations were measured using an ELISA test.

RESULTS

LPS administration did not change adiponectin concentration; however, PACAP 38 administered alone decreased serum adiponectin concentration after 2 h (p<0.05) and 4 h (p<0.01). In the group that received LPS+PACAP38, compared with LPS alone, no difference in adiponectin concentration was observed.

CONCLUSIONS

We conclude that PACAP 38 may directly modulate adiponectin secretion by adipocytes in basal conditions.

摘要

背景

垂体腺苷酸环化酶激活肽（PACAP 38）是一种具有抗炎活性的神经肽。血管活性肠肽（VIP）/PACAP受体存在于免疫细胞、内分泌腺以及脂肪组织中。脂联素是一种由脂肪细胞产生的蛋白质激素，具有抗炎、抗糖尿病和抗动脉粥样硬化特性。本研究旨在探讨PACAP 38在基础条件下以及脂多糖（LPS）诱导的急性炎症过程中对脂联素释放的影响。