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Updated: Jul 15, 2026

Measurement of Basal and Forskolin-stimulated Lipolysis in Inguinal Adipose Fat Pads
Published on: July 21, 2017
PACAP 38 inhibits adiponectin release
Wojciech Bik1, Ewa Wolinska-Witort, Agnieszka Baranowska-Bik
1Neuroendocrinology Department, Medical Centre of Postgraduate Education, Warsaw, Poland. zncmkp@op.pl
Pituitary adenylate cyclase activating peptide (PACAP 38) reduced adiponectin levels in rats under normal conditions. However, PACAP 38 did not affect adiponectin levels during acute inflammation induced by lipopolysaccharide (LPS).
Area of Science:
- Endocrinology
- Immunology
- Metabolic Research
Background:
- Pituitary adenylate cyclase activating peptide (PACAP 38) is a neuropeptide with known anti-inflammatory effects.
- PACAP receptors are present in immune cells, endocrine glands, and adipose tissue.
- Adiponectin, an adipocyte hormone, has anti-inflammatory, antidiabetic, and antiatherogenic properties.
Purpose of the Study:
- To investigate the effect of PACAP 38 on adiponectin release.
- To examine adiponectin response to PACAP 38 during lipopolysaccharide (LPS)-induced inflammation.
Main Methods:
- Male Wistar-Kyoto rats were used and divided into four experimental groups.
- Groups received intraperitoneal injections of saline, LPS, PACAP 38, or LPS + PACAP 38.
- Serum adiponectin concentrations were quantified using ELISA.
Main Results:
- Lipopolysaccharide (LPS) administration did not alter serum adiponectin levels.
- PACAP 38 administered alone significantly decreased adiponectin concentration at 2 and 4 hours.
- Co-administration of LPS and PACAP 38 showed no significant difference in adiponectin levels compared to LPS alone.
Conclusions:
- PACAP 38 appears to directly modulate adiponectin secretion from adipocytes under basal conditions.
- PACAP 38's effect on adiponectin may be altered during acute inflammatory states induced by LPS.
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