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Updated: Aug 6, 2026
09:41
Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
Published on: March 17, 2023
Glucose-dependent insulinotropic polypeptide modulates adipocyte lipolysis and reesterification
Lisa Getty-Kaushik1, Diane H Song, Michael O Boylan
1Obesity Research Center, Department of Molecular Medicine, Boston University School of Medicine, Boston, MA 02118, USA.
Obesity (Silver Spring, Md.)
|August 11, 2006
Summary
Glucose-dependent insulinotropic polypeptide (GIP) promotes obesity by stimulating fat storage and lipolysis in adipocytes. A GIP receptor antagonist reversed these effects, suggesting GIP is a potential target for obesity and type 2 diabetes treatments.
Area of Science:
- Endocrinology
- Metabolic Research
- Pharmacology
Background:
- Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone secreted postprandially.
- Previous research suggests GIP may contribute to obesity development.
- The GIP receptor is a potential therapeutic target for anti-obesity strategies.
Purpose of the Study:
- To investigate the mechanisms by which GIP influences adipocyte metabolism, specifically lipolysis and reesterification.
- To determine if a GIP receptor antagonist (ANTGIP) can counteract GIP-mediated effects on adipocytes.
Main Methods:
- Isolated rat adipocytes were perifused and treated with GIP, insulin, isoproterenol, or ANTGIP.
- Adipocyte metabolism was assessed by measuring glycerol and free fatty acid (FFA) release.
- Lactate release was also measured as an indicator of metabolic activity.
Main Results:
- GIP significantly increased FFA reesterification (25% decrease in FFA release) and stimulated lipolysis (22% increase in glycerol release).
- GIP attenuated the lipolytic response to isoproterenol by 43%, exhibiting insulin-like effects on adipocytes.
- ANTGIP effectively reversed the metabolic effects of GIP on both basal and stimulated adipocytes.
Conclusions:
- GIP plays a significant physiological role in lipid homeostasis.
- GIP's actions on adipocytes suggest a role in obesity pathogenesis.
- The GIP receptor presents a promising therapeutic target for obesity and related type 2 diabetes.
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