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Related Experiment Video

Updated: Oct 5, 2025

An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function

An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function

Published on: May 4, 2021

S1P/S1PR3 signalling axis protects against obesity-induced metabolic dysfunction.

Sagarika Chakrabarty¹, Quyen Bui¹, Leylla Badeanlou¹

¹Department of Cell Biology, San Diego Biomedical Research Institute, San Diego, CA, USA.

|January 31, 2022

Summary

Sphingosine-1-phosphate (S1P) shows anti-diabetic effects by improving glucose homeostasis. S1P-S1PR3 signaling in adipose and liver tissues protects against inflammation and fat accumulation, maintaining metabolic health.

Keywords:

S1PR3 Sphingosine 1 phosphate T2D adipogenesis adipose inflammation hepatic inflammation hepatic steatosis obesity

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Area of Science:

Metabolic disease
Endocrinology
Lipid signaling

Background:

Sphingosine-1-phosphate (S1P) is a bioactive lipid regulating cell growth, immune cell trafficking, and inflammation via G-protein coupled receptors (S1PR1-5).
Type 2 diabetes (T2D) is a metabolic disorder characterized by impaired glucose homeostasis and inflammation.

Purpose of the Study:

To investigate the role of S1P and its receptor S1PR3 in metabolic regulation, particularly in the context of Type 2 diabetes and obesity.
To explore the therapeutic potential of S1P in improving metabolic parameters.

Main Methods:

Analysis of plasma S1P levels in Type 2 diabetic subjects treated with rosiglitazone.
Gene expression analysis of S1PR3 in adipose tissue and liver of mice fed a high-fat diet (HFD).
Phenotypic characterization of S1PR3 knockout (S1PR3-/-) mice on an HFD, including metabolic assessments and immune cell profiling.
Investigation of S1P effects on adipogenesis and PPARγ expression in 3T3-L1 preadipocytes.

Main Results:

Plasma S1P levels increased with rosiglitazone treatment in T2D subjects, correlating with improved glucose homeostasis.
HFD-induced obesity increased S1PR3 expression in adipose tissue and liver.
S1PR3-/- mice on HFD exhibited partial lipodystrophy, exacerbated insulin resistance, glucose intolerance, adipose and hepatic inflammation, and hepatic steatosis.
S1P promoted adipogenesis and S1P-S1PR3 signaling regulated PPARγ expression in preadipocytes.

Conclusions:

S1P exerts anti-diabetic effects and improves glucose homeostasis.
S1P-S1PR3 signaling in adipose and liver tissues plays a protective role against inflammation and steatosis, crucial for maintaining metabolic homeostasis.
Targeting the S1P-S1PR3 pathway may offer a novel therapeutic strategy for managing metabolic disorders like Type 2 diabetes and obesity.