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Updated: Jun 13, 2026

Rapid In Situ Hybridization using Oligonucleotide Probes on Paraformaldehyde-prefixed Brain of Rats with Serotonin Syndrome

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Published on: September 23, 2015

Serotonin (5-HT) receptor 5A sequence variants affect human plasma triglyceride levels.

Y Zhang¹, E M Smith, T M Baye

¹Human and Molecular Genetics Center, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.

Physiological Genomics

|April 15, 2010

Summary

Genetic variations in the serotonin receptor gene HTR5A are linked to higher triglyceride levels in a Northern European population. This suggests HTR5A may play a role in brain-based regulation of plasma triglycerides.

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Area of Science:

Neuroscience
Genetics
Metabolic Disorders

Background:

Serotonin (5-hydroxytryptamine, 5-HT) interacts with leptin and insulin to regulate metabolic and neuroendocrine functions.
Reduced sensitivity to food intake can lead to obesity, diabetes, and behavioral issues.
The role of specific serotonin receptor subtypes in integrating metabolic signals and genetic influences on metabolic disorder susceptibility remains unclear.

Purpose of the Study:

To investigate the association between serotonin receptor gene variants and plasma triglyceride levels.
To identify specific genetic variations in HTR5A influencing metabolic traits.
To explore the functional impact of identified genetic variants on HTR5A expression and regulation.

Main Methods:

Genome-wide linkage and targeted association analyses were performed on a cohort of 2,209 individuals of Northern European descent.
28 publicly available and 12 newly discovered single nucleotide polymorphisms (SNPs) in HTR5A were analyzed.
Bayesian quantitative trait nucleotide (BQTN) analysis and electrophoretic mobility shift assays (EMSA) were used for SNP analysis and functional validation.

Main Results:

The serotonin type 5A receptor gene (HTR5A) was identified as a significant factor influencing plasma triglyceride (TG) levels.
Three SNPs in HTR5A showed strong association with plasma TG levels (P < 0.00125).
A putative causal promoter SNP (rs3734967) was identified, with distinct nuclear protein binding patterns observed for its alleles via EMSA.

Conclusions:

Sequence variants in HTR5A are strongly associated with elevated plasma TG levels in a Northern European population.
This finding suggests a novel role for the serotonin receptor system in human metabolic regulation.
The results indicate a potential brain-specific regulation of plasma TG levels, possibly mediated by altered HTR5A expression.