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LCoRL Regulates Growth and Metabolism
Steven C Wyler1, Surbhi Gahlot1, Lara Bideyan1
1Center for Hypothalamic Research, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Endocrinology
|October 28, 2024
Summary
Ligand-dependent corepressor-like (LCoRL) regulates body weight and glucose homeostasis. LCoRL knockout mice exhibit improved metabolic health, reduced food intake, and protection against high-fat diets, validating GWAS findings.
Area of Science:
- Metabolic regulation
- Genetics
- Physiology
Background:
- Genome-wide association studies (GWAS) link genes to metabolic traits, but causality remains unclear.
- Ligand-dependent corepressor-like (LCoRL) is associated with body size and glucose homeostasis in humans and livestock.
- Functional analysis of LCoRL's role in metabolic regulation is lacking.
Purpose of the Study:
- To investigate the functional role of LCoRL in metabolic homeostasis.
- To characterize the metabolic traits of Lcorl knockout mice.
- To elucidate the mechanisms underlying LCoRL's metabolic regulation.
Main Methods:
- Generation and characterization of Lcorl knockout mice (Lcorl-/-).
- Assessment of body weight, food intake, glucose tolerance, and insulin sensitivity.
- Measurement of circulating IGF-1 levels and gene expression analysis in the liver.
- Evaluation of response to high-fat diet and exercise stress test.
Main Results:
- Lcorl-/- mice exhibit reduced birth weight but normalize by adulthood, remaining leaner with decreased food intake.
- Improved glucose tolerance and insulin sensitivity were observed in Lcorl-/- mice.
- Reduced circulating IGF-1 levels were linked to stunted growth.
- Liver gene expression related to GH signaling, glucose, and lipid metabolism was altered.
- Lcorl-/- mice showed protection against high-fat diet and reduced exercise capacity.
Conclusions:
- LCoRL is a critical regulator of body weight and glucose homeostasis.
- Lcorl deficiency confers protection against metabolic challenges.
- These findings validate GWAS associations and highlight LCoRL as a potential therapeutic target for metabolic disorders.
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