Large-scale analysis of circulating glutamate and adipose gene expression in relation to abdominal obesity.
Document Type
Article
Publication Date
9-2022
Identifier
DOI: 10.1007/s00726-022-03181-1
Abstract
Circulating levels of the amino acid glutamate are associated with central fat accumulation, yet the pathophysiology of this relationship remains unknown. We aimed to (i) refine and validate the association between circulating glutamate and abdominal obesity in a large twin cohort, and (ii) investigate whether transcriptomic profiles in adipose tissue could provide insight into the biological mechanisms underlying the association. First, in a cohort of 4665 individuals from the TwinsUK resource, we identified individuals with abdominal obesity and compared prevalence of the latter across circulating glutamate quintiles. Second, we used transcriptomic signatures generated from adipose tissue, both subcutaneous and visceral, to investigate associations with circulating glutamate levels. Individuals in the top circulating glutamate quintile had a sevenfold higher prevalence of abdominal obesity compared to those in the bottom quintile. The adipose tissue transcriptomic analyses identified GLUL, encoding Glutamate-Ammonia Ligase, as being associated with circulating glutamate and abdominal obesity, with pronounced signatures in the visceral depot. In conclusion, circulating glutamate is positively associated with the prevalence of abdominal obesity which relates to dysregulated GLUL expression specifically in visceral adipose tissue.
Journal Title
Amino acids
Volume
54
Issue
9
First Page
1287
Last Page
1294
MeSH Keywords
Adipose Tissue; Body Mass Index; Gene Expression; Glutamic Acid; Humans; Obesity; Obesity, Abdominal
Keywords
Abdominal obesity; Adipose tissue; Amino acids; Glutamate
Recommended Citation
Maltais-Payette I, Vijay J, Simon MM, et al. Large-scale analysis of circulating glutamate and adipose gene expression in relation to abdominal obesity. Amino Acids. 2022;54(9):1287-1294. doi:10.1007/s00726-022-03181-1