Glo1 reduction in mice results in age- and sex-dependent metabolic dysfunction.

ABSTRACT:

Objectives

Advanced glycation end products (AGEs) have been implicated as an important mediator of metabolic disorders including obesity, insulin resistance, and coronary artery disease. Glyoxalase 1 (Glo1) is a critical enzyme in the clearance of toxic dicarbonyl such as methylglyoxal, precursors of AGEs. The role of AGE-independent mechanisms that underly Glo1-induced metabolic disorders have yet to be elucidated.

Methods

We performed a longitudinal study of female and male Glo1 heterozygous knockdown (Glo1 ^+/- ) mice with ~50% gene expression and screened metabolic phenotypes such as body weight, adiposity, glycemic control and plasma lipids. We also evaluated atherosclerotic burden, AGE levels, and gene expression profiles across cardiomet

SUBMITTER: Cely I 

PROVIDER: S-EPMC11785252 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature