We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Agrp-Specific Ablation of Scly Protects against Diet-Induced Obesity and Leptin Resistance.
- Authors
Torres, Daniel J.; Pitts, Matthew W.; Hashimoto, Ann C.; Berry, Marla J.
- Abstract
Selenium, an essential trace element known mainly for its antioxidant properties, is critical for proper brain function and regulation of energy metabolism. Whole-body knockout of the selenium recycling enzyme, selenocysteine lyase (Scly), increases susceptibility to metabolic syndrome and diet-induced obesity in mice. Scly knockout mice also have decreased selenoprotein expression levels in the hypothalamus, a key regulator of energy homeostasis. This study investigated the role of selenium in whole-body metabolism regulation using a mouse model with hypothalamic knockout of Scly. Agouti-related peptide (Agrp) promoter-driven Scly knockout resulted in reduced weight gain and adiposity while on a high-fat diet (HFD). Scly-Agrp knockout mice had reduced Agrp expression in the hypothalamus, as measured by Western blot and immunohistochemistry (IHC). IHC also revealed that while control mice developed HFD-induced leptin resistance in the arcuate nucleus, Scly-Agrp knockout mice maintained leptin sensitivity. Brown adipose tissue from Scly-Agrp knockout mice had reduced lipid deposition and increased expression of the thermogenic marker uncoupled protein-1. This study sheds light on the important role of selenium utilization in energy homeostasis, provides new information on the interplay between the central nervous system and whole-body metabolism, and may help identify key targets of interest for therapeutic treatment of metabolic disorders.
- Subjects
ANIMAL experimentation; BIOLOGICAL models; DIET; FAT content of food; HYPOTHALAMUS; IMMUNOHISTOCHEMISTRY; MICE; NEUROPEPTIDES; OBESITY; PROTEINS; SELENIUM; WESTERN immunoblotting; LEPTIN; METABOLIC syndrome; CYSTEINE
- Publication
Nutrients, 2019, Vol 11, Issue 7, p1693
- ISSN
2072-6643
- Publication type
Article
- DOI
10.3390/nu11071693