129S6/SvEvTac mice are protected from high-fat diet-induced metabolic syndrome compared to C57BL/6 mice due to a >700-fold higher number of UCP1-positive brown fat cells in intermuscular fat.
Ectopic brown adipose tissue in intermuscular depots with regulatable UCP1 expression provides a genetically based mechanism of protection from high-fat diet-induced metabolic syndrome in mice.
Effect estimate: >700-fold higher
C57BL/6 (B6) mice subjected to a high-fat diet develop metabolic syndrome with obesity, hyperglycemia, and insulin resistance, whereas 129S6/SvEvTac (129) mice are relatively protected from this disorder because of differences in higher basal energy expenditure in 129 mice, leading to lower weight gain. At a molecular level, this difference correlates with a marked higher expression of uncoupling protein 1 (UCP1) and a higher degree of uncoupling in vitro in mitochondria isolated from muscle of 129 versus B6 mice. Detailed histological examination, however, reveals that this UCP1 is in mitochondria of brown adipocytes interspersed between muscle bundles. Indeed, the number of UCP1-positive brown fat cells in intermuscular fat in 129 mice is >700-fold higher than in B6 mice. These brown fat cells are subject to further up-regulation of UCP1 after stimulation with a beta3-adrenergic receptor agonist. Thus, ectopic deposits of brown adipose tissue in intermuscular depots with regulatable expression of UCP1 provide a genetically based mechanism of protection from weight gain and metabolic syndrome between strains of mice.
Almind et al. (Tue,) conducted a other in Metabolic syndrome. 129S6/SvEvTac (129) strain vs. C57BL/6 (B6) strain was evaluated on Number of UCP1-positive brown fat cells in intermuscular fat (>700-fold higher). 129S6/SvEvTac mice are protected from high-fat diet-induced metabolic syndrome compared to C57BL/6 mice due to a >700-fold higher number of UCP1-positive brown fat cells in intermuscular fat.