Fatty Acid Oxidation Prevents Obesity in Ob/ob Mice!!

So this article talks about how scientists have found that when endogenous ligands sustain the activation of PPAR{alpha}, hepatic fatty acid oxidation is increased, resulting in the prevention of obesity in ob/ob mice. An ob/ob (or obese) mouse is a mutant mouse that eats excessively and becomes extremely obese.

Mice that lacked acyl-CoA oxidase 1 (Acox1), the first enzyme of the peroxisomal fatty acid β-oxidation system, are characterized as having an increased energy expenditure and a lean body phenotype. This is because of sustained activation of peroxisome proliferator-activated receptor α (PPARα) by endogenous ligands in liver that remain unmetabolized in the absence of Acox1.Scientists wanted to see what would happen if an ob/ob mice lacked Acox1. So, they made generated some ob/ob mice deficient in Acox1 and conducted tests comparing them to regular ob/ob mice.
When compared, the regular ob/ob mice were severely obese and had more epididymal fat content. The reason why the Acox1 deficient ob/ob mice were more resistant to obesity is because there is an increase in PPARα-mediated up-regulation of genes involving fatty acid oxidation in liver. The activation of PPARα in Acox1-deficient ob/ob mice also reduced the serum glucose and insulin levels, and improved glucose tolerance and insulin sensitivity. There are negatives as well though. For example, Acox1 deficient ob/ob mice manifested hepatic endoplasmic reticulum stress and also develop hepatocellular carcinomas.