The infusion of either caprylic acid or oleic acid into the hepatic portal vein results in liver fatty acid oxidation and a concomitant reduction in food intake ( and therefore probably also bodyweight ). (1, 2)
The same thing was also seen in a mutant mouse model, they over-express Fructose 1,6-bisphosphatase in the liver of rodents and it decreases food intake and bodyweight. ( 3 ) Infact this paper puts forward very strong support for the idea that the liver can actually directly control appetite by changing orexin proteins in the brain, NPY/AgRP.
What else can enhance liver fat oxidation? Metformin! It does this by increasing liver AMPK.
There is an ugly one for the ladies next, ovariectomized rats have decreased liver fat oxidation ( 4 ). Estrogen-deficient states are associated with hepatic steatosis. ( fatty liver ). Fatty acid oxidation rate was lowered by 34% (p<0.05), associated with 114% higher (p<0.01) hepatic triacylgylcerol content in the liver of ovariectomized as compared to intact rats. Estrogen replacement prevented all of these changes.
This is further evidence why women have problems with their weight post-meno. And another reason why CICO is complete bullshit. All the evidence seems to support the idea that CICO is an affect, not a cause. ( 5 ) Higher respiratory qutioent strongly predicts weight gain, the way that I personally think it works is like this.....
Fat oxidation -> low respiratory quotient -> reduced food intake -> reduced bodyweight. There are quite a few studies on pubmed showing that if you inhibit fat oxidation with drugs this immediately stimulates food intake in rodents.