Recently it was found that failure to increase PPARα-regulated free fatty acid oxidation may be more prone to developing obesity because PPARα deficiency in ob/ob obese mice makes the mice become more obese (ref.17). Fat is mainly stored in adipose tissue in the form of triglyceride. When the fat in adipose tissue is saturated, the fat “overflows” from adipose tissue to liver, which contributes to hepatic steatosis (ref.34). Indeed, liver fat is mainly from adipose tissue (ref.35). In this study, while fatty liver was more severe in P-/A- mice than in P+/A- mice, body weight gain (obesity) was less in P-/A- mice than in P+/A- mice. When fat is subjected to lipolysis in adipose tissue, free fatty acids will be released into blood, so fat flow from adipose tissue to liver is in the form of serum free fatty acids. Compared with P+A- mice, P-/A- mice exhibited higher serum free fatty acids, suggesting a stronger adipose lipolysis, which may cause less obese and more severe fatty liver. Therefore, this observation is still in agreement with the notion that “fat flow”
