Those opposing actions of DGAT1 may explain the reasons why the reintroduction of DGAT1 into the intestine of DGAT1 null mice is sufficient to lose metabolic phenotypes such as resistance to hepatic steatosis and diet-induced obesity, and why long-time treatment with Compound B showed beneficial metabolic effects such as insulin-sensitization and reduction of the body weight gain and hepatic lipids. This evidence concerns the gene INS and fatty liver disease.