The distinct features related to the mechanism behind the two obese animal models may play a role in the response to the UT treatment against the NAFLD co-morbity: (1) absence of functional leptin versus leptin resistance, (2) hypogonadism due to persistent immaturity of the hypothalamus-pituitary gonadal axis in the ob/ob mice, (3) the degree of sarcopenia associated with obesity and insulin sensitivity impairment, and (4) the degree of chronic inflammation. Here, LEP is linked to metabolic dysfunction-associated steatotic liver disease.