INS and metabolic syndrome: For example, there is evidence that apoptosis-effector caspases cleave PPAR-γ and GLUT-4, leading to decreased lipogenic gene transcription and impaired glucose uptake, effects that promote insulin resistance.35 In aggregate, these data suggest a unifying hypothesis whereby adipocyte apoptosis both leads to a massive decrease in adipose tissue capacity for fat storage by limiting the expansibility of the adipose tissue and induces an insulin resistant and pro-inflammatory state that promotes the metabolic syndrome.