Based on these findings, it is possible that male EtOH-exposed offspring of the present study may have had either increased gluconeogenesis or peripheral insulin resistance, however in the absence of performing biochemical studies on either fasted EtOH-exposed offspring of the same age or EtOH-exposed offspring at the conclusion of first phase insulin secretion during the insulin challenge we are unable to determine the molecular mechanisms of this insulin resistance. The gene discussed is INS; the disease is Insulin resistance.