Available evidence suggests that insulin resistance may be involved, with metabolic disturbances more likely to lead to relative or absolute excess insulin secretion.[16] Hyperinsulinemia reduces renal serum uric acid excretion, leading to subsequent hyperuricemia.[17] But it is unclear whether metabolically healthy obese individuals can maintain insulin sensitivity throughout life, or whether metabolically healthy obesity simply represents a delayed onset of obesity-related insulin resistance.[16]. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.