Figure 4

Model depicting thrifty metabolism underlying catch-up fat and hyperinsulinemia during catch-up growth. In response to fat depletion and/or delayed fat stores expansion (resulting from energy deficit and growth retardation), energy conservation mechanisms operate via suppressed thermogenesis [8], leading to diminished insulin sensitivity in skeletal muscle [9, 17] during increased food availability, so that the spared energy leads to accelerated replenishment of the fat stores (catch-up fat) in adipose tissue. The glucose spared from utilization in skeletal muscle is thus redirected to an adipose tissue that shows increased insulin hyperresponsiveness [9] and enhanced lipogenic machinery [18], under orchestration by hyperinsulinemia which is sustained by pancreatic β-cell hyperresponsiveness (as reported here). In this model, the 'adipostat' signals (?) that dictate suppress thermogenesis and insulin resistance in skeletal muscle are postulated to also dictate the pancreatic beta-cell hyperresponsiveness that will sustain glucose redistribution between skeletal muscle and adipose tissue, thereby contributing to the thrifty 'catch-up fat' phenotype associated with hyperinsulinemia.