recently, the fetal insulin hypothesis has cited observations in families with maturity onset diabetes of the young to illustrate the dependence of fetal growth on the genetics of fetal and maternal insulin secretion . It predicts that a gene or combination of genes responsible for insulin resistance will be found which leads both to low weight at birth through insulin resistance and to glucose intolerance later in life (fig. 1).
There is a common theme to all three hypotheses: insulin resistance, which might arguably have favored survival in times of famine, leaves many in today's 'coke and burger' culture unable to control their blood sugar. None of the theories, however, estimates how much of today's diabetes (the attributable proportion) can be accounted for by congenital insulin resistance already present at birth, nor explains the rising incidence of type-2 diabetes which, according to the logic of all three hypotheses, should by now be stable or falling as nutrition in pregnancy improves and gene selection operates to select out the less fit. Insulin resistance acquired through lifestyle change is more likely than genes or gestational experience to underlie the recent rise in diabetes and its ever-younger presentation.
Importantly for the hypothesis, glucose clamp studies 20 years ago showed that noninsulinized adults with type-1 diabetes were as insulin resistant as metabolic diabetics of comparable glucose tolerance  and there has been further evidence recently. Furthermore, the rise in proinsulin/insulin ratio that has long been the hallmark of insulin resistance in pre-type-2 diabetes has been shown to characterize pre-type-1 diabetes as well . Most seropositive type-2 diabetic adults become type 1 more rapidly than those who are seronegative  and these observations together provide robust support for the 'overlay' and 'accelerator' concepts. The slower tempo of progression in adults has thus provided the means of demonstrating that all diabetes is associated with insulin resistance (the second accelerator), that a subgroup advances more rapidly to insulin dependency as a result of autoimmunity (the third accelerator), and that (by implication) this subgroup, had it been free of autoimmunity, would have progressed to diabetes in any case, albeit at a later date.
Was this article helpful?
Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...