Relative contributions of insulin deficiency and insulin resistance in maturity-onset diabetes

Lancet. 1982 Mar 13;1(8272):596-8. doi: 10.1016/s0140-6736(82)91753-6.


The effects of raised insulin resistance and decreased beta-cell function on basal plasma glucose and insulin concentrations have been estimated by means of a mathematical model which uses the available data on control of glucose and insulin flux. The model shows that near-normal basal plasma insulin levels could be maintained by means of basal hyperglycaemia when beta-cell function is deficient. The hyperglycaemia does not become pronounced until more than 80% of beta-cell function has been lost. However, when only 5-10% of beta-cell remains, plasma insulin levels fall in spite of hyperglycaemic stimulation. Conversely, raised insulin resistance in the absence of decreased beta-cell function induces only a small rise in basal plasma glucose concentrations, which stimulates a compensatory increase in basal plasma insulin concentrations from a normal beta-cell capacity. However, if the beta-cell dysfunction is sufficient to induce a basal plasma glucose concentration of 5-6 mmol/l, a slight rise in insulin resistance causes pronounced basal hyperglycaemia.

MeSH terms

  • Adipose Tissue / metabolism
  • Adult
  • Blood Glucose / analysis
  • Central Nervous System / metabolism
  • Diabetes Mellitus / metabolism
  • Diabetes Mellitus / physiopathology*
  • Humans
  • Insulin / blood
  • Insulin / deficiency*
  • Insulin Resistance*
  • Islets of Langerhans / physiopathology
  • Models, Biological*
  • Muscles / metabolism
  • Obesity


  • Blood Glucose
  • Insulin