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Concept
Pancreatic beta cell function
Summary
Pancreatic beta cell function (synonyms Gβ or, if calculated from fasting concentrations of insulin and glucose, HOMA-Beta or SPINA-GBeta) is one of the preconditions of euglycaemia, i.e. normal blood sugar regulation. It is defined as insulin secretory capacity, i.e. the maximum amount of insulin to be produced by beta cells in a given unit of time.
Beta cells play a paramount role in glucose homeostasis. Progressive loss of insulin secretory capacity is a key defect associated with the transition from a healthy glycaemic state to hyperglycaemia, characteristic of untreated diabetes mellitus. In type 1 diabetes mellitus and pancreatogenic diabetes beta cell destruction is a primary event from the perspective of the feedback loop. In type 2 diabetes beta cell dysfunction is an essential constituent as well, but subsequent to the development of insulin resistance. Other mechanisms, including lipotoxicity, amyloid deposition, oxidative stress, mitochondrial dysfunction, ER stress and inflammation may be involved as well. The beta cell loss in type 2 diabetes is mainly caused by reduced beta cell number rather than size. Hyperglycaemia becomes clinically significant once insulin over-secretion can no longer compensate for the degree of insulin resistance.
Measuring beta-cell function is a challenge, since insulin secretory capacity cannot be readily assessed. Therefore, indirect methods of measurement have been developed. They include dynamic and static function tests.
Dynamic function tests for beta-cell function include:
Oral glucose tolerance testing (OGTT)
Intravenous glucose tolerance tests (IVGTT)
Meal tolerance tests
Hyperglycaemic clamp
Static function tests for the assessment of beta-cell function comprise:
Insulin-glucose ratio
Amended insulin-glucose ratio
HOMA-Beta
SPINA-GBeta
Measuring beta-cell function requires the rate of secretion to be interpreted in relation to the prevailing glucose concentration. Therefore, a mathematical model is needed that links the time courses of insulin secretion and glucose concentration as a mechanistic causal relationship.
Official source
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