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Despite signalling pathways situations, the endocrine pancreas can change

Linguer Li*

The capacity of the endocrine pancreas to modify the beta-cell mass in response to changes in the demand for insulin is known as endocrine pancreatic plasticity. For instance, the increase in beta-cell bulk, together with beta-cell hyperactivity, during late pregnancy and obesity leads to insulin over secretion in response to insulin resistance. There is mounting evidence that adult animals have significantly greater capacity for beta-cell mass expansion than previously believed. The variations in beta-cell mass during pregnancy are mostly caused by placental hormones, particularly placental lactogens. Although the major contender appears to be an increase in free fatty acids, the exact variables that contribute to beta-cell development in obesity are still unclear.