Transgenic mice overproducing islet amyloid polypeptide have increased insulin storage and secretion in vitro
CB Verchere, DA D'Alessio, RD Palmiter, SE Kahn - Diabetologia, 1994 - Springer
CB Verchere, DA D'Alessio, RD Palmiter, SE Kahn
Diabetologia, 1994•SpringerTo determine whether chronic overproduction of islet amyloid polypeptide alters beta-cell
function, we studied a line of transgenic mice which overexpress islet amyloid polypeptide in
their beta-cells. At 3 months of age, these transgenic mice had greater pancreatic content of
both islet amyloid polypeptide and insulin. Further, basal and glucose-stimulated secretion
of both islet amyloid polypeptide and insulin were also elevated in the perfused pancreas of
the transgenic animals. These findings demonstrate that chronic overproduction and …
function, we studied a line of transgenic mice which overexpress islet amyloid polypeptide in
their beta-cells. At 3 months of age, these transgenic mice had greater pancreatic content of
both islet amyloid polypeptide and insulin. Further, basal and glucose-stimulated secretion
of both islet amyloid polypeptide and insulin were also elevated in the perfused pancreas of
the transgenic animals. These findings demonstrate that chronic overproduction and …
Summary
To determine whether chronic overproduction of islet amyloid polypeptide alters beta-cell function, we studied a line of transgenic mice which overexpress islet amyloid polypeptide in their beta-cells. At 3 months of age, these transgenic mice had greater pancreatic content of both islet amyloid polypeptide and insulin. Further, basal and glucose-stimulated secretion of both islet amyloid polypeptide and insulin were also elevated in the perfused pancreas of the transgenic animals. These findings demonstrate that chronic overproduction and secretion of islet amyloid polypeptide are associated with increased insulin storage and enhanced secretion of insulin in vitro. This increase in insulin storage and secretion may be due to a direct effect of islet amyloid polypeptide on the beta-cell or a betacell adaptation to islet amyloid polypeptide-induced insulin resistance.
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