The Goto-Kakisaki (GK) @entity35 is a genetic model of @entity2175 . At 21.5 d of age we found that GK fetuses had an increased plasma @entity413 concentration, a decreased plasma insulin level, and a reduced pancreatic beta cell mass. To investigate the beta cell function during fetal life we used a hyperglycemic clamp protocol applied to the mothers, which allowed us to obtain a steady-state @entity4854 in the corresponding fetuses. At variance, with @entity35 (W) fetuses, plasma insulin concentration in GK fetuses did not rise in response to @entity4854 . In contrast, GK fetal pancreas released insulin in response to @entity413 in vitro to the same extent as W fetal pancreas. Such a discrepancy between the in vivo and in vitro results suggests that the lack of pancreatic reactivity to @entity413 as seen in vivo is extrinsic to the fetal GK beta cell. Finally, the importance of gestational @entity4854 was investigated by performing crosses between GK and @entity35 . Fetuses issued from crosses between W mother and GK father or GK mother and W father had a beta cell mass close to normal values and were still able to increase their plasma insulin levels in response to @entity4854 in vivo. Our data suggest that @entity4854 in utero does not influence the severity of the decrease of the beta cell mass or the lack of the insulin secretory response to @entity413 in the fetal GK @entity35 . Moreover they indicate that conjunction of GK genes originating from both parents is necessary in order for these defects to be fully expressed.

Impaired pancreatic beta cell function in the fetal GK XXXX . Impact of diabetic inheritance.

@entity35 :: ('10116', 'Species') :: ['rat', 'W rats', 'Wistar'] @entity4854 :: ('MESH:D006943', 'Disease') :: ['hyperglycemia'] @entity413 :: ('MESH:D005947', 'Chemical') :: ['glucose'] @entity2175 :: ('MESH:D003924', 'Disease') :: ['non-insulin-dependent diabetes']
@entity35 :: (10116,Species) :: ['rat']
