Glucose homeostasis in pregnant rats submitted to dietary protein restriction


Autoria(s): Rostom de Mello, Maria Alice; Luciano, Eliete; Magalhães Carneiro, Everardo; Queiroz Latorraca, Márcia; Machado de Oliveira, Camila Aparecida; Boschero, Antonio Carlos
Contribuinte(s)

Universidade Estadual Paulista (UNESP)

Data(s)

27/05/2014

27/05/2014

01/12/2003

Resumo

In the present work, we examined the effects of feeding a low protein diet during pregnancy on glucose-induced insulin secretion and glucose homeostasis in rats. Young (60 days), pregnant (P) or non-pregnant (NP) rats were fed during pregnancy or for 21 days (the NP) a normal (17%) or a low (6%) protein diet. Serum glucose and insulin levels and pancreas insulin content in the fed state; total area under serum glucose curve (AG) after a glucose load and serum glucose disappearance rate (Kitt) after insulin administration; as well as 86Rb outflow, 45Ca uptake and insulin secretion by isolated pancreatic islets in response to glucose were evaluated. Serum glucose was lower in 17%-P (12%) and 6%-P (27%) than in corresponding NP-rats. Serum insulin was higher in 17%- P (153%) and 6%-P (77%) compared to the corresponding NP-rats. Pancreatic insulin was higher in 6%-rats (55%) than in 17%-rats. No differences were found in AG among the groups whereas Kitt was lower in 6%-NP and higher in 6%-P than in the equivalent 17% rats. Increasing glucose concentration from 2.8 to 16.7 mmol/l, reduced 86Rb outflow from isolated islets from all groups. Increasing glucose concentration from 2.8 to 16.7 mmol/l elevated 45Ca uptake by 17%-NP (47%), 17%-P (40%) and 6%-P (214%) islets but not by 6%-NP ones. The increase in 45Ca uptake was followed by an increase in insulin release by the 17%-NP (2767%), 17%-P (2850%) and 6%-P (1200%) islets. In conclusion, 6%-P rats show impaired glucose induced insulin secretion related to reduced calcium uptake by pancreatic islets. However, the poor insulin secretion did not fully compensate the high peripheral sensitivity to the hormone, resulting in hypoglycemia.

Formato

229-246

Identificador

Research Communications in Molecular Pathology and Pharmacology, v. 113-114, p. 229-246.

1078-0297

http://hdl.handle.net/11449/67581

2-s2.0-13144266686

Idioma(s)

eng

Relação

Research Communications in Molecular Pathology and Pharmacology

Direitos

closedAccess

Palavras-Chave #45Ca uptake #86Rb outflow #Glucose metabolism #Insulin secretion #Pancreatic islets #Pregnancy #Protein malnutrition #Rat #calcium #glucose #rubidium #animal experiment #calcium transport #controlled study #glucose blood level #glucose homeostasis #glucose metabolism #insulin blood level #insulin release #nonhuman #pancreas islet #pregnancy #priority journal #protein diet #protein restriction #rat #Animals #Calcium #Fatty Acids, Nonesterified #Female #Glucose #Homeostasis #Insulin #Islets of Langerhans #Liver #Protein Deficiency #Rats #Rats, Wistar
Tipo

info:eu-repo/semantics/article