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Antenatal Maternal Protein Deprivation and Sexually Dimorphic Programming of the Pancreatic Renin‐Angiotensin System
Author(s) -
Goyal Ravi,
Wong Christine,
Longo Lawrence D.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.686.9
Subject(s) - offspring , medicine , endocrinology , sexual dimorphism , pancreatic islets , renin–angiotensin system , pancreas , pregnancy , gestation , insulin , biology , low protein diet , islet , blood pressure , genetics
Alterations in the local pancreatic renin‐angiotensin system (RAS) may play a role in the underlying mechanisms of antenatal maternal malnutrition‐induced type 2 diabetes mellitus (T2DM). In the present study, we tested the hypothesis that antenatal maternal protein deprivation (AMPD) leads to alterations in the local pancreatic RAS, with associated hyperglycemia in the adult progeny. Mice dams were fed either control or 50% protein restricted diet starting 1 week before conception and maintained during complete gestation. From 3‐week old control and AMPD mice offspring (n= 5), we isolated pancreas to examine the RAS mRNA and protein expression. We also examined birth weight, catch‐up growth, insulin, and blood glucose levels of control and AMPD mice offspring. Our results demonstrate low birth weight and sexually dimorphic programming of the pancreatic RAS, with development of hyperglycemia in the mice offspring as a consequence of AMPD during pregnancy. Only female offspring from the AMPD group developed hyperglycemia with no significant difference serum insulin concentration. We conclude that sexually dimorphic programming of the pancreatic RAS expression is associated with AMPD diet‐mediated development of hyperglycemia.