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Maternal low protein diet: Developmental origin of adult hypertension
Author(s) -
Goyal Ravi,
Leitzke Arthur,
Goyal Dipali,
Longo Lawrence D.
Publication year - 2009
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.23.1_supplement.776.6
Subject(s) - offspring , endocrinology , medicine , low protein diet , blood pressure , biology , renin–angiotensin system , epigenetics , messenger rna , western blot , methylation , fetus , pregnancy , dna methylation , gene expression , gene , genetics
Objective We hypothesized that maternal isocaloric, low‐protein, diet during pregnancy programs the Renin Angiotensin System in the fetus leading to hypertension in the adult. We conducted studies on pregnant mice, on isocaloric, normal or low protein diet (50% and 33% less protein). Methods Proteins and mRNA levels were measured using western blot and real time PCR technique and blood pressure was recorded by the non‐invasive tail cuff system. Results Maternal low protein diet (MLPD) resulted in low birth weight and rapid catch up growth in both male and female offspring. MLPD induced hypertension in female mice offspring at 11 weeks of age, whereas no hypertension was observed in male offspring by 20 th week of age. Our results indicate increased AGT and ACE, but decreased AT2, expression of mRNA, with no change in the protein expression of AGT but decreased protein expression of both, ACE and AT2 receptors with MLPD. Promoter methylation analysis of ACE gene showed hypo‐methylation of the CpG islands as a consequence of maternal protein deprivation. Conclusions Our studies establish that MLPD programs hypertension in female offspring by epigenetic programming of the renin‐angiotensin system.