Abstract
Perinatal diets may affect the cardiovascular-renal functions of offspring. To understand effects of maternal diet on the renal function and blood pressure (BP) of offspring, protein (10% low, LP; 23% normal, NP) and/or NaCl (4% high salt, HS; 0.6% normal, NS) diets were started at pre-pregnancy through pups' weaning to either a 4% high NaCl (hs) or 0.6% NaCl (ns) diet. Telemetered BP data was analyzed by methods of linear least square rhythmometry. Systolic BPs (circadian mean ±SE mm Hg) were: NPNSns, 131±2; NPNShs, 137±2; NPHSns, 137±0.2; NPHShs, 134±3; LPNSns, 138±1; LPNShs, 138±0.6; LPHSns, 135±2; LPHShs, 142±2. Offspring in NPNShs and NPHSns had significantly increased SBPs versus NPNSns (both P<0.05). Most LP-offspring had increased SBP (P<0.01 to <0.05) and lower body weight (BW) with smaller glomerular filtration rate changes (renal reserve, RR-GFR) following overnight acute highprotein loads: RR-GFRs (inulin, ml/min/g kidney) for groups stated above were, respectively: 0.935; 0.927; 0.537; -0.064; -0.229; 0.057; -0.515; -0.404. The kidney weight/BW ratio of offspring was higher on hs- than on ns-diets (all P<0.001). Rats on a low caloric diet had reduced sclerotic glomerular numbers compared to those on normal diets (11.2±1 vs. 15.7±2, P<0.001), though glomerular numbers were similar in both groups. In summary, perinatal LP-HS diets significantly affected the BW, BP, renal injuries and kidney function of offspring. RR was seriously reduced, especially among offspring in hs- and perinatal LP groups. The most interesting result was the glomerular maturation staging in the pups, which suggests delayed nephrogenesis by a maternal LP diet.
Highlights
Genetic and environmental factors play an important role in disease expression on offspring by exerting diverse and predominant modulatory effects [1,2,3]
chronic kidney disease (CKD) is an independent predictor of MI, stroke, and mortality risk among men and women younger than 55 and 65 years of age, respectively, which has been defined by levels of estimated glomerular filtration rate as markers of kidney damage [4,5,6]
We examined perinatal dietary protein and salt effects on the kidney maturation of offspring with a moderate protein restriction and subtoxic levels of dietary salt and assessed progeny responses to the perinatal and post-maternal diet on body weight (BW), SBP, GFR and RR in the Lewis rat, which is known to have a high degree of homozygosity [25]
Summary
Genetic and environmental factors play an important role in disease expression on offspring by exerting diverse and predominant modulatory effects [1,2,3]. Cardiac disease and chronic kidney disease (CKD) commonly coexist, sharing cardiovascular disease (CVD) risk factors such as hypertension, dyslipidemia and diabetes. Some authors have addressed epigenetic effects – in the relationship between longevity and food availability in the transgeneration response to swings in nutrition – on the regulation of reproduction with disease risk [7]. The effects of perinatal nutrition impact health and disease later in adult life in manifesting the altered epigenetic regulation of gene expression caused by defective epigenetic regulation [8]. Barker et al hypothesized that adult disease may originate from fetal stage developmental plasticity and compensatory biological phenomena [9]
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