Early renal structure alteration in rat offspring from dams fed low protein diet

Pires, Karla Maria Pereira; Águila, Márcia Barbosa; Mandarim-de-Lacerda, Carlos Alberto

doi:10.1016/j.lfs.2006.07.006

Cited by 25 publications

(3 citation statements)

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“…In addition, it was observed that severe protein restriction during pregnancy decreased offspring's life span [47] and impaired nephrogenesis [48], in accordance with Brenner's hypothesis [49]. The reason why severe protein restriction in the mother turns into a reduced number of glomeruli at birth (20% to 30% fewer glomeruli than in controls) [50,51] has been explained as an imbalance between actively proliferating cells and apoptosis in the metanephros, in favor of apoptosis [51] and with higher p53 expression [52]. Moreover, protein deprivation from conception to the 5th-6th week of gestation alters gene expression in embryonic kidneys, downregulating the expression of prox-1 and cofilin-1, the genes that are pivotal in the normal development of the lymphatic vessels [53] and cytoskeleton [54], respectively [55].…”

Section: Models Of Protein Deprivation During Pregnancy In Rodents Ansupporting

confidence: 57%

Of Mice and Men: The Effect of Maternal Protein Restriction on Offspring’s Kidney Health. Are Studies on Rodents Applicable to Chronic Kidney Disease Patients? A Narrative Review

et al. 2020

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In the almost 30 years that have passed since the postulation of the “Developmental Origins of Health and Disease” theory, it has been clearly demonstrated that a mother’s dietary habits during pregnancy have potential consequences for her offspring that go far beyond in utero development. Protein malnutrition during pregnancy, for instance, can cause severe alterations ranging from intrauterine growth retardation to organ damage and increased susceptibility to hypertension, diabetes mellitus, cardiovascular diseases and chronic kidney disease (CKD) later in life both in experimental animals and humans. Conversely, a balanced mild protein restriction in patients affected by CKD has been shown to mitigate the biochemical derangements associated with kidney disease and even slow its progression. The first reports on the management of pregnant CKD women with a moderately protein-restricted plant-based diet appeared in the literature a few years ago. Today, this approach is still being debated, as is the optimal source of protein during gestation in CKD. The aim of this report is to critically review the available literature on the topic, focusing on the similarities and differences between animal and clinical studies.

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Section: Models Of Protein Deprivation During Pregnancy In Rodents Ansupporting

confidence: 57%

Of Mice and Men: The Effect of Maternal Protein Restriction on Offspring’s Kidney Health. Are Studies on Rodents Applicable to Chronic Kidney Disease Patients? A Narrative Review

et al. 2020

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“…The fractionator method was used to estimate the number of glomeruli in a slice (starting with a random number for each 10th section). The total number of glomeruli per kidney, adjusted to the entire organ, was estimated from the analyzed fraction of the kidney [17], [18]. The “fraction” of the kidney that we used to count glomeruli considered the size of the glomeruli.…”

Section: Methodsmentioning

confidence: 99%

Maternal Vitamin D Deficiency Delays Glomerular Maturity in F1 and F2 Offspring

et al. 2012

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BackgroundThere is a high prevalence of vitamin D insufficiency in women of reproductive age.MethodsThis work studied the first two generations of offspring (F1 and F2) of Swiss mice from mothers fed one of two diets: SC (standard chow) or VitD- (vitamin D-deficient). Functional and developmental kidney measurements were taken.ResultsThe first two generations of the VitD- group had higher blood pressure at 6 months of age than the offspring of the SC group as well as an increase in renin and AT1r expression. However, at all ages, both F1 and F2 VitD- mice had shorter glomerular diameters, and diet played a significant role in the total variation. Both the F1 and F2 generations of the VitD- group had more immature glomeruli than offspring from the SC group. Immature glomeruli begin to disappear at 10 days, but at this age, F1-VitD- mice had more immature and mature glomeruli than F1-SC mice. At 6 months of age, F1-VitD- mice exhibited more glomeruli, while F2-VitD- mice exhibited the same number of glomeruli as F2-SC mice, but fewer glomeruli compared to the F1-VitD group. Both diet and generation account for the total variation in the number of glomeruli. Decreases in urine output and podocin expression and increases in urea and creatinine in the urine were observed in F1 offspring.ConclusionThese findings demonstrate that maternal vitamin D deficiency accompanies changes in the renal expression of important factors that may retard the maturation of glomeruli by extending the period of nephrogenesis.

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“…The nutritional status of the mother is an important factor that affects fetal programming (Langley-Evans et al, 1994;Vehaskari et al, 2001;Woods et al, 2001;Lamireau et al, 2002;Manning et al, 2002;McMullen and Langley-Evans, 2005;Welham et al, 2005;Maria Pereira Pires et al, 2006;Pladys et al, 2006;Zambrano et al, 2006;Hocher, 2007;Dörsam et al, 2019;Rughani et al, 2020;Zhou et al, 2020). To investigate the impact of SGK1 on fetal programming and hypertension (blood pressure), Rexhepaj et al, mated wild-type (sgk1 +/+ ) male mice with sgk1 −/− female mice, and sgk1 −/− males with sgk1 +/+ females, resulting in heterozygotic (sgk1 −/+ ) offspring in both cases (Rexhepaj et al, 2008).…”

Section: Sgk1 In Fetal Programmingmentioning

confidence: 99%

The Enigmatic Role of Serum & Glucocorticoid Inducible Kinase 1 in the Endometrium

Läng

Rajaxavier

Singh

et al. 2020

Front. Cell Dev. Biol.

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The serum-and glucocorticoid-inducible kinase 1 (SGK1) is subject to genetic up-regulation by diverse stimulators including glucocorticoids, mineralocorticoids, dehydration, ischemia, radiation and hyperosmotic shock. To become active, the expressed kinase requires phosphorylation, which is accomplished by PI3K/PDK1 and mTOR dependent signaling. SGK1 enhances the expression/activity of various transport proteins including Na + /K +-ATPase as well as ion-, glucose-, and amino acid-carriers in the plasma membrane. SGK1 can further up-regulate diverse ion channels, such as Na +-, Ca 2+-, K +-and Cl − channels. SGK1 regulates expression/activity of a wide variety of transcription factors (such as FKHRL1/Foxo3a, β-catenin, NFκB and p53). SGK1 thus contributes to the regulation of transport, glycolysis, angiogenesis, cell survival, immune regulation, cell migration, tissue fibrosis and tissue calcification. In this review we summarized the current findings that SGK1 plays a crucial function in the regulation of endometrial function. Specifically, it plays a dual role in the regulation of endometrial receptivity necessary for implantation and, subsequently in pregnancy maintenance. Furthermore, fetal programming of blood pressure regulation requires maternal SGK1. Underlying mechanisms are, however, still ill-defined and there is a substantial need for additional information to fully understand the role of SGK1 in the orchestration of embryo implantation, embryo survival and fetal programming.

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Early renal structure alteration in rat offspring from dams fed low protein diet

Cited by 25 publications

References 50 publications

Of Mice and Men: The Effect of Maternal Protein Restriction on Offspring’s Kidney Health. Are Studies on Rodents Applicable to Chronic Kidney Disease Patients? A Narrative Review

Of Mice and Men: The Effect of Maternal Protein Restriction on Offspring’s Kidney Health. Are Studies on Rodents Applicable to Chronic Kidney Disease Patients? A Narrative Review

Maternal Vitamin D Deficiency Delays Glomerular Maturity in F1 and F2 Offspring

The Enigmatic Role of Serum & Glucocorticoid Inducible Kinase 1 in the Endometrium

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