Mechanisms involved in developmental programming of hypertension and renal diseases. Gender differences

Tomat, Analia Lorena; Salazar, Francisco

doi:10.1515/hmbci-2013-0054

Cited by 28 publications

(25 citation statements)

References 143 publications

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“…There is emerging evidence that sex differences exist in the fetal programming of kidney disease [11,38], showing that males are more vulnerable than females. The important sex-dependent differences in the developmental programming of diseases seem to be related to sex hormones [38].…”

Section: Discussionmentioning

confidence: 99%

High Fat Diets Sex-Specifically Affect the Renal Transcriptome and Program Obesity, Kidney Injury, and Hypertension in the Offspring

et al. 2017

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Obesity and related disorders have increased concurrently with an increased consumption of saturated fatty acids. We examined whether post-weaning high fat (HF) diet would exacerbate offspring vulnerability to maternal HF-induced programmed hypertension and kidney disease sex-specifically, with a focus on the kidney. Next, we aimed to elucidate the gene–diet interactions that contribute to maternal HF-induced renal programming using the next generation RNA sequencing (NGS) technology. Female Sprague-Dawley rats received either a normal diet (ND) or HF diet (D12331, Research Diets) for five weeks before the delivery. The offspring of both sexes were put on either the ND or HF diet from weaning to six months of age, resulting in four groups of each sex (maternal diet/post-weaning diet; n = 5–7/group): ND/ND, ND/HF, HF/ND, and HF/HF. Post-weaning HF diet increased bodyweights of both ND/HF and HF/HF animals from three to six months only in males. Post-weaning HF diet increased systolic blood pressure in male and female offspring, irrespective of whether they were exposed to maternal HF or not. Male HF/HF offspring showed greater degrees of glomerular and tubular injury compared to the ND/ND group. Our NGS data showed that maternal HF diet significantly altered renal transcriptome with female offspring being more HF-sensitive. HF diet induced hypertension and renal injury are associated with oxidative stress, activation of renin-angiotensin system, and dysregulated sodium transporters and circadian clock. Post-weaning HF diet sex-specifically exacerbates the development of obesity, kidney injury, but not hypertension programmed by maternal HF intake. Better understanding of the sex-dependent mechanisms that underlie HF-induced renal programming will help develop a novel personalized dietary intervention to prevent obesity and related disorders.

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Section: Discussionmentioning

confidence: 99%

High Fat Diets Sex-Specifically Affect the Renal Transcriptome and Program Obesity, Kidney Injury, and Hypertension in the Offspring

et al. 2017

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“…In contrast, we found higher HRV in females than males, specifically among those who were not exposed to ANCS. There is evidence supporting sex differences for other outcomes such as blood pressure, markers of the renin-angiotensin system, and sympathoadrenal function, with females generally exhibiting more favorable outcomes (33,34). Our colleagues have also reported sex differences in ANCS programming effects on renal function in the sheep model, with some of the differences being age-dependent, possibly mediated via changes in sex steroid hormones with maturation (18,19).…”

Section: Discussionmentioning

confidence: 99%

Antenatal steroid exposure and heart rate variability in adolescents born with very low birth weight

et al. 2016

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BackgroundReduced heart rate variability (HRV) suggests autonomic imbalance in the control of heart rate and is associated with unfavorable cardiometabolic outcomes. We examined whether antenatal corticosteroid (ANCS) exposure had long-term programming effects on heart rate variability (HRV) in adolescents born with very low birth weight (VLBW).MethodsFollow-up study of a cohort of VLBW 14 year-olds born between 1992 and 1996 with 50% exposed to ANCS. HRV in both the time and frequency domains using Nevrokard Software was determined from a 5 minute electrocardiogram tracing.ResultsHRV data from 89 (35 male, 53 non-black) exposed (ANCS+) and 77 (28 male, 29 non-black) unexposed (ANCS−) adolescents were analyzed. HRV did not differ between ANCS+ and ANCS− black participants. However, in non-black participants, a significant interaction between ANCS and sex was observed, with ANCS− females having significantly greater HRV than ANCS+ females and males, and ANCS− males for both time and frequency domain variables.ConclusionsAmong non-black adolescents born with VLBW, ANCS exposure is associated with reduced HRV with apparent sex-specificity. Reduced HRV has been associated with development of adverse cardiometabolic outcomes, thus supporting the need to monitor these outcomes in VLBW adolescents as they mature.

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“…There is increasing evidence that sex differences exist in the fetal programming of kidney disease and hypertension [97,98], showing that males are more vulnerable than females. In fact, several hypothetical mechanisms of renal programming, such as the RAS [99] and oxidative stress [100], have been reported to respond to environmental stress in a sex-specific manner.…”

Section: Mechanisms Of Renal Programmingmentioning

confidence: 99%

Developmental Origins of Chronic Kidney Disease: Should We Focus on Early Life?

Tain

Hsu

2017

IJMS

103

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Chronic kidney disease (CKD) is becoming a global burden, despite recent advances in management. CKD can begin in early life by so-called “developmental programming” or “developmental origins of health and disease” (DOHaD). Early-life insults cause structural and functional changes in the developing kidney, which is called renal programming. Epidemiological and experimental evidence supports the proposition that early-life adverse events lead to renal programming and make subjects vulnerable to developing CKD and its comorbidities in later life. In addition to low nephron endowment, several mechanisms have been proposed for renal programming. The DOHaD concept opens a new window to offset the programming process in early life to prevent the development of adult kidney disease, namely reprogramming. Here, we review the key themes on the developmental origins of CKD. We have particularly focused on the following areas: evidence from human studies support fetal programming of kidney disease; insight from animal models of renal programming; hypothetical mechanisms of renal programming; alterations of renal transcriptome in response to early-life insults; and the application of reprogramming interventions to prevent the programming of kidney disease.

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Mechanisms involved in developmental programming of hypertension and renal diseases. Gender differences

Cited by 28 publications

References 143 publications

High Fat Diets Sex-Specifically Affect the Renal Transcriptome and Program Obesity, Kidney Injury, and Hypertension in the Offspring

High Fat Diets Sex-Specifically Affect the Renal Transcriptome and Program Obesity, Kidney Injury, and Hypertension in the Offspring

Antenatal steroid exposure and heart rate variability in adolescents born with very low birth weight

Developmental Origins of Chronic Kidney Disease: Should We Focus on Early Life?

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