Feeding pregnant rats a low-protein diet alters the hepatic expression of SREBP-1c in their offspring via a glucocorticoid-related mechanism

Erhuma, Aml; McMullen, Sarah; Langley‐Evans, Simon C.; Bennett, Andrew J.

doi:10.1007/s12020-009-9225-8

Cited by 26 publications

(18 citation statements)

References 44 publications

(60 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, protein restriction in pregnant rats reduces methylation of the promoter region of the gene that codes for glucocorticoid receptor in offspring liver cells , Erhuma et al 2009). This leads to the amplification of the liver metabolic response to stress hormones.…”

Section: Epigenetic Mechanismsmentioning

confidence: 99%

Obesity-related hypertension: possible pathophysiological mechanisms

Vaněčková¹,

Maletı́nská²,

Behuliak³

et al. 2014

Journal of Endocrinology

123

View full text Add to dashboard Cite

Hypertension is one of the major risk factors of cardiovascular diseases, but despite a century of clinical and basic research, the discrete etiology of this disease is still not fully understood. The same is true for obesity, which is recognized as a major global epidemic health problem nowadays. Obesity is associated with an increasing prevalence of the metabolic syndrome, a cluster of risk factors including hypertension, abdominal obesity, dyslipidemia, and hyperglycemia. Epidemiological studies have shown that excess weight gain predicts future development of hypertension, and the relationship between BMI and blood pressure (BP) appears to be almost linear in different populations. There is no doubt that obesity-related hypertension is a multifactorial and polygenic trait, and multiple potential pathogenetic mechanisms probably contribute to the development of higher BP in obese humans. These include hyperinsulinemia, activation of the renin-angiotensin-aldosterone system, sympathetic nervous system stimulation, abnormal levels of certain adipokines such as leptin, or cytokines acting at the vascular endothelial level. Moreover, some genetic and epigenetic mechanisms are also in play. Although the full manifestation of both hypertension and obesity occurs predominantly in adulthood, their roots can be traced back to early ontogeny. The detailed knowledge of alterations occurring in the organism of experimental animals during particular critical periods (developmental windows) could help to solve this phenomenon in humans and might facilitate the age-specific prevention of human obesity-related hypertension. In addition, better understanding of particular pathophysiological mechanisms might be useful in so-called personalized medicine. Key Words" obesity " hypertension " sympathetic nervous system " renin-angiotensin system " critical developmental periods " epigenetics " rat

show abstract

Section: Epigenetic Mechanismsmentioning

confidence: 99%

Obesity-related hypertension: possible pathophysiological mechanisms

Vaněčková¹,

Maletı́nská²,

Behuliak³

et al. 2014

Journal of Endocrinology

123

View full text Add to dashboard Cite

show abstract

“…LXRs, the nuclear hormone receptors that form active heterodimers with retinoid X receptors, are known to regulate SREBP-1c gene expression ( 54,55 ). In rats, GCs are involved in the regulation of the expression of LXR ␣ and SREBP-1c ( 56,57 ). In the fasting state, however, the SREBP-1c mRNA level was upregulated following CORT administration without any measurable change in the expression of LXR ␣ , indicating the different mechanisms of regulation in chickens.…”

Section: Gcs Decrease Yolk Precursor Secretion By Suppressing Apolipomentioning

confidence: 99%

Corticosterone regulation of ovarian follicular development is dependent on the energy status of laying hens

Wang¹,

Li²,

Song³

et al. 2013

Journal of Lipid Research

View full text Add to dashboard Cite

This article is available online at http://www.jlr.org secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus stimulates the release of the pituitary gonadotropins, luteinizing hormone (LH), and folliclestimulating hormone (FSH), which in turn activate gonadal development and release of sex steroids, including estradiol (E2) and testosterone. Stress is a common problem disrupting breeding in either wild birds or domestic chickens ( 1 ). Glucocorticoids (GC), as the fi nal effectors of the hypothalamic-pituitary-adrenal axis, participate in the control of whole body homeostasis and the arousal of stress responses. GCs transmit information about environmental conditions to the HPG axis, which ultimately infl uences the timing of breeding.Female kittiwakes with low baseline LH levels and elevated levels of baseline corticosterone (CORT), the main form of GCs in avians, were more likely to skip breeding ( 2 ). An experimental reduction of CORT release during the prelaying period was associated with an advancement of egg laying in female kittiwakes ( 3 ). In domestic chickens, an acute infusion of CORT resulted in a pause in laying and a severely reduced ovarian weight ( 4 ). Chronic and repeated exposure to CORT during the rearing phrase suppressed reproductive performance, resulting in a delay of fi rst egg laid and a reduction of egg production ( 5 ).In avians, the development of ovarian follicles is accompanied by the deposition of a large amount of yolk. During a laying cycle, follicular development is matched with a supply of yolk precursors. Triacylglycerols (TG), the main

show abstract

“…The findings of this study are, therefore, highly suggestive of the maternal pituitary-adrenal axis playing a central role in mediating the adverse effects of the LP diet [9]. In pregnant rats, protein restriction during gestation reduces methylation of the promoter region of the gene that codes for the glucocorticoid receptor in offspring liver cells [27,67]. This leads to the amplification of the liver's metabolite response to stress hormones.…”

Section: The Missing Bp Heritabilitymentioning

confidence: 57%

Programming of Essential Hypertension: What Pediatric Cardiologists Need to Know

et al. 2015

View full text Add to dashboard Cite

Hypertension is recognized as one of the major contributing factors to cardiovascular disease, but its etiology remains incompletely understood. Known genetic and environmental influences can only explain a small part of the variability in cardiovascular disease risk. The missing heritability is currently one of the most important challenges in blood pressure and hypertension genetics. Recently, some promising approaches have emerged that move beyond the DNA sequence and focus on identification of blood pressure genes regulated by epigenetic mechanisms such as DNA methylation, histone modification and microRNAs. This review summarizes information on gene-environmental interactions that lead toward the developmental programming of hypertension with specific reference to epigenetics and provides pediatricians and pediatric cardiologists with a more complete understanding of its pathogenesis.

show abstract

Feeding pregnant rats a low-protein diet alters the hepatic expression of SREBP-1c in their offspring via a glucocorticoid-related mechanism

Cited by 26 publications

References 44 publications

Obesity-related hypertension: possible pathophysiological mechanisms

Obesity-related hypertension: possible pathophysiological mechanisms

Corticosterone regulation of ovarian follicular development is dependent on the energy status of laying hens

Programming of Essential Hypertension: What Pediatric Cardiologists Need to Know

Contact Info

Product

Resources

About