Developmental programming: the role of growth hormone

Oberbauer, Anita M.

doi:10.1186/s40104-015-0001-8

Cited by 26 publications

(23 citation statements)

References 95 publications

(105 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…There is a body of evidence indicating that in utero exposure to maternal factors such as obesity, poor diet and smoking can modify gene expression though DNA methylation and histones, which can exacerbate obesity in later life [ 8 , 39 ]. It is now known that these epigenetic changes can be inherited, and their effects continue over several generations [ 40 ]. In principle, epigenetic effects may be harmful or protective.…”

Section: Discussionmentioning

confidence: 99%

Changes in prevalence of obesity and high waist circumference over four years across European regions: the European male ageing study (EMAS)

Han¹,

Correa

Lean

et al. 2016

Endocrine

View full text Add to dashboard Cite

Diversity in lifestyles and socioeconomic status among European populations, and recent socio-political and economic changes in transitional countries, may affect changes in adiposity. We aimed to determine whether change in the prevalence of obesity varies between the socio-politically transitional North-East European (Łódź, Poland; Szeged, Hungary; Tartu, Estonia), and the non-transitional Mediterranean (Santiago de Compostela, Spain; Florence, Italy) and North-West European (Leuven, Belgium; Malmö, Sweden; Manchester, UK) cities. This prospective observational cohort survey was performed between 2003 and 2005 at baseline and followed up between 2008 and 2010 of 3369 community-dwelling men aged 40–79 years. Main outcome measures in the present paper included waist circumference, body mass index and mid-upper arm muscle area. Baseline prevalence of waist circumference ≥ 102 cm and body mass index ≥ 30 kg/m2, respectively, were 39.0, 29.5 % in North-East European cities, 32.4, 21.9 % in Mediterranean cities, and 30.0, 20.1 % in North-West European cities. After median 4.3 years, men living in cities from transitional countries had mean gains in waist circumference (1.1 cm) and body mass index (0.2 kg/m2), which were greater than men in cities from non-transitional countries (P = 0.005). North-East European cities had greater gains in waist circumference (1.5 cm) than in Mediterranean cities (P < 0.001). Over 4.3 years, the prevalence of waist circumference ≥ 102 cm had increased by 13.1 % in North-East European cities, 5.8 % in the Mediterranean cities, 10.0 % in North-West European cities. Odds ratios (95 % confidence intervals), adjusted for lifestyle factors, for developing waist circumference ≥ 102 cm, compared with men from Mediterranean cities, were 2.3 (1.5–3.5) in North-East European cities and 1.6 (1.1–2.4) in North-West European cities, and 1.6 (1.2–2.1) in men living in cities from transitional, compared with cities from non-transitional countries. These regional differences in increased prevalence of waist circumference ≥ 102 cm were more pronounced in men aged 60–79 years than in those aged 40–59 years. Overall there was an increase in the prevalence of obesity (body mass index ≥ 30 kg/m2) over 4.3 years (between 5.3 and 6.1 %) with no significant regional differences at any age. Mid-upper arm muscle area declined during follow-up with the greatest decline among men from North-East European cities. In conclusion, increasing waist circumference is dissociated from change in body mass index and most rapid among men living in cities from transitional North-East European countries, presumably driven by economic and socio–political changes. Information on women would also be of value and it would be of interest to relate the changes in adiposity to dietary and other behavioural habits.

show abstract

Section: Discussionmentioning

confidence: 99%

Changes in prevalence of obesity and high waist circumference over four years across European regions: the European male ageing study (EMAS)

Han¹,

Correa

Lean

et al. 2016

Endocrine

View full text Add to dashboard Cite

show abstract

“…In both regions, we detected several haplotypes that are preferentially transmitted to one sex or the other, which is in concordance with the prediction of theoretical works (Úbeda and Haig 2005;Burt and Trivers 2006;Patten et al 2010;Ubeda et al 2011;Patten 2014). The chromosome 17 region encompasses the growth hormone locus, notably the GH gene, which encodes a protein in the placenta that is important for in utero development (Oberbauer 2015), and affects adult traits such as height and bone mineral density (Timasheva et al 2013). Interestingly, there is evidence for ongoing IASC on human height (Stulp et al 2012).…”

Section: Discussionmentioning

confidence: 99%

Detection of sexually antagonistic transmission distortions in trio datasets

Lucotte

Albiñana

Laurent

et al. 2020

Preprint

View full text Add to dashboard Cite

Sex dimorphisms are widespread in animals and plants, for morphological as well as physiological traits. Understanding the genetic basis of sex dimorphism and its evolution is crucial for understanding biological differences between the sexes. Genetic variants with sex-antagonistic effects on fitness are expected to segregate in populations at the early phases of sexual dimorphism emergence. Detecting such variants is notoriously difficult, and the few genome-scan methods employed so far have limited power and little specificity. Here, we propose a new framework to detect a signature of sexually antagonistic selection. We rely on trio datasets where sex-biased transmission distortions can be directly tracked from parents to offspring, and allows identifying signal of sexually antagonistic transmission distortions in genomic regions. We report the genomic location and recombination pattern surrounding 66 regions detected as potentially under sexually antagonist selection. We find an enrichment of genes associated with embryonic development within these regions. Last, we highlight two candidates regions for sexually antagonistic selection in humans.

show abstract

“…It has been suggested that the extended elevation of GH can disrupt the normal physiological response to hyperleptinemia [ 54 ], thus predisposing towards leptin resistance and obesity, with the most likely mechanism underpinning leptin signaling impairment being at the level of the ARC. It has been well-established that adverse developmental programming disrupts the normal wiring of the pathways that regulate energy balance via a disruption in neurite outgrowth in the ARC and changes in the expression of anorixigenic/orexigenic factors, including neuropeptide Y (NPY), proopiomelanocortin (POMC), and agouti-related peptide (AgRP).…”

Section: Animal Models Of Manipulation Of the Gh-igf Axismentioning

confidence: 99%

Manipulation of the Growth Hormone-Insulin-Like Growth Factor (GH-IGF) Axis: A Treatment Strategy to Reverse the Effects of Early Life Developmental Programming

Reynolds

Perry

Vickers

2017

IJMS

View full text Add to dashboard Cite

Evidence from human clinical, epidemiological, and experimental animal models has clearly highlighted a link between the early life environment and an increased risk for a range of cardiometabolic disorders in later life. In particular, altered maternal nutrition, including both undernutrition and overnutrition, spanning exposure windows that cover the period from preconception through to early infancy, clearly highlight an increased risk for a range of disorders in offspring in later life. This process, preferentially termed “developmental programming” as part of the developmental origins of health and disease (DOHaD) framework, leads to phenotypic outcomes in offspring that closely resemble those of individuals with untreated growth hormone (GH) deficiency, including increased adiposity and cardiovascular disorders. As such, the use of GH as a potential intervention strategy to mitigate the effects of developmental malprogramming has received some attention in the DOHaD field. In particular, experimental animal models have shown that early GH treatment in the setting of poor maternal nutrition can partially rescue the programmed phenotype, albeit in a sex-specific manner. Although the mechanisms remain poorly defined, they include changes to endothelial function, an altered inflammasome, changes in adipogenesis and cardiovascular function, neuroendocrine effects, and changes in the epigenetic regulation of gene expression. Similarly, GH treatment to adult offspring, where an adverse metabolic phenotype is already manifest, has shown efficacy in reversing some of the metabolic disorders arising from a poor early life environment. Components of the GH-insulin-like growth factor (IGF)-IGF binding protein (GH-IGF-IGFBP) system, including insulin-like growth factor 1 (IGF-1), have also shown promise in ameliorating programmed metabolic disorders, potentially acting via epigenetic processes including changes in miRNA profiles and altered DNA methylation. However, as with the use of GH in the clinical setting of short stature and GH-deficiency, the benefits of treatment are also, in some cases, associated with potential unwanted side effects that need to be taken into account before effective translation as an intervention modality in the DOHaD context can be undertaken.

show abstract

Developmental programming: the role of growth hormone

Cited by 26 publications

References 95 publications

Changes in prevalence of obesity and high waist circumference over four years across European regions: the European male ageing study (EMAS)

Changes in prevalence of obesity and high waist circumference over four years across European regions: the European male ageing study (EMAS)

Detection of sexually antagonistic transmission distortions in trio datasets

Manipulation of the Growth Hormone-Insulin-Like Growth Factor (GH-IGF) Axis: A Treatment Strategy to Reverse the Effects of Early Life Developmental Programming

Contact Info

Product

Resources

About