The Developmental Origins of Health and Disease (DOHaD)

Lacagnina, Salvatore

doi:10.1177/1559827619879694

Cited by 67 publications

(44 citation statements)

References 22 publications

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“…On the other hand, according to the Developmental Origins of Health and Disease ( 51 ) hypothesis, most of the individual metabolic phenotypes are determined in utero. In particular, exposure to a hostile uterine environment has been associated—in humans and model organisms—with adult hyperphagia and late onset metabolic disorders, due to impaired placenta development and function ( 52 , 53 ).…”

Section: Resultsmentioning

confidence: 99%

Disruption of paternal circadian rhythm affects metabolic health in male offspring via nongerm cell factors

et al. 2021

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Circadian rhythm synchronizes each body function with the environment and regulates physiology. Disruption of normal circadian rhythm alters organismal physiology and increases disease risk. Recent epidemiological data and studies in model organisms have shown that maternal circadian disruption is important for offspring health and adult phenotypes. Less is known about the role of paternal circadian rhythm for offspring health. Here, we disrupted circadian rhythm in male mice by night-restricted feeding and showed that paternal circadian disruption at conception is important for offspring feeding behavior, metabolic health, and oscillatory transcription. Mechanistically, our data suggest that the effect of paternal circadian disruption is not transferred to the offspring via the germ cells but initiated by corticosterone-based parental communication at conception and programmed during in utero development through a state of fetal growth restriction. These findings indicate paternal circadian health at conception as a newly identified determinant of offspring phenotypes.

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Section: Resultsmentioning

confidence: 99%

Disruption of paternal circadian rhythm affects metabolic health in male offspring via nongerm cell factors

et al. 2021

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“…This concept is based on Barker’s theory of the evolutionary origins of adult health and disease (DOHaD). This theory defines the relationship between early developmental influences on health and disease in adulthood and aging [ 52 – 54 ]. We observed that long-term programming was sex-dependent in both non-stressed and PRS aged rats.…”

Section: Discussionmentioning

confidence: 99%

Maternal stress programs a demasculinization of glutamatergic transmission in stress-related brain regions of aged rats

et al. 2021

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Brain aging may be programmed by early-life stress. Aging affects males and females differently, but how perinatal stress (PRS) affects brain aging between sexes is unknown. We showed behavioral and neurobiological sex differences in non-stressed control rats that were strongly reduced or inverted in PRS rats. In particular, PRS decreased risk-taking behavior, spatial memory, exploratory behavior, and fine motor behavior in male aged rats. In contrast, female aged PRS rats displayed only increased risk-taking behavior and reduced exploratory behavior. PRS induced large reductions in the expression of glutamate receptors in the ventral and dorsal hippocampus and prefrontal cortex only in male rats. PRS also reduced the expression of synaptic vesicle-associated proteins, glucocorticoid receptors (GR), and mineralocorticoid receptors (MR) in the ventral hippocampus of aged male rats. In contrast, in female aged rats, PRS enhanced the expression of MRs and brain-derived neurotrophic factor (BDNF) in the ventral hippocampus and the expression of glial fibrillary acidic protein (GFAP) and BDNF in the prefrontal cortex. A common PRS effect in both sexes was a reduction in exploratory behavior and metabotropic glutamate (mGlu2/3) receptors in the ventral hippocampus and prefrontal cortex. A multidimensional analysis revealed that PRS induced a demasculinization profile in glutamate-related proteins in the ventral and dorsal hippocampus and prefrontal cortex, as well as a demasculinization profile of stress markers only in the dorsal hippocampus. In contrast, defeminization was observed only in the ventral hippocampus. Measurements of testosterone and 17-β-estradiol in the plasma and aromatase in the dorsal hippocampus were consistent with a demasculinizing action of PRS. These findings confirm that the brains of males and females differentially respond to PRS and aging suggesting that females might be more protected against early stress and age-related inflammation and neurodegeneration. Taken together, these results may contribute to understanding how early environmental factors shape vulnerability to brain aging in both sexes and may lay the groundwork for future studies aimed at identifying new treatment strategies to improve the quality of life of older individuals, which is of particular interest given that there is a high growth of aging in populations around the world.

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“…In addition to genetic predisposition, environmental factors experienced during fetal life and childhood have been found to influence brain and nervous system functions through epigenetic changes. For example, the DOHaD theory (developmental origins of health and disease) has been proposed that inadequate nutrition during fetal life may lead to the risk of chronic diseases such as hypertension in adulthood [72]. It has also been pointed out that excess salt also may induce epigenetic saltsensitive hypertension [73].…”

Section: Epigenetics In Salt-sensitive Hypertensionmentioning

confidence: 99%

Hypertension as Three Systematic Dysregulations of Na⁺ Homeostasis in Terrestrial Mammal, and Salt in Gut Might Cause Brain Inflammation

Mifune¹,

Kanno²

2021

Psychology and Pathophysiological Outcomes of Eating

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Although Na+ homeostasis in vivo is essential for mammals, it is known that excessive salt (NaCl) intake has played a major role in the development of hypertension. In vivo, there is a hormonal system, the renin-angiotensin-aldosterone system (RAAS), that specializes in regulating Na+ retention, especially the amount of Na+ in plasma. Na+ homeostasis in vivo has been achieved mainly by the RAAS, through regulation of vascular tonus (blood pressure) and Na+ handling in the kidney (Na+ diuresis). Recent studies have revealed a third mechanism of Na+ homeostasis in vivo: regulation of interstitial Na+ levels in tissues, such as subcutaneous tissues, by tissue macrophage immunity. In the pathogenesis of salt-sensitive hypertension, Recent research have been revealed that three molecular axes (Ang II - Rho/NOX-eNOS system, Aldosterone-rac1 -ENaC system, and tissue Na+ − TonEBP in macrophage -VEGF-c) are significantly involved in maintaining Na+ homeostasis in salt induced hypertension. Furthermore, the mechanism by which salt causes hypertension via the immune system (intestinal, local mucosal, and tissue immunity) has also been reported. In this article, we would like to propose that three molecular dysfunctions are involved in the development of salt-sensitive hypertension through three immunological mechanisms in the maintenance of Na+ homeostasis. Next, I would like to explain the importance of gut-RAAS and abnormality of intestinal microflora (dysbiosis) in salt-sensitive hypertension. It has been known that the metabolites (e.g., short-chain fatty acid neural amino) produced by microflora are deeply involved in central (CNS) and sympathetic nervous system (SNS) activity. In addition, we would like to explain of the importance of brain-RAAS and cerebral inflammation in salt-sensitive hypertension. Moreover, recent research have revealed that the detection-mechanism in the brain for Na+ concentration([Na+]) in vivo and in the tongue for [Na+] in diet. These finding suggests that excessive salt intake may cause brain dysfunction, most delicate organ, before the onset of salt sensitive hypertension, and may also destroy brain structure after the onset of salt sensitive hypertension. Thus, we would like to insist that excessive salt intake might not only induce hypertension, but also be toxic especially for brain. Finally, we would like to explain that The DASH diet (Dietary Approaches to Stop Hypertension) is one of the universal diets for adult human, not only by reducing salt, but also by reducing metabolic stress and improving of dysbiosis.

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The Developmental Origins of Health and Disease (DOHaD)

Cited by 67 publications

References 22 publications

Disruption of paternal circadian rhythm affects metabolic health in male offspring via nongerm cell factors

Disruption of paternal circadian rhythm affects metabolic health in male offspring via nongerm cell factors

Maternal stress programs a demasculinization of glutamatergic transmission in stress-related brain regions of aged rats

Hypertension as Three Systematic Dysregulations of Na⁺ Homeostasis in Terrestrial Mammal, and Salt in Gut Might Cause Brain Inflammation

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The Developmental Origins of Health and Disease (DOHaD)

Cited by 67 publications

References 22 publications

Disruption of paternal circadian rhythm affects metabolic health in male offspring via nongerm cell factors

Disruption of paternal circadian rhythm affects metabolic health in male offspring via nongerm cell factors

Maternal stress programs a demasculinization of glutamatergic transmission in stress-related brain regions of aged rats

Hypertension as Three Systematic Dysregulations of Na+ Homeostasis in Terrestrial Mammal, and Salt in Gut Might Cause Brain Inflammation

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Hypertension as Three Systematic Dysregulations of Na⁺ Homeostasis in Terrestrial Mammal, and Salt in Gut Might Cause Brain Inflammation