| 1. |
- Delpierre, Cyrille, et al.
(författare)
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Origins of heath inequalities : the case for Allostatic Load
- 2016
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Ingår i: Longitudinal and Life Course Studies. - : Bristol University Press. - 1757-9597. ; 7:1, s. 79-103
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Tidskriftsartikel (refereegranskat)abstract
- In an opening paper Delpierre et al. explore the concept of allostatic load. The impact of the environment on our biological systems is summarised by the concept of embodiment. The biological embedding of social conditions could therefore be a relevant mechanism to partly explain the social gradient in health. A key issue is how to measure the 'physiological reality' the biological expression of embodiment at individual and population levels. Allostatic load (AL) has been proposed as a measure of the overall cost of adapting to the environment and may be a relevant tool or concept for measuring the way we have embodied our environment. Social inequalities in health may be partly explained by the embodiment of social environments, and AL may allow us to measure and compare embodiment between socioeconomic groups. However, before operationalising AL, a number of issues deserve further exploration. Among these, the choice of biological systems, and variables within each system, that should be included to remain 'loyal' to the theory of biological multisystem wastage underlying AL and the most appropriate methodological approach to be used to build an AL score, are particularly important. Moreover, studies analysing the link between adverse environments (physical, chemical, nutritional, psychosocial) across the life course and AL remain rare. Such studies require cohorts with data on socioeconomic and psychosocial environments over the life course, with multiple biological measures, made at various stages across the life span. The development and maintenance of these cohorts is essential to continue exploring the promising results that could enhance our understanding of the genesis of the social gradient in health by measuring embodiment. These points are then debated in commentaries by Linn Getz and Margret Olafia Tomasdottir, Tony Robertson and Per Gustafson. The commentaries are followed by a response from the authors of the opening paper.
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| 2. |
- Mairesse, Jérôme, et al.
(författare)
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Maternal stress alters endocrine function of the feto-placental unit in rats.
- 2007
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Ingår i: American journal of physiology. Endocrinology and metabolism. - : American Physiological Society. - 0193-1849 .- 1522-1555. ; 292:6, s. E1526-33
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Tidskriftsartikel (refereegranskat)abstract
- Prenatal stress (PS) can cause early and long-term developmental effects resulting in part from altered maternal and/or fetal glucocorticoid exposure. The aim of the present study was to assess the impact of chronic restraint stress during late gestation on feto-placental unit physiology and function in embryonic (E) day 21 male rat fetuses. Chronic stress decreased body weight gain and food intake of the dams and increased their adrenal weight. In the placenta of PS rats, the expression of glucose transporter type 1 (GLUT1) was decreased, whereas GLUT3 and GLUT4 were slightly increased. Moreover, placental expression and activity of the glucocorticoid "barrier" enzyme 11beta-hydroxysteroid dehydrogenase type 2 was strongly reduced. At E21, PS fetuses exhibited decreased body, adrenal pancreas, and testis weights. These alterations were associated with reduced pancreatic beta-cell mass, plasma levels of glucose, growth hormone, and ACTH, whereas corticosterone, insulin, IGF-1, and CBG levels were unaffected. These data emphasize the impact of PS on both fetal growth and endocrine function as well as on placental physiology, suggesting that PS could program processes implied in adult biology and pathophysiology.
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| 3. |
- Rincel, Marion, et al.
(författare)
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Maternal high-fat diet and early-life stress differentially modulate spine density and dendritic morphology in the medial prefrontal cortex of juvenile and adult rats.
- 2018
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Ingår i: Brain Structure and Function. - : Springer. - 1863-2653 .- 1863-2661. ; 223:2, s. 883-895
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Tidskriftsartikel (refereegranskat)abstract
- The medial prefrontal cortex (mPFC) is a key area for the regulation of numerous brain functions including stress response and cognitive processes. This brain area is also particularly affected by adversity during early life. Using an animal model in rats, we recently demonstrated that maternal exposure to a high-fat diet (HFD) prevents maternal separation (MS)-induced gene expression alterations in the developing PFC and attenuates several long-term deleterious behavioral effects of MS. In the present study, we ask whether maternal HFD could protect mPFC neurons of pups exposed to early life stress by examining dendritic morphology and spine density in juvenile [postnatal day (PND) 21] and adult rats submitted to MS. Dams were fed either a control or an HFD throughout gestation and lactation, and pups were submitted to MS from PND2 to PND14. We report that maternal HFD prevents MS-induced spine loss at PND21 and dendritic atrophy at adulthood. Furthermore, we show in adult MS rats that PFC-dependent memory extinction deficits are prevented by maternal HFD. Finally, perinatal HFD exposure reverses gut leakiness following stress in pups and seems to exert an anti-stress effect in dams. Overall, our work demonstrates that maternal HFD affects the developing brain and suggests that nutrition, possibly through gut–brain interactions, could modulate mPFC sensitivity to early stress.
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