Maternal stress alters endocrine function of the feto-placental unit in rats

2007 ◽  
Vol 292 (6) ◽  
pp. E1526-E1533 ◽  
Author(s):  
Jérôme Mairesse ◽  
Jean Lesage ◽  
Christophe Breton ◽  
Bernadette Bréant ◽  
Tom Hahn ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Body Weight Gain ◽  
Cell Mass ◽  
Late Gestation ◽  
Endocrine Function ◽  
Male Rat ◽  
And Function ◽  
The Impact

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 11β-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 β-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.

scholarly journals High Doses of Caffeine during the Peripubertal Period in the Rat Impair the Growth and Function of the Testis

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Minji Park ◽  
Yuri Choi ◽  
Hyeonhae Choi ◽  
Ju-Yearn Yim ◽  
Jaesook Roh
Keyword(s):  
Leydig Cells ◽  
Ex Vivo ◽  
Body Weight Gain ◽  
Male Rats ◽  
Male Rat ◽  
Control Group ◽  
High Doses ◽  
And Function ◽  
The Impact ◽  
Caffeine Exposure

Prenatal caffeine exposure adversely affects the development of the reproductive organs of male rat offspring. Thus, it is conceivable that peripubertal caffeine exposure would also influence physiologic gonadal changes and function during this critical period for sexual maturation. This study investigated the impact of high doses of caffeine on the testes of prepubertal male rats. A total of 45 immature male rats were divided randomly into three groups: a control group and 2 groups fed 120 and 180 mg/kg/day of caffeine, respectively, via the stomach for 4 weeks. Caffeine caused a significant decrease in body weight gain, accompanied by proportional decreases in lean body mass and body fat. The caffeine-fed animals had smaller and lighter testes than those of the control that were accompanied by negative influences on the histologic parameters of the testes. In addition, stimulated-testosterone ex vivo production was reduced in Leydig cells retrieved from the caffeine-fed animals. Our results demonstrate that peripubertal caffeine consumption can interfere with the maturation and function of the testis, possibly by interrupting endogenous testosterone secretion and reducing the sensitivity of Leydig cells to gonadotrophic stimulation. In addition, we confirmed that pubertal administration of caffeine reduced testis growth and altered testis histomorphology.

scholarly journals Imaginary Worlds: The Status of Simulation Modeling in Claims for Cost-Effectiveness In Diabetes Mellitus

2016 ◽  
Vol 7 (2) ◽  
Author(s):  
Paul C Langley ◽  
Taeho Greg Rhee
Keyword(s):  
Diabetes Mellitus ◽  
Cost Effectiveness ◽  
Simulation Modeling ◽  
Decision Makers ◽  
The Past ◽  
The Status ◽  
The Impact

Over the past 20 years a number of simulations or models have been developed as a basis for tracking and evaluating the impact of pharmacological and other interventions in type 1 and type 2 diabetes mellitus. These models have typically tracked the natural course of these diseases generating long-term composite claims for cost-effectiveness. These claims can extend over the lifetime of the modeled patient cohort. Set against the standards of normal science, however, these claims lack credibility. The claims presented are all too often either immune to failure or are presented in a form that is non-testable. As such they fail to meet the key experimental requirements of falsification and replication. Unfortunately, there is a continuing belief that long-term or lifetime models are essential to decision-making. This is misplaced. The purpose of this review is to argue that there is a pressing need to reconsider the needs of health system decision makers and focus on modeled or simulated claims that are meaningful, testable, reportable and replicable in evaluating interventions in diabetes mellitus.   Type: Commentary

scholarly journals Distinct Roles of β-Cell Mass and Function During Type 1 Diabetes Onset and Remission

Diabetes ◽  
2015 ◽  
Vol 64 (6) ◽  
pp. 2148-2160 ◽  
Author(s):  
Helena Chmelova ◽  
Christian M. Cohrs ◽  
Julie A. Chouinard ◽  
Cathleen Petzold ◽  
Matthias Kuhn ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Cell Mass ◽  
Β Cell ◽  
Diabetes Onset ◽  
And Function

scholarly journals Long-Term Neuroinflammation Induced by Influenza A Virus Infection and the Impact on Hippocampal Neuron Morphology and Function

2018 ◽  
Vol 38 (12) ◽  
pp. 3060-3080 ◽  
Author(s):  
Shirin Hosseini ◽  
Esther Wilk ◽  
Kristin Michaelsen-Preusse ◽  
Ingo Gerhauser ◽  
Wolfgang Baumgärtner ◽  
...  
Keyword(s):  
Virus Infection ◽  
Influenza A Virus ◽  
Influenza A ◽  
Hippocampal Neuron ◽  
Neuron Morphology ◽  
Influenza A Virus Infection ◽  
And Function ◽  
The Impact

scholarly journals Intrauterine growth restriction induced by maternal low protein diet causes long-term alterations of thymic structure and function in adult male rat offspring – CORRIGENDUM

2020 ◽  
pp. 1-1
Author(s):  
Jean-Baptiste Armengaud ◽  
Zelie Dennebouy ◽  
Danny Labes ◽  
Catherine Fumey ◽  
Anne Wilson ◽  
...  
Keyword(s):  
Adult Male ◽  
Intrauterine Growth Restriction ◽  
Structure And Function ◽  
Male Rat ◽  
Intrauterine Growth ◽  
Rat Offspring ◽  
Low Protein ◽  
Adult Male Rat ◽  
And Function

scholarly journals A Dual Infection/Competition Assay Shows a Correlation between Ex Vivo Human Immunodeficiency Virus Type 1 Fitness and Disease Progression

2000 ◽  
Vol 74 (19) ◽  
pp. 9222-9233 ◽  
Author(s):  
Miguel E. Quiñones-Mateu ◽  
Sarah C. Ball ◽  
Andre J. Marozsan ◽  
Vincent S. Torre ◽  
Jamie L. Albright ◽  
...  
Keyword(s):  
Immune Response ◽  
Human Immunodeficiency Virus ◽  
Disease Progression ◽  
Ex Vivo ◽  
Relative Fitness ◽  
Immunodeficiency Virus ◽  
The Impact ◽  
Hiv 1

ABSTRACT This study was designed to examine the impact of human immunodeficiency virus type 1 (HIV-1) fitness on disease progression through the use of a dual competition/heteroduplex tracking assay (HTA). Despite numerous studies on the impact of HIV-1 diversity and HIV-specific immune response on disease progression, we still do not have a firm understanding of the long-term pathogenesis of this virus. Strong and early CD8-positive cytotoxic T-cell and CD4-positive T-helper cell responses directed toward HIV-infected cells appear to curb HIV pathogenesis. However, the rate at which the virus infects the CD4+ T-cell population and possibly destroys the HIV-specific immune response may also alter the rate of disease progression. For HIV-1 fitness studies, we established conditions for dual HIV-1 infections of peripheral blood mononuclear cells (PBMC) and a sensitive HTA to measure relative virus production. A pairwise comparison was then performed to estimate the relative fitness of various non-syncytium-inducing/CCR5-tropic (NSI/R5) and syncytium-inducing/CXCR4-tropic (SI/X4) HIV-1 isolates. Four HIV-1 strains (two NSI/R5 and two SI/X4) with moderate ex vivo fitness were then selected as controls and competed against primary HIV-1 isolates from an HIV-infected Belgian cohort. HIV-1 isolates from long-term survivors (LTS) were outcompeted by control strains and were significantly less fit than HIV-1 isolates from patients with accelerated progression to AIDS (PRO). In addition, NSI/R5 HIV-1 isolates from PRO overgrew control SI/X4 strains, suggesting that not all SI/X4 HIV-1 isolates replicate more efficiently than all NSI/R5 isolates. Finally, there were strong, independent correlations between viral load and the total relative fitness values of HIV-1 isolates from PRO (r = 0.84, P = 0.033) and LTS (r = 0.86, P = 0.028). Separation of the PRO and LTS plots suggest that HIV-1 fitness together with viral load may be a strong predictor for the rate of disease progression.

scholarly journals Adrenocortical and Adipose Responses to High-Altitude-Induced, Long-Term Hypoxia in the Ovine Fetus

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Dean A. Myers ◽  
Charles A. Ducsay
Keyword(s):  
High Altitude ◽  
Hpa Axis ◽  
Anterior Pituitary ◽  
Late Gestation ◽  
Integrative Model ◽  
Adaptive Responses ◽  
Fetal Plasma ◽  
Pregnant Sheep ◽  
The Impact

By late gestation, the maturing hypothalamo-pituitary-adrenal (HPA) axis aids the fetus in responding to stress. Hypoxia represents a significant threat to the fetus accompanying situations such as preeclampsia, smoking, high altitude, and preterm labor. We developed a model of high-altitude (3,820 m), long-term hypoxia (LTH) in pregnant sheep. We describe the impact of LTH on the fetal HPA axis at the level of the hypothalamic paraventricular nucleus (PVN), anterior pituitary corticotrope, and adrenal cortex. At the PVN and anterior pituitary, the responses to LTH are consistent with hypoxia being a potent activator of the HPA axis and potentially maladaptive, while the adrenocortical response to LTH appears to be primarily adaptive. We discuss mechanisms involved in the delicate balance between these seemingly opposing responses that preserve the normal ontogenic rise in fetal plasma cortisol essential for organ maturation and in this species, birth. Further, we examine the response to, and ramifications of, an acute secondary stressor in the LTH fetus. We provide an integrative model on the potential role of adipose in modulating these responses to LTH. Integration of these adaptive responses to LTH plays a key role in promoting normal fetal growth and development under conditions of a chronic stress.

scholarly journals Dichotomy between regulation of coral bacterial communities and calcification physiology under ocean acidification conditions

2021 ◽  
Author(s):  
A. Shore ◽  
R. D. Day ◽  
J. A. Stewart ◽  
C.A. Burge
Keyword(s):  
Ocean Acidification ◽  
Bacterial Communities ◽  
16S Rrna Gene Sequencing ◽  
Ph Gradient ◽  
Rrna Gene ◽  
Seawater Ph ◽  
Coral Health ◽  
And Function ◽  
The Impact

Ocean acidification (OA) threatens the growth and function of coral reef ecosystems. A key component to coral health is the microbiome, but little is known about the impact of OA on coral microbiomes. A submarine CO2 vent at Maug Island in the Northern Marianas Islands provides a natural pH gradient to investigate coral responses to long-term OA conditions. Three coral species (Pocillopora eydouxi, Porites lobata, and Porites rus) were sampled from three sites where mean seawater pH is 8.04, 7.98, and 7.94. We characterized coral bacterial communities (using 16S rRNA gene sequencing) and determined pH of the extracellular calcifying fluid (ECF) (using skeletal boron isotopes) across the seawater pH gradient. Bacterial communities of both Porites species stabilized (decreases in community dispersion) with decreased seawater pH, coupled with large increases in the abundance of Endozoicomonas, an endosymbiont. P. lobata experienced a significant decrease in ECF pH near the vent, whereas P. rus experienced a trending decrease in ECF pH near the vent. By contrast, Pocillopora exhibited bacterial community destabilization (increases in community dispersion), with significant decreases in Endozoicomonas abundance, while its ECF pH remained unchanged across the pH gradient. Our study shows that OA has multiple consequences on Endozoicomonas abundance and suggests that Endozoicomonas abundance may be an indicator of coral response to OA. We reveal an interesting dichotomy between two facets of coral physiology (regulation of bacterial communities and regulation of calcification), highlighting the importance of multidisciplinary approaches to understanding coral health and function in a changing ocean. IMPORTANCE Ocean acidification (OA) is a consequence of anthropogenic CO2 emissions that is negatively impacting marine ecosystems such as coral reefs. OA affects many aspects of coral physiology, including growth (i.e. calcification) and disrupting associated bacterial communities. Coral-associated bacteria are important for host health, but it remains unclear how coral-associated bacterial communities will respond to future OA conditions. We document changes in coral-associated bacterial communities and changes to calcification physiology with long-term exposure to decreases in seawater pH that are environmentally relevant under mid-range IPCC emission scenarios (0.1 pH units). We also find species-specific responses that may reflect different responses to long-term OA. In Pocillopora, calcification physiology was highly regulated despite changing seawater conditions. In Porites spp., changes in bacterial communities do not reflect a breakdown of coral-bacterial symbiosis. Insights into calcification and host-microbe interactions are critical to predicting the health and function of different coral taxa to future OA conditions.

scholarly journals A zebrafish model of developmental joint dysplasia: Manipulating the larval mechanical environment to drive the malformation and recovery of joint shape

2017 ◽  
Author(s):  
Karen A Roddy ◽  
Roddy EH Skinner ◽  
Lucy H Brunt ◽  
Erika Kague ◽  
Stephen Cross ◽  
...  
Keyword(s):  
Developmental Dysplasia ◽  
Human Condition ◽  
Zebrafish Model ◽  
Element Analysis ◽  
Joint Health ◽  
Long Term Impact ◽  
And Function ◽  
Joint Shape ◽  
The Impact

AbstractDevelopmental dysplasia of the hip (DDH), a malformation of the acetabulum, is a frequent cause of early onset osteoarthritis. The disease encompasses a spectrum of severities, some of which are more amenable to treatment. Embryonic immobilisation significantly impairs the development of joint shape however the impact of this malformation to the function and growth of the joint in the short to medium term is unclear. We developed a novel model of developmental joint dysplasia using the zebrafish jaw joint to identify the mechanisms regulating cellular plasticity and ability to recover joint shape and function. Larval zebrafish were immobilised either pharmacologically or using targeted ablation of jaw muscles to induce an altered joint shape. Following restoration of muscle activity we dynamically monitored the joint shape and function in individuals at cellular resolution impossible in other vertebrate species. Reflecting the variability of the human condition we found a proportion of joints will recover both their shape and function, while others will not; despite coming from a genetically homogenous population. This allowed us to study what controls likelihood of recovery; we identified a number of cellular changes that predict likelihood of functional recovery, including position of precursor cells, and specific patterns of proliferation, migration and differentiation in joints and associated connective tissues. These factors together predict recovery better than severity of malformation alone. Using Finite Element Analysis we studied the mechanics of joints representative of ones that recover and those that fail to identify differences in patterns of strain that could explain the cellular behaviours that underpin likelihood of recovery. Thus, this model would enable the study of the short to long term impact of altered joint shape on function and could help to identify the changes that render an individual more receptive to treatment and therefore may potentially be indicative of long term joint health.

scholarly journals Beta-cell function and human islet transplantation: can we improve?

2021 ◽  
Author(s):  
Jennifer Chen ◽  
Jenny E Gunton
Keyword(s):  
Islet Transplantation ◽  
Cell Function ◽  
Therapeutic Option ◽  
Human Islets ◽  
Post Transplantation ◽  
Human Islet Transplantation ◽  
And Function ◽  
Islet Survival

Islet transplantation, a therapeutic option to treat type 1 diabetes, is not yet as successful as whole-pancreas transplantation as a treatment for diabetes. Mouse models are commonly used for islet research. However, it is clear disparities exist between islet transplantation outcomes in mice and humans. Given the shortage of transplant-grade islets, it is crucial that we further our understanding of factors that determine long-term islet survival and function post-transplantation. In turn, that may lead to new therapeutic targets and strategies that to improve transplant outcomes. Here, we summarise the current landscape in clinical transplantation, highlight underlying similarities and differences between mouse and human islets, and review interventions that are being considered to create a new pool of β-cells for clinical application.

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