scholarly journals The Roles of PPARs in the Fetal Origins of Metabolic Health and Disease

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
William D. Rees ◽  
Christopher J. McNeil ◽  
Christopher A. Maloney
Keyword(s):  
Epigenetic Modification ◽  
Fetal Liver ◽  
Maternal Diet ◽  
Subsequent Development ◽  
Adaptive Responses ◽  
Fetal Origins ◽  
Methylation Of Dna ◽  
Health And Disease ◽  
Cell Growth And Differentiation

Beyond the short-term effects on fertility, there is increasing evidence that obesity or the consumption of an inappropriate diet by the mother during pregnancy adversely affects the long-term health of her offspring. PPAR and RXR isotypes are widely expressed in reproductive tissues and in the developing fetus. Through their interactions with fatty acids, they may mediate adaptive responses to the changes in the maternal diet. In the maturing follicle, PPAR-γhas an important role in the granulosa cells that surround the maturing oocyte. After fertilisation, PPAR-γand PPAR-β/δare essential regulators of placentation and the subsequent development of key metabolic tissues such as skeletal muscle and adipose cells. Activation of PPAR-γand PPAR-β/δduring fetal development has the potential to modify the growth and development of these tissues. PPAR-αis expressed at low levels in the fetal liver, however, this expression may be important, as changes in the methylation of DNA in its promoter region are reported to take place during this period of development. This epigenetic modification then programmes subsequent expression. These findings suggest that two separate PPAR-dependent mechanisms may be involved in the fetal adaptations to the maternal diet, one, mediated by PPAR-γand PPAR-β/δ, regulating cell growth and differentiation; and another adapting long-term lipid metabolism via epigenetic changes in PPAR-αto optimise postnatal survival.

Fetal programming of hypertension

2006 ◽  
Vol 290 (1) ◽  
pp. R1-R10 ◽  
Author(s):  
Barbara T. Alexander
Keyword(s):  
Fetal Programming ◽  
Animal Studies ◽  
Subsequent Development ◽  
Epidemiological Studies ◽  
Fetal Life ◽  
Adaptive Responses ◽  
Renal Functions ◽  
Regulatory Systems ◽  
Physiological Alterations

Numerous epidemiological studies suggest an inverse relationship between low birth weight (LBW) and hypertension, an observation now supported by numerous animal studies. The mechanisms linking LBW and hypertension appear to be multifactorial and involve alterations in the normal regulatory systems and renal functions involved in the long-term control of arterial pressure. Recent studies using animal models of fetal programming suggest that programming during fetal life occurs in response to an adverse fetal environment and results in permanent adaptive responses that lead to structural and physiological alterations and the subsequent development of hypertension. This review summarizes the adaptive responses observed in the different models used to induce a suboptimal fetal environment and discusses insights into the mechanisms mediating the fetal programming of hypertension.

Nutrition and Fetal Origins of Diseases in Adults

2018 ◽  
Author(s):  
Amanda K Barks ◽  
Phu V Tran ◽  
Michael K Georgieff ◽  
Anne Maliszewski-Hall
Keyword(s):  
Health Outcomes ◽  
Fetal Programming ◽  
Epigenetic Modification ◽  
Nutrient Deficiency ◽  
Nutrient Deficiencies ◽  
Critical Periods ◽  
Fetal Origins ◽  
Organ Systems ◽  
Postnatal Environment

Accumulating evidence suggests that the early-life environment has lasting effects on health and disease into adulthood. The current concept of developmental origins of adulthood disease has expanded beyond the original observation by Barker and colleagues correlating low birth weight with adulthood cardiovascular and metabolic disorders. Notably, the fetal-neonatal nutritional environment has a significant role in influencing an individual’s wellness in adulthood. During critical periods of fetal and neonatal development, tissues and organ systems are most vulnerable to nutrient deficiencies. Through fetal programming mechanisms such as epigenetic modification, a biochemical process that regulates gene expression without altering the genetic code, developing tissues adapt to nutrient-poor environments to preserve normal development of critical organ systems, including the brain. However, these programmed adaptations can have negative long-term health consequences if the postnatal environment does not match the fetal-neonatal environment in which the programming occurred. These long-term adverse health outcomes constitute the true cost to society, in both increased medical costs and the indirect cost of lost productivity. Here we review the effects of nutrient deficiencies on fetal programming and subsequent health outcomes, as well as the potential mechanisms that underlie fetal programming. This review contains 3 Figures, 2 Tables and 115 references Key words: critical period, epigenetics, fetal programming, iron, long-chain polyunsaturated fatty acids, neurodevelopment, nutrient deficiency, protein-energy, vitamins, zinc

scholarly journals The Role of Cell Metabolism in Innate Immune Memory

2020 ◽  
pp. 1-9
Author(s):  
Anaisa Valido Ferreira ◽  
Jorge Domiguéz-Andrés ◽  
Mihai Gheorghe Netea
Keyword(s):  
Metabolic Pathways ◽  
Tricarboxylic Acid Cycle ◽  
Cell Metabolism ◽  
Innate Immune ◽  
Immune Memory ◽  
Functional Changes ◽  
Trained Immunity ◽  
Health And Disease

Immunological memory is classically attributed to adaptive immune responses, but recent studies have shown that challenged innate immune cells can display long-term functional changes that increase nonspecific responsiveness to subsequent infections. This phenomenon, coined <i>trained immunity</i> or <i>innate immune memory</i>, is based on the epigenetic reprogramming and the rewiring of intracellular metabolic pathways. Here, we review the different metabolic pathways that are modulated in trained immunity. Glycolysis, oxidative phosphorylation, the tricarboxylic acid cycle, amino acid, and lipid metabolism are interplaying pathways that are crucial for the establishment of innate immune memory. Unraveling this metabolic wiring allows for a better understanding of innate immune contribution to health and disease. These insights may open avenues for the development of future therapies that aim to harness or dampen the power of the innate immune response.

scholarly journals Cariogenic Biofilm: Pathology-Related Phenotypes and Targeted Therapy

2021 ◽  
Vol 9 (6) ◽  
pp. 1311
Author(s):  
Xiuqin Chen ◽  
Eric Banan-Mwine Daliri ◽  
Akanksha Tyagi ◽  
Deog-Hwan Oh
Keyword(s):  
Treatment Strategies ◽  
High Specificity ◽  
Low Ph ◽  
Oral Microbiota ◽  
Extracellular Polymers ◽  
Dental Biofilm ◽  
Health And Disease ◽  
Promising Treatment ◽  
Cariogenic Biofilm

The initiation and development of cariogenic (that is, caries-related) biofilms are the result of the disruption of homeostasis in the oral microenvironment. There is a daily accumulation of dental biofilm on the surface of teeth and its matrix of extracellular polymers supports the host in its defense against invading microbes, thus helping to achieve oral microbial homeostasis. However, the homeostasis can be broken down under certain circumstances such as during long-term exposure to a low pH environment which results in the dominance of acidogenic and acid-tolerating species in the dental biofilm and, thus, triggers the shift of harmless biofilm to an acidic one. This work aims to explore microbial diversity and the quorum sensing of dental biofilm and their important contributions to oral health and disease. The complex and multispecies ecosystems of the cariogenic biofilm pose significant challenges for the modulation of the oral microenvironment. Promising treatment strategies are those that target cariogenic niches with high specificity without disrupting the balance of the surrounding oral microbiota. Here, we summarized the recent advances in modulating cariogenic biofilm and/or controlling its pathogenic traits.

scholarly journals Advancement in long-distance bird migration through individual plasticity in departure

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jesse R. Conklin ◽  
Simeon Lisovski ◽  
Phil F. Battley
Keyword(s):  
Bird Migration ◽  
Population Level ◽  
Breeding Site ◽  
Environmental Constraints ◽  
Adaptive Responses ◽  
Long Distance ◽  
Direct Observations ◽  
Breeding Resources ◽  
Plastic Responses

AbstractGlobally, bird migration is occurring earlier in the year, consistent with climate-related changes in breeding resources. Although often attributed to phenotypic plasticity, there is no clear demonstration of long-term population advancement in avian migration through individual plasticity. Using direct observations of bar-tailed godwits (Limosa lapponica) departing New Zealand on a 16,000-km journey to Alaska, we show that migration advanced by six days during 2008–2020, and that within-individual advancement was sufficient to explain this population-level change. However, in individuals tracked for the entire migration (50 total tracks of 36 individuals), earlier departure did not lead to earlier arrival or breeding in Alaska, due to prolonged stopovers in Asia. Moreover, changes in breeding-site phenology varied across Alaska, but were not reflected in within-population differences in advancement of migratory departure. We demonstrate that plastic responses can drive population-level changes in timing of long-distance migration, but also that behavioral and environmental constraints en route may yet limit adaptive responses to global change.

scholarly journals Long-Lasting Hyperexcitability Induced by Depolarization in the Absence of Detectable Ca2+ Signals

2009 ◽  
Vol 101 (3) ◽  
pp. 1351-1360 ◽  
Author(s):  
Kumud K. Kunjilwar ◽  
Harvey M. Fishman ◽  
Dario J. Englot ◽  
Roger G. O'Neil ◽  
Edgar T. Walters
Keyword(s):  
Protein Synthesis ◽  
Neuronal Injury ◽  
Adaptive Responses ◽  
Neuronal Responses ◽  
Local Protein Synthesis ◽  
Neuronal Viability ◽  
Nerve Ganglion ◽  
Dissociated Cell Culture ◽  
Activity Dependent

Learning and memory depend on neuronal alterations induced by electrical activity. Most examples of activity-dependent plasticity, as well as adaptive responses to neuronal injury, have been linked explicitly or implicitly to induction by Ca2+ signals produced by depolarization. Indeed, transient Ca2+ signals are commonly assumed to be the only effective transducers of depolarization into adaptive neuronal responses. Nevertheless, Ca2+-independent depolarization-induced signals might also trigger plastic changes. Establishing the existence of such signals is a challenge because procedures that eliminate Ca2+ transients also impair neuronal viability and tolerance to cellular stress. We have taken advantage of nociceptive sensory neurons in the marine snail Aplysia, which exhibit unusual tolerance to extreme reduction of extracellular and intracellular free Ca2+ levels. The axons of these neurons exhibit a depolarization-induced memory-like hyperexcitability that lasts a day or longer and depends on local protein synthesis for induction. Here we show that transient localized depolarization of these axons in an excised nerve–ganglion preparation or in dissociated cell culture can induce short- and intermediate-term axonal hyperexcitability as well as long-term protein synthesis–dependent hyperexcitability under conditions in which Ca2+ entry is prevented (by bathing in nominally Ca2+ -free solutions containing EGTA) and detectable Ca2+ transients are eliminated (by adding BAPTA-AM). Disruption of Ca2+ release from intracellular stores by pretreatment with thapsigargin also failed to affect induction of axonal hyperexcitability. These findings suggest that unrecognized Ca2+-independent signals exist that can transduce intense depolarization into adaptive cellular responses during neuronal injury, prolonged high-frequency activity, or other sustained depolarizing events.

Offspring’s hydromineral adaptive responses to maternal undernutrition during lactation

2015 ◽  
Vol 6 (6) ◽  
pp. 520-529 ◽  
Author(s):  
P. Nuñez ◽  
J. Arguelles ◽  
C. Perillan
Keyword(s):  
Salt Intake ◽  
Maternal Diet ◽  
Plasma Osmolality ◽  
Control Mechanisms ◽  
Lactation Period ◽  
Adaptive Responses ◽  
Long Term Effects ◽  
Molecular Alterations ◽  
Maternal Undernutrition ◽  
Renal Histology

Early development, throughout gestation and lactation, represents a period of extreme vulnerability during which susceptibility to later metabolic and cardiovascular injuries increases. Maternal diet is a major determinant of the foetal and newborn developmental environment; maternal undernutrition may result in adaptive responses leading to structural and molecular alterations in various organs and tissues, such as the brain and kidney. New nephron anlages appear in the renal cortex up to postnatal day 4 and the last anlages to be formed develop into functional nephrons by postnatal day 10 in rodents. We used a model of undernutrition in rat dams that were food-restricted during the first half of the lactation period in order to study the long-term effects of maternal diet on renal development, behaviour and neural hydromineral control mechanisms. The study showed that after 40% food restriction in maternal dietary intake, the dipsogenic responses for both water and salt intake were not altered; Fos expression in brain areas investigated involved in hydromineral homeostasis control was always higher in the offspring in response to isoproterenol. This was accompanied by normal plasma osmolality changes and typical renal histology. These results suggest that the mechanisms for the control of hydromineral balance were unaffected in the offspring of these 40% food-restricted mothers. Undernutrition of the pups may not be as drastic as suggested by dams’ restriction.

scholarly journals Is “transgenerational response” a hidden cause of failed corporate turnarounds and chronic underperformance?

2017 ◽  
Vol 45 (3) ◽  
pp. 23-29
Author(s):  
John Oliver
Keyword(s):  
Financial Performance ◽  
Case Studies ◽  
Corporate Culture ◽  
Ceo Turnover ◽  
Business Leaders ◽  
Adaptive Responses ◽  
Content Type ◽  
Organizational Policies ◽  
And Performance

Purpose CEO turnover and chronic corporate underperformance are examined through the lens of Transgenerational Response. Design/methodology/approach The criteria for investigating Transgenerational Response in corporations consisted of identifying a Critical Corporate Incident, the number of corporate generations and the resultant corporate financial performance. Findings The evidence presented in the case studies illustrates how a Critical Corporate Incident has produced the consequential effect of chronic financial performance in the years following the incident. Research limitations/implications These case studies have not presented the “actual” adaptive responses, inherited attitudes and behaviours that have subsequently embedded themselves in a new corporate culture, post the Critical Corporate Incident, to the detriment of the long-term health and performance of each firm. Practical implications Examining CEO turnover and chronic corporate underperformance through the lens of Transgenerational Response means that business leaders can identify how a historic event has affected the performance of their firm in subsequent generations. With this knowledge in hand, they will be able to examine the inherited attitudes and behaviours, organizational policies, strategy and adaptive cultural routines that have combined to consolidate the firms chronic under performance. Originality/value This is a highly original, evidence based, idea that has the potential to reshape our current understanding of CEO turnover and underperforming firms. It will help business leaders identify how a historic event has affected the performance of a firm in subsequent generations.

Sign in / Sign up

Export Citation Format

Share Document