Implications of accumulative stress burdens during critical periods of early postnatal life for mortality risk among Guale interred in a colonial era cemetery in Spanish Florida (ca. AD 1605–1680)

2020 ◽  
Vol 172 (4) ◽  
pp. 621-637
Author(s):  
Carey J. Garland
Keyword(s):  
Mortality Risk ◽  
Postnatal Life ◽  
Critical Periods ◽  
Colonial Era ◽  
Spanish Florida ◽  
Early Postnatal Life

Early-life programming of adipose tissue

2020 ◽  
Vol 33 (2) ◽  
pp. 244-259 ◽  
Author(s):  
Ericka Moreno-Mendez ◽  
Saray Quintero-Fabian ◽  
Cristina Fernandez-Mejia ◽  
Maria-Luisa Lazo-de-la-Vega-Monroy
Keyword(s):  
Adipose Tissue ◽  
Fetal Growth ◽  
Early Life ◽  
Maternal Obesity ◽  
Tissue Expansion ◽  
Tissue Cell ◽  
Postnatal Life ◽  
Critical Periods ◽  
Early Life Programming ◽  
Early Postnatal Life

AbstractWorldwide obesity is increasing at an alarming rate in children and adolescents, with the consequent emergence of co-morbidities. Moreover, the maternal environment during pregnancy plays an important role in obesity, contributing to transgenerational transmission of the same and metabolic dysfunction. White adipose tissue represents a prime target of metabolic programming induced by maternal milieu. In this article, we review adipose tissue physiology and development, as well as maternal influences during the perinatal period that may lead to obesity in early postnatal life and adulthood. First, we describe the adipose tissue cell composition, distribution and hormonal action, together with the evidence of hormonal factors participating in fetal/postnatal programming. Subsequently, we describe the critical periods of adipose tissue development and the relationship of gestational and early postnatal life with healthy fetal adipose tissue expansion. Furthermore, we discuss the evidence showing that adipose tissue is an important target for nutritional, hormonal and epigenetic signals to modulate fetal growth. Finally, we describe nutritional, hormonal, epigenetic and microbiome changes observed in maternal obesity, and whether their disruption alters fetal growth and adiposity. The presented evidence supports the developmental origins of health and disease concept, which proposes that the homeostatic system is affected during gestational and postnatal development, impeding the ability to regulate body weight after birth, thereby resulting in adult obesity. Consequently, we anticipate that promoting a healthy early-life programming of adipose tissue and increasing the knowledge of the mechanisms by which maternal factors affect the health of future generations may offer novel strategies for explaining and addressing worldwide health problems such as obesity.

Regulation of motor neuron dendrite growth by NMDA receptor activation

Development ◽  
1994 ◽  
Vol 120 (11) ◽  
pp. 3063-3071 ◽  
Author(s):  
R.G. Kalb
Keyword(s):  
Nmda Receptor ◽  
Motor Neuron ◽  
Cell Body ◽  
Motor Neurons ◽  
Receptor Activation ◽  
Dendrite Growth ◽  
Postnatal Life ◽  
Receptor Antagonism ◽  
Neuron Cell Body ◽  
Early Postnatal Life

Spinal motor neurons undergo great changes in morphology, electrophysiology and molecular composition during development. Some of this maturation occurs postnatally when limbs are employed for locomotion, suggesting that neuronal activity may influence motor neuron development. To identify features of motor neurons that might be regulated by activity we first examined the structural development of the rat motor neuron cell body and dendritic tree labeled with cholera toxin-conjugated horseradish peroxidase. The motor neuron cell body and dendrites in the radial and rostrocaudal axes grew progressively over the first month of life. In contrast, the growth of the dendritic arbor/cell and number of dendritic branches was biphasic with overabundant growth followed by regression until the adult pattern was achieved. We next examined the influence of neurotransmission on the development of these motor neuron features. We found that antagonism of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor inhibited cell body growth and dendritic branching in early postnatal life but had no effect on the maximal extent of dendrite growth in the radial and rostrocaudal axes. The effects of NMDA receptor antagonism on motor neurons and their dendrites was temporally restricted; all of our anatomic measures of dendrite structure were resistant to NMDA receptor antagonism in adults. These results suggest that the establishment of mature motor neuron dendritic architecture results in part from dendrite growth in response to afferent input during a sensitive period in early postnatal life.

scholarly journals A STEREOLOGICAL ANALYSIS OF THE EFFECT OF EARLY POSTNATAL ETHANOL EXPOSURE ON NEURONAL NUMBERS IN RAT DENTATE GYRUS

2011 ◽  
Vol 19 (2) ◽  
pp. 99 ◽  
Author(s):  
Takanori Miki ◽  
Simon J Harris ◽  
Peter Wilce ◽  
Yoshiki Takeuchi ◽  
Kuldip S Bedi
Keyword(s):  
Dentate Gyrus ◽  
Hippocampal Formation ◽  
Ethanol Exposure ◽  
Learning Ability ◽  
Ethanol Ingestion ◽  
High Dose ◽  
Postnatal Life ◽  
Numerical Density ◽  
Rat Pups ◽  
Early Postnatal Life

Maternal ethanol ingestion during pregnancy can cause fetal alcohol syndrome (FAS) in their offspring. Among the symptoms of FAS, damage to the central nervous system has emerged as one of the most serious problems. We have previously shown that a relatively high dose of ethanol exposure during early postnatal life can cause alterations in spatial learning ability. This ability is controlled, at least in part, by the hippocampal formation. The purpose of the present study was to determine whether exposure of rat pups to ethanol during early postnatal life had effects on the total number of the dentate gyrus neurons. Wistar rats were exposed to a relatively high daily dose of ethanol between postnatal days 10 to 15. Ethanol exposure was achieved by placing rat pups in a chamber containing ethanol vapour for 3 hours a day. The blood ethanol concentration was found to be about 430 mg/dL at the end of the exposure period. Groups of ethanol treated (ET), separation controls (SC) and mother reared controls (MRC) were anaesthetised and killed at 16-days-of-age by perfusion with phosphate-buffered 2.5% glutaraldehyde. The Cavalieri principle was used to determine the volume of subdivisions of the dentate gyrus, and the physical disector method was used to estimate the numerical densities of neurons within each subdivision. The total number of neurons was calculated by multiplying estimates of the numerical density with the volume. There was, on average, about 421,000 granule cells in all three treatment groups. In the hilus region, ET rats had about 27,000 neuronal cells. This value was significantly smaller than the average of 38,000 such neurons estimated to be present in both MRC and SC animals. It is concluded that neurons in the hilus region of the dentate gyrus may be particularly vulnerable to the effects of a high dose of ethanol exposure during PND 10-15. It is likely that this deficit was due to neuronal death induced by some mechanisms related to the ethanol exposure.

scholarly journals Leptin levels at birth and in early postnatal life in small- and appropriate-for-gestational-age infants

Medicina ◽  
2007 ◽  
Vol 43 (10) ◽  
pp. 784 ◽  
Author(s):  
Margarita Valūnienė ◽  
Rasa Verkauskienė ◽  
Margaret Boguszewski ◽  
Jovanna Dahlgren ◽  
Danutė Lašienė ◽  
...  
Keyword(s):  
Birth Weight ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Venous Blood ◽  
Postnatal Life ◽  
Abrupt Decrease ◽  
Blood Samples ◽  
Appropriate For Gestational Age ◽  
Early Postnatal Life ◽  
The Impact

The aim of this study was to evaluate leptin concentration at birth and in early postnatal life in small- and appropriate-for-gestational-age infants and to assess its relationship with infants’ anthropometry at birth and some characteristics of maternal pregnancy. Materials and methods. A total of 367 infants born after 32–42 weeks of gestation were enrolled in the study. Umbilical cord blood samples were collected from 80 small- and 287 appropriate- for-gestational-age newborns. Altogether, 166 venous blood samples were taken from these neonates on days 2–6 of life. Results. Cord leptin levels were significantly lower in small- compared to appropriate-forgestational- age infants. We observed a positive correlation between cord leptin and birth weight, all neonatal anthropometric parameters, placental weight, and some maternal nutritional factors. In multivariate analysis, cord leptin concentration explained up to 15% of the variation in sum of newborn’s skinfold thickness but only 5% of the variation in birth weight. Postnatally, leptin concentration decreased markedly to the similar low levels in both infant groups and remained so during the first postnatal week. Conclusions. Significantly lower cord leptin concentration in small-for-gestational-age neonates reflects a lower fat mass content compared to appropriate-for-gestational-age infants. However, an abrupt decrease in leptin levels shortly after birth in both groups suggests that placenta could be an important source of leptin in fetal circulation. The impact of low leptin levels at birth in small-for-gestational-age infants on their postnatal appetite and weight gain remains to be elucidated in future studies.

Nutritional challenges during development induce sex-specific changes in glucose homeostasis in the adult sheep

2007 ◽  
Vol 292 (1) ◽  
pp. E32-E39 ◽  
Author(s):  
Kirsten R. Poore ◽  
Jane K. Cleal ◽  
James P. Newman ◽  
Julian P. Boullin ◽  
David E. Noakes ◽  
...  
Keyword(s):  
Body Composition ◽  
Insulin Sensitivity ◽  
Glucose Homeostasis ◽  
Area Under The Curve ◽  
Postnatal Growth ◽  
Female Offspring ◽  
Postnatal Life ◽  
Intravenous Glucose ◽  
Ad Libitum ◽  
Early Postnatal Life

The early-life environment has implications for risk of adult-onset diseases, such as glucose intolerance, insulin insensitivity, and obesity, effects that may occur with or without reduced birth weight. We determined the consequences of nutrient restriction in early gestation and early postnatal life and their interactions on postnatal growth, body composition, and glucose handling. Ewes received 100% (C, n = 39) or 50% nutritional requirements (U, n = 41) from 1 to 31 days gestation and 100% thereafter. Male and female offspring (singleton/twin) from C and U ewes were then fed either ad libitum (CC n = 22, UC n = 19) or to reduce body weight to 85% of target from 12 to 25 wk of age (CU n = 17, UU n = 22) and ad libitum thereafter. At 1.5 and 2.5 yr, glucose handling was determined by area under the curve (AUC) for glucose and insulin concentrations following intravenous glucose (0.5 g/kg body wt). Insulin sensitivity was determined at 2.5 yr following intravenous insulin (0.5 IU/kg). In females, postnatal undernutrition reduced ( P < 0.05) glucose AUC at both ages, regardless of prenatal nutrition. Postnatal undernutrition did not affect insulin secretion in females but enhanced insulin-induced glucose disappearance in singletons. Poor early postnatal growth was associated with increased fat in females. In males, glucose tolerance was unaffected by undernutrition despite changes in insulin AUC dependent on age, treatment, and single/twin birth. Nutrition in early postnatal life has long-lasting, sex-specific effects on glucose handling in sheep, likely due, in females, to enhanced insulin sensitivity. Improved glucose utilization may aid weight recovery but have negative implications for glucose homeostasis and body composition over the longer term.

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