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Biomedical subjects

Terence Stephenson

Publications and source records attributed to Terence Stephenson.

At least 19 recordsLinked to original sources
PubMed2007

Effects of maternal parity and late gestational nutrition on mRNA abundance for growth factors in the liver of postnatal sheep.

The liver is a major metabolic and endocrine organ in growing neonates, but the extent to which its hormone receptor (R) sensitivity is potentially determined by maternal parity and the mother's nutritional environment is unknown. This was therefore investigated by sampling livers from postnatal sheep born to nulliparous or multiparous mothers. Offspring were sampled 1 or 30 days after birth from mothers consuming either 100 or 50% [i.e., nutrient-restricted (NR) group] of total metabolizable energy requirements from 110 days gestation to term ( approximately 147 days). Regardless of maternal diet, offspring of nulliparous mothers were lighter at birth and had smaller livers. By 1 mo of age, they exhibited catch-up growth, an adaptation not seen when mothers were NR, but they retained their lighter livers. At both sampling ages, livers from offspring born to nulliparous mothers exhibited increased mRNA abundance for growth hormone (GH) receptor, IGF-IR, plus hepatocyte growth factor (HGF); and at day 1 only IGF-I, but not IGF-IIR mRNA was decreased. In addition, mRNA for IGF-II, the HGFR, c-Met, and Bax were persistently reduced in these offspring. Effects of parity were largely unaffected by maternal nutrient restriction. Maternal parity therefore has a substantial effect on liver size during postnatal development and its receptor population that is not dependent on maternal diet. First-born offspring appear to exhibit a resetting of the endocrine control of hepatic growth within the HGF and GH-IGF axis, which could have later consequences after their growth has caught up.

Aging↗
PubMed2007

Infant nutrition and stereoacuity at age 4-6 y.

BACKGROUND: Breastfeeding has been reported to benefit visual development in children. A higher concentration of docosahexaneoic acid (DHA) in breast milk than in formula has been proposed as one explanation for this association and as a rationale for adding DHA to infant formula, but few long-term data support this possibility. OBJECTIVE: The objectives of the study were, first, to test the hypothesis that breastfeeding benefits stereoscopic visual maturation and, second, if that benefit is shown, to ascertain whether it is mediated by the dietary intake of DHA. DESIGN: Stereoacuity was measured by using the random dot E test (primary outcome), and visual acuity was measured by using the Sonksen-Silver acuity system (secondary outcome) in previously breastfed (n = 78) or formula-fed (n = 184) children aged 4-6 y who had been followed prospectively from birth. In the formula-fed group, children were randomly assigned to receive formula with either DHA or arachidonic acid (n = 94) or a control formula (n = 90) for the first 6 mo. RESULTS: Breastfed children had a significantly (P = 0.001) greater likelihood of foveal stereoacuity (high-grade or < 100 s/arc) than did formula-fed children (odds ratio: 2.5; 95% CI: 1.4, 4.5) independent of potential confounding (P = 0.005). Stereoacuity did not differ significantly between children randomly assigned to DHA-supplemented or control formula. None of the groups differed in Sonksen-Silver visual acuity. CONCLUSIONS: These findings support the hypothesis that breastfeeding benefits long-term stereoscopic development. An effect of DHA cannot be excluded, but the lack of difference in stereoacuity between infants randomly assigned to DHA-containing and those assigned to control formula raises the hypothesis that factors in breast milk other than DHA account for the observed benefits.

Breast Feeding↗
PubMed2006

Promotion of faster weight gain in infants born small for gestational age: is there an adverse effect on later blood pressure?

BACKGROUND: Being born small for gestational age is associated with later risk factors for cardiovascular disease, such as high blood pressure. Promotion of postnatal growth has been proposed to ameliorate these effects. There is evidence in animals and infants born prematurely, however, that promotion of growth by increased postnatal nutrition increases rather than decreases later cardiovascular risk. We report the long-term impact of growth promotion in term infants born small for gestational age (birth weight <10th percentile). METHODS AND RESULTS: Blood pressure was measured at 6 to 8 years in 153 of 299 (51%) of a cohort of children born small for gestational age and randomly assigned at birth to receive either a standard or a nutrient-enriched formula. The enriched formula contained 28% more protein than standard formula and promoted weight gain. Diastolic and mean (but not systolic) blood pressure was significantly lower in children assigned to standard compared with nutrient-enriched formula (unadjusted mean difference for diastolic blood pressure, -3.2 mm Hg; 95% CI, -5.8 to -0.5; P=0.02) independent of potential confounding factors (adjusted difference, -3.5 mm Hg; P=0.01). In observational analyses, faster weight gain in infancy was associated with higher later blood pressure. CONCLUSIONS: In the present randomized study targeted to investigate the effect of early nutrition on long-term cardiovascular health, we found that a nutrient-enriched diet increased later blood pressure. These findings support an adverse effect of relative "overnutrition" in infancy on long-term cardiovascular disease risk, have implications for the early origins of cardiovascular disease hypothesis, and do not support the promotion of faster weight gain in infants born small for gestational age.

Adult↗
PubMed2006

The medicines for children agenda in the UK.

Children can expect the medicines prescribed for them to have at least as good an evidence base as in adult practice. Current licensing arrangements in the UK ensure a rigorous assessment of most drugs used for adults, whereas prescribing outside the licence is relatively common for children. Until the evidence base is increased, consensus guidelines or formularies, such as the new British National Formulary for Children, provide some protection for children and prescribers. For the future, there is optimism that the dearth of research on which to base children's prescribing will be addressed by new initiatives, such as the UK Medicines for Children Research Network and draft EU legislation providing incentives to industry.

Biomedical Research↗
PubMed2005

Ontogeny and nutritional programming of adiposity in sheep: potential role of glucocorticoid action and uncoupling protein-2.

Increased glucocorticoid action and adipose tissue inflammation contribute to excess adiposity. These adaptations may be enhanced in offspring exposed to nutrient restriction (NR) in utero, thereby increasing their susceptibility to later obesity. We therefore determined the developmental ontogeny of glucocorticoid receptor (GR), 11beta-hydroxysteroid dehydrogenase (11betaHSD) types 1 and 2, and uncoupling protein (UCP)-2 mRNA in perirenal adipose tissue between late gestation and 6 mo after birth in the sheep, as well as the effect of maternal NR targeted between early to mid (28-80 days, term approximately 147 days)- or late (110-147 days) gestation. GR and 11betaHSD1 mRNA increased with fat mass and were all maximal within the 6-mo observation period. 11betaHSD2 mRNA abundance demonstrated a converse decline, whereas UCP2 peaked at 30 days. GR and 11betaHSD1 mRNA abundance were strongly correlated with total and relative perirenal adipose tissue weight, and UCP2 was strongly correlated with GR and 11betaHSD1 mRNA. Early- to midgestational NR increased GR, 11betaHSD1, and UCP2 mRNA, but decreased 11betaHSD2 mRNA abundance, an adaptation reversed with late-gestational NR. We conclude that the continual rise in glucocorticoid action and fat mass after birth may underlie the development of later obesity. The magnitude of this adaptation is partly dependent on maternal food intake through pregnancy.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed2005

Maternal nutritional programming of fetal adipose tissue development: long-term consequences for later obesity.

As obesity reaches epidemic levels in the United States there is an urgent need to understand the developmental pathways leading to this condition. Obesity increases the risk of hypertension and diabetes, symptoms of which are being seen with increased incidence in children. Adipocyte development begins in the fetus and, in contrast to all other tissues whose growth ceases in late juvenile life, it has the capacity for "unlimited" growth. In normal healthy individuals, the increase in fat mass with age is accompanied by a parallel increase in cortisol sensitivity, i.e., increased glucocorticoid receptor abundance and increased activity of the enzyme 11beta hydroxysteroid dehydrogenase type 1. Enhanced adipocyte sensitivity to cortisol is promoted in offspring born to mothers that were nutrient-restricted in utero in conjunction with increased peroxisome proliferator activated receptor alpha. This adaptation only appears to be associated with greater fat mass in the offspring when maternal nutrient restriction is confined to late gestation, coincident with the period of maximal fetal growth. In these offspring, increased fat mass is accompanied by glucose intolerance and insulin resistance, in conjunction with an adipose tissue specific reduction in glucose transporter 4 abundance. In conclusion, changes in maternal and, therefore, fetal nutrient supply at specific stages of gestation have the potential to substantially increase the risk of those offspring becoming obese in later life. The extent to which changes in dietary habits, both during pregnancy and in later life, may act to contribute to the current explosion in childhood and adult obesity remains a scientific and public health challenge to us all.

Adipocytes↗
PubMed2005

How children's responses to drugs differ from adults.

Children are not small adults. However, the main thesis of this review will be that children's responses to drugs have much in common with the responses in adults and indeed in other mammals. Often, it is assumed that drug effects differ in children but in reality this perception often arises because the drugs have not been adequately studied in paediatric populations of different ages and with different diseases. There may also be difficulties in measuring small but significant effects because the outcome measures are more difficult to assess in children. In some cases, stage of development can alter the action of, and response to, a drug - a truly age-dependent difference in pharmacodynamics. This may be true of both the desired action and adverse events. Examples are given. Programming by drugs is also a phenomenon almost exclusive to early life, i.e. permanent effects result from a stimulus applied at a sensitive point in development ('critical window'), often in fetal or neonatal life. Again, examples are discussed. Different pathophysiology, different disease variants, different pharmacodynamics, different 'host' response and different adverse drug reactions can all explain why some drugs behave differently in children. However, we need to explore ways to avoid re-inventing the wheel by determining how data from adult animal and human models can help inform research and practice for children.

Adult↗
PubMed2004

Peri-implantation undernutrition programs blunted angiotensin II evoked baroreflex responses in young adult sheep.

An adverse environment around conception and implantation influences later fetal growth and development to term in humans and sheep. Indeed, preimplantation undernutrition of rats elevated the systolic blood pressure of the resultant adult offspring. In this study, adult cardiovascular function is examined in a slower growing, non-litter-bearing species after peri-implantation undernutrition. Eight ewes were fed to 50% equivalent food intake of 12 control ewes from 1 to 30 days (term approximately 147 days) only. Following consumption of an adequate diet to term, natural lambing, and then weaning, resting cardiovascular status and baroreflex function were examined in the resultant young adult offspring. Birth weight and postnatal growth to 1 year of age were unaffected by early undernutrition; however, nutrient-restricted sheep had increased pulse pressure, a reduced rate pressure product, and a leftward shift in their baroreflex function curve. Baroreflex sensitivity during angiotensin II infusion was also blunted in early nutrient-restricted sheep but the tachycardia following a reduction in central blood pressure appeared potentiated, relative to controls. The data suggest that peri-implantation undernutrition may program long-term cardiovascular dysfunction that ultimately increases the risk of hypertension later in life. An increase in regional angiotensin II activity during this critical early phase of development is a likely candidate mechanism for the effects observed. The data have broad implications for the health outcome of those offspring from mothers who were poorly nourished during early, often unknown pregnancy and for embryos artificially manipulated because of infertility treatment.

Angiotensin II↗
PubMed2004

Ontogeny and nutritional manipulation of the hepatic prolactin-growth hormone-insulin-like growth factor axis in the ovine fetus and in neonate and juvenile sheep.

The somatotrophic axis is the main endocrine system regulating postnatal growth; however, prenatal growth is independent of growth hormone (GH). Fetal development relies on the coordinated actions of a range of hormones, including insulin-like growth factors (IGF), and prolactin (PRL), in the control of differentiation, growth and maturation. In the sheep the abundance peaks for liver IGF-II and PRL receptors occur during late gestation while that for IGF-I receptor occurs at birth. All receptors, with the exception of GH receptor subsequently decrease by age 6 months. It has been proposed that maternal undernutrition during gestation regulates the maturation of the fetal hypothalmic-pituitary-adrenal axis and endocrine sensitivity. Critically, the timing of the nutritional insult may affect the magnitude of reprogramming. Maternal malnutrition during early to mid-gestation (3.2-3.8 MJ/d (60% total metabolisable energy requirements) v. 8.7-9.9 MJ/d (150% total metabolisable energy requirements) between 28 and 80 d of gestation) had no effect on body or liver weight. Nutrient-restricted (NR) fetuses sampled at 80 d (mid-gestation) showed up-regulation of hepatic PRL receptor, but following refeeding the normal gestational rise in PRL and GH receptors did not occur. Hepatic IGF-II receptor was down regulated in NR fetuses at both mid- and late gestation. Conversely, 6-month-old offspring showed no difference in the abundance of either GH receptor or PRL receptor, while IGF-II mRNA was increased. Offspring of ewes malnourished during late gestation (9.1 MJ/d (60% total metabolisable energy requirements) v. 12.7 MJ/d (100% total metabolisable energy requirements) from 110 d of gestation to term) showed reduced abundance of hepatic GH and PRL receptor mRNA. In conclusion, maternal undernutrition during the various stages of gestation reprogrammed the PRL-GH-IGF axis. Nutritional regulation of cytokine receptors may contribute to altered liver function following the onset of GH-dependent growth, which may be important in regulating endocrine adaptations during subsequent periods of nutritional deprivation.

Animal Nutritional Physiological Phenomena↗
PubMed2004

Timing of nutrient restriction and programming of fetal adipose tissue development.

It is apparent from epidemiological studies that the timing of maternal nutrient restriction has a major influence on outcome in terms of predisposing the resulting offspring to adult obesity. The present review will consider the extent to which maternal age, parity and nutritional restriction at defined stages of gestation can have important effects on fat deposition and endocrine sensitivity of adipose tissue in the offspring. For example, in 1-year-old sheep the offspring of juvenile mothers have substantially reduced fat deposition compared with those born to adult mothers. Offspring of primiparous adult mothers, however, show increased adiposity compared with those born to multiparous mothers. These offspring of multiparous ewes show retained abundance of the brown adipose tissue-specific uncoupling protein 1 at 1 month of age. A stimulated rate of metabolism in brown fat of these offspring may act to reduce adipose tissue deposition in later life. In terms of defined windows of development that can programme adipose tissue growth, maternal nutrient restriction targetted over the period of maximal placental growth results in increased adiposity at term in conjunction with enhanced abundance of mRNA for the insulin-like growth factor-I and -II receptors. In contrast, nutrient restriction in late gestation, coincident with the period of maximal fetal growth, has no major effect on adiposity but results in greater abundance of specific mitochondrial proteins, i.e. voltage-dependent anion channel and/or uncoupling protein 2. These adaptations may increase the predisposal of these offspring to adult obesity. Increasing maternal nutrition in late gestation, however, can result in proportionately less fetal adipose tissue deposition in conjunction with enhanced abundance of uncoupling protein 1.

Adipose Tissue↗
PubMed2004

Neurodevelopment in children born small for gestational age: a randomized trial of nutrient-enriched versus standard formula and comparison with a reference breastfed group.

OBJECTIVE: Many studies have shown that children born small for gestational age (SGA) are at a neurodevelopmental disadvantage. We have shown that nutrient enrichment of formula fed to term SGA infants improves their growth and hypothesized that it also would improve their neurodevelopmental outcome. DESIGN: A randomized, controlled trial of standard term-infant (n = 147) or nutrient-enriched (n = 152) formula for the first 9 months. A reference group of 175 breastfed SGA infants was also recruited. SETTING: Subjects were recruited in 5 maternity hospitals in Cambridge, Nottingham, and Leicester, all in the United Kingdom. PARTICIPANTS: Healthy, term infants (gestation: > or =37 weeks) with birth weight <10th centile. OUTCOME MEASURES: Bayley mental and psychomotor scores at 18 months (primary) and developmental scores from Knobloch, Pasamanick, and Sherrard's developmental screening inventory at 9 months (secondary). RESULTS: There was no significant intergroup difference in Bayley Mental Development Index (MDI) or Psychomotor Development Index (PDI) scores at 18 months. However, at 9 months, children fed the enriched formula had a significantly lower developmental quotient (99.5 vs 102.0; 95% confidence interval [CI] for difference: -4.6, -0.4). A significant disadvantage was seen in girls (-5.1; 95% CI: -7.8, -2.4) but not in boys (0.9; 95% CI: -2.4, 4.2). Breastfed infants had significantly higher MDI and PDI scores at 18 months than formula-fed infants. Confounding factors accounted for approximately 34% of the observed association between breastfeeding and MDI score and none of the association between breastfeeding and PDI score. CONCLUSIONS: The previously reported enhanced linear growth in SGA children fed enriched formula was not matched by a neurodevelopmental advantage. At 9 months, girls fed the enriched formula had a significant developmental disadvantage, although this was not seen at 18 months. Later follow-up will determine any long-term effects on health or development. Meanwhile, use of enriched formula for term SGA children should not be promoted. It seems that breastfeeding may be especially beneficial for neurodevelopment in children born SGA.

Breast Feeding↗
PubMed2003

Growth and development of premature infants fed predominantly human milk, predominantly premature infant formula, or a combination of human milk and premature formula.

BACKGROUND: In a recent meta-analysis, human milk feeding of low birth-weight (LBW) infants was associated with a 5.2 point improvement in IQ tests. However, in the studies in this meta-analysis, feeding regimens were used (unfortified human milk, term formula) that no longer represent recommended practice. OBJECTIVE: To compare the growth, in-hospital feeding tolerance, morbidity, and development (cognitive, motor, visual, and language) of LBW infants fed different amounts of human milk until term chronologic age (CA) with those of LBW infants fed nutrient-enriched formulas from first enteral feeding. METHODS: The data in this study were collected in a previous randomized controlled trial assessing the benefit of supplementing nutrient-enriched formulas for LBW infants with arachidonic acid and docosahexaenoic acid. Infants (n = 463, birth weight, 750-1,800 g) were enrolled from nurseries located in Chile, the United Kingdom, and the United States. If human milk was fed before hospital discharge, it was fortified (3,050-3,300 kJ/L, 22-24 kcal/oz). As infants were weaned from human milk, they were fed nutrient-enriched formula with or without arachidonic and docosahexaenoic acids (3,300 kJ/L before term, 3,050 kJ/L thereafter) until 12 months CA. Formula fed infants were given nutrient-enriched formula with or without added arachidonic and docosahexaenoic acids (3,300 kJ/L to term, 3,050 kJ/L thereafter) until 12 months CA. For the purposes of this evaluation, infants were categorized into four mutually exclusive feeding groups: 1) predominantly human milk fed until term CA (PHM-T, n = 43); 2) >/= 50% energy from human milk before hospital discharge (>/= 50% HM, n = 98); 3) < 50% of energy from human milk before hospital discharge (< 50% HM, n = 203); or 4) predominantly formula fed until term CA (PFF-T, n = 119). RESULTS: PFF-T infants weighed approximately 500 g more at term CA than did PHM-T infants. This absolute difference persisted until 6 months CA. PFF-T infants were also longer (1.0-1.5 cm) and had larger head circumferences (0.3-1.1 cm) than both PHM-T and >/= 50% HM infants at term CA. There was a positive association between duration of human milk feeding and the Bayley Mental Index at 12 months CA (P = 0.032 full and P = 0.073 reduced, statistical models) after controlling for the confounding variables of home environment and maternal intelligence. Infants with chronic lung disease fed >/= 50% HM until term CA (n = 22) had a mean Bayley Motor Index about 11 points higher at 12 months CA compared with infants PFF-T (n = 24, P = 0.033 full model). CONCLUSION: Our data suggest that, despite a slower early growth rate, human milk fed LBW infants have development at least comparable to that of infants fed nutrient-enriched formula. Exploratory analysis suggests that some subgroups of human milk fed LBW infants may have enhanced development, although this needs to be confirmed in future studies.

Adult↗
PubMed2003

Differential effects of age and sex on the postnatal responsiveness of brown adipose tissue to prolactin administration in rats.

Previous studies have shown that prolactin administration to pregnant rats results in offspring with enhanced abundance of the brown adipose tissue-specific uncoupling protein (UCP) 1. The present study therefore aimed to determine whether a similar effect was observed after birth and if the sex of the animal further influenced the responsiveness of brown adipose tissue mitochondria to prolactin administration. Daily prolactin injections were therefore commenced at 15, 35 or 60 days of age and continued for 4 days. The abundance of UCP1 was unchanged with age in females but decreased between 15 and 35 days in males and was lower in males than females by 60 days of age. Cytochrome c abundance remained unchanged with postnatal age in both males and females and was consistently higher in males at each sampling age. Prolactin decreased the abundance of UCP1 and cytochrome c when administered to female rats at 35 and 60 days of age, but had no effect at 15 days. In contrast, prolactin had no effect on UCP1 in male rats at any age, but did stimulate the abundance of cytochrome c at 15 days of age. In conclusion, the administration of prolactin to postnatal rats over the period in which maturation of the hypothalamic-pituitary axis and brown adipose tissue function is occurring did not enhance UCP1 abundance. In females, prolactin actually caused a reduction in UCP1 suggesting that in rats it is only prior to birth that prolactin has a stimulatory role on brown adipose tissue development.

Adipose Tissue, Brown↗
PubMed2003

Differential effects of fetal number and maternal nutrition in late gestation on prolactin receptor abundance and adipose tissue development in the neonatal lamb.

The present study examined the extent to which abundance of the prolactin receptor (PRLR) and a range of primary mitochondrial proteins are influenced by either maternal nutrition and/or fetal number in adipose tissue. Pregnant sheep were control fed [consuming 100% of total metabolizable energy (ME) requirements (taking into account requirements for both ewe maintenance and growth of the conceptus to produce a 4.5-kg lamb at term) for that stage of gestation] or were nutrient restricted (consuming 60% of total ME requirements). All ewes lambed normally at term and both perirenal adipose and hepatic tissues were sampled within 6 h of birth. Plasma membranes and mitochondria were prepared and analyzed using immunoblotting for abundance of PRLR and/or cytochrome c, voltage-dependent anion channel (VDAC), and uncoupling protein-1 (UCP1). Irrespective of maternal nutrition, abundance of specific isoforms of PRLR were significantly higher in adipose tissue sampled from twins compared with singletons and total UCP1 concentration per milligram of tissue was increased (p < 0.05). There was no effect of fetal number on PRLR abundance in the liver. Maternal nutrient restriction resulted in an increased abundance of both cytochrome c (p < 0.001) and VDAC in adipose tissue of twins but not singletons. This occurred despite maternal nutrition having no effect on either lamb body or adipose tissue weights, although both were lower (p < 0.05) in twins compared with singletons. In conclusion, fetal adipose tissue development is highly sensitive to nutritionally mediated changes in late gestation. An increase in fetal number results in greater PRLR abundance, which, in conjunction with a decrease in maternal nutrition, results in up-regulation of specific mitochondrial proteins.

Adipose Tissue↗
PubMed2002

Differential effects of leptin on thermoregulation and uncoupling protein abundance in the neonatal lamb.

As the role of leptin in energy balance in neonate is unknown, we investigated the effect of acute (2 h) and chronic (7 days) administration of leptin (100 microg/day) on thermoregulation and mitochondrial protein abundance in adipose tissue. The concentration of uncoupling protein (UCP)1 and voltage-dependent anion channel (VDAC) located on the inner and outer mitochondrial membranes, respectively, were measured. Administration of leptin prevented the normal decline in colonic temperature over the first few hours and days after birth. It subsequently accelerated the loss of both mRNA and protein for UCP1 but had no effect on VDAC abundance. At seven days of age, colonic temperature was correlated strongly with both mRNA abundance and thermogenic potential of UCP1 in leptin-treated but not control lambs, indicating more effective use of UCP1 for heat production following leptin administration. Leptin had no effect on weight gain or adipose tissue deposition; at one day of age only, leptin mRNA was correlated positively with adipose tissue weight. In conclusion, leptin administration to neonatal lambs improves thermoregulation and promotes the loss of UCP1 in brown adipose tissue.

Adipose Tissue, Brown↗
PubMed2002

Ambient temperature, maternal dexamethasone, and postnatal ontogeny of leptin in the neonatal lamb.

The influence of route of delivery, ambient temperature, maternal dexamethasone treatment, and postnatal age on plasma concentrations of leptin or leptin mRNA abundance in perirenal adipose tissue was examined from 6-h-old lambs, born vaginally or delivered by cesarean section into warm (30 degrees C) or cool (15 degrees C) ambient temperatures, and from cesarean section-delivered lambs whose mothers had been treated with dexamethasone beginning 2 d before parturition. The ontogeny of leptin during the first month of postnatal life was also examined. In lambs born into a cool ambient temperature, but not in those born to dexamethasone-treated mothers, leptin mRNA abundance decreased within 6 h of birth. Plasma concentrations of leptin decreased during the first 6 h of life, an adaptation delayed by cesarean section birth. After the first day of postnatal life, both plasma concentrations of leptin and its mRNA increased to peak at 7 d of age and were positively correlated with each other, as well as with whole-body and perirenal adipose tissue weights. A similar relationship was not observed after 7 d of age, as plasma leptin declined despite an increase in adipose tissue weight. In conclusion, route of delivery, ambient temperature, or maternal dexamethasone therefore delays the rate of leptin disappearance after birth. Concomitantly, leptin abundance was only associated with body and adipose tissue weights for 1 week after birth, which may be coincident with the onset of peak lactation and the time at which nutrient supply should no longer be limiting to the neonate.

Adaptation, Physiological↗