Lower ghrelin levels have been related to slower growth in small for gestational age infants, and infants with higher cord leptin levels have been reported to gain weight more slowly from birth to 2 yr. This study investigated whether cord blood ghrelin and leptin levels are related to weight gain up to 12 wk of age. One hundred infants were weighed at birth and at 12 wk, and cord blood was assayed for ghrelin and leptin. The mean (؎SD) birth weight was 3.458 (0.433) kg (median, 3.390; range, 2.510 -4.615 kg). The mean (؎SD) leptin level was 10.1 (6.7) ng/ml (median, 8.4; range, 1.6 -36.7 ng/ml), and that of ghrelin was 760.9 (282.9) pg/ml (median, 770; range, 210-1670 pg/ml). Higher birth weight was associated with slower weight gain. Leptin was correlated with birth weight, but ghrelin was not, and leptin and ghrelin levels were not significantly correlated with one another. With birth weight as a control variable, ghrelin was significantly associated with slow weight gain ( 2 ؍ 7.20 with 1 df; P < 0.01), although leptin was not ( 2 ؍ 1.59 with 1 df; P > 0.1). In conclusion, lower cord ghrelin levels are associated with slower weight gain from birth to 3 months of age. R ESEARCH IN BOTH rodents and humans has shownthat leptin is an important regulator of appetite and energy balance (1, 2). Rare forms of childhood obesity arising from leptin gene (3, 4) and receptor (5) mutations have demonstrated the crucial importance of leptin in the regulation of appetite and weight gain. These infants were of normal birth weight, but gained weight rapidly between 2 and 4 months of age. Healthy infants with higher cord leptin levels at birth have since been shown to gain weight more slowly over the period from birth to 4 months (6). More recently, the gut peptide ghrelin has been described (7), and it has also been detected in cord blood (8). Ghrelin may be implicated in the stimulation of appetite and GH release in both rodents (9, 10) and humans (11). Human subjects administered ghrelin by iv injection reported increased ratings of hunger on a visual analog scale (11). High fasting ghrelin levels have also been reported in young adults with Prader-Willi syndrome (12, 13); therefore, altered ghrelin concentrations could be linked to the hyperphagia and rapid weight gain in childhood and adolescence that are characteristic of this syndrome. High circulating ghrelin concentrations have been described in small for gestational age (SGA) neonates (14), and SGA infants showing slower weight gain over the first year of life had lower ghrelin levels after an iv glucose load (15). These findings suggest that leptin and ghrelin may be important regulators of weight gain in early infancy, and we therefore examined the relationship between cord blood ghrelin and leptin in relation to weight gain up to 3 months of age. Subjects and Methods SubjectsWomen with singleton term pregnancies were recruited consecutively from the delivery suite of the Royal Victoria Infirmary (Newcastleupon-Tyne, UK). The mothers recruited were in good he...
ABSTRACT:Our aim was to study the feeding behavior of healthy term infants in the first week of life and determine whether this was related to cord blood leptin, ghrelin, and insulin. A total of 100 healthy bottle-fed infants were studied by weighing bottles of milk before and after feeds. Leptin, total ghrelin, and insulin concentrations were measured in cord blood. Mean (SD) birth weight was 3.46 (0.43) kg. Mean milk intake increased from 196.7 (83.0) g on d 1 to 585.0 (128.4) g on d 7. Milk intake over the first 6 d was significantly associated with weight gain to d 7. There was no relationship between cord ghrelin or leptin and milk intake or feed frequency. Cord blood insulin was inversely related to the mean daily number of feeds over the first 6 d (r ϭ Ϫ0.21, p Ͻ 0.05). Birth weight and milk intake are the major determinants of weight gain in the first week of life in healthy bottle-fed infants. Total cord ghrelin and leptin are not directly related to milk intake or feed frequency in the first week of life. Circulating insulin concentrations may have a role in the initiation of feeding behavior. Ghrelin is a 28-amino-acid peptide secreted primarily by the stomach (1) and by other tissues including the pancreas in fetal life. Ghrelin is the first natural ligand for the growth hormone secretagogue receptor (GHS-R). In addition to stimulating growth hormone (GH) release, ghrelin has a potent orexigenic effect (2,3) and is involved in feeding initiation and termination. At least some of these actions appear to be mediated via the vagus nerve (4). Ghrelin secretion is pulsatile, with increased secretion during fasting and lower levels after food intake (5,6).Leptin is expressed and secreted by adipocytes in white adipose tissue. Leptin circulates in plasma at concentrations that are proportional to fat mass and provides the CNS with feedback regarding overall nutritional status. Leptin deficient patients are hyperphagic and develop morbid obesity, while leptin has anorectic effects in humans (7). The relationship between obesity and insulin resistance is widely recognized (8), and humoral signals from compounds like ghrelin, leptin, and insulin act on a hypothalamic neuronal network involved in the central regulation of appetite. One network of neurons is associated with appetite inhibition (including proopiomelanocortin or POMC) and one with appetite stimulation (neuropeptide-Y or NPY) (9,10).Whether the hormonal regulators of feeding behavior in adults function in a similar manner in infancy is less well known, although there is evidence to suggest that this is the case. The fact that infants will consume more of a low-energy than a high-energy feed (11,12) suggests that a homeostatic mechanism regulates feeding behavior. Growth in infancy is related to nutritional intake and therefore potentially to the circulating levels of compounds like ghrelin, insulin, and leptin. Ghrelin secretion has been found to be relatively refractory to the effects of feeding in the neonatal period, and the authors have suggest...
This study confirms that suckling is a potent stimulus to thirst in the mother, and is not associated with vasopressin release or dependent on any measurable alterations in osmoregulation. What actually stimulates thirst during breast feeding remains unknown, but there are two potential explanations for these observations: (1) suckling sends nerve impulses to the paraventricular and supraoptic nuclei in the hypothalamus which may have afferents within the central nervous system which stimulates a thirst response simultaneous with oxytocin release; (ii) a learned anticipation of thirst may be occurring in a situation associated with expectant fluid loss to preserve homeostasis.
<p>Strong winds and extremes in precipitation are capable of producing devastating socio-economic impacts across Europe. Although it is well known that individually these drivers cause billions of Euros of damage, their combined impacts are less well understood. Previous work has typically either focused on daily or seasonal timescales, demonstrating that compound wind and precipitation events are commonly associated with passing cyclones or particularly wet and windy years respectively. This study systematically investigates the relationships between national wind and flood damage metrics at all timescales ranging from daily to seasonal during the winter season. This work is completed using high resolution meteorological reanalysis and river flow datasets to explore the historical period (1980-present). As well as this, data from the UKCP18 climate projections at 2.2km and 12km resolution is used to understand historical sampling uncertainty, and the possible impacts of future climate change.</p><p>The correlation between national aggregate wind gusts and precipitation peaks at ~10 days; whereas, the correlation between national aggregate wind gusts and river flows peaks at ~3 weeks. When using more impact focussed metrics of compound wind and flood events, such as storm severity and flooding indices, the strongest correlations are seen at seasonal timescales. Results show the historical correlation between wind and flood damage becomes weaker as the definition of the metrics become more impact focussed, and this is true across all timescales from daily to seasonal. This change in relationship is of key importance to the insurance industry who require actionable information based on both the meteorological hazards and on the exposure of their portfolios. The work is designed to support climate analytics for financial institutions, as part of the UK Centre for Greening Finance and Investments (UKCGFI). Results incorporating the impacts of climate change on compound wind and flood events will also be discussed.</p>
Excess body weight is thought to increase the risk of aggressive prostate cancer (PCa), although the biological mechanism is currently unclear. Body fatness is positively associated with a diminished cellular response to insulin and biomarkers of insulin signalling have been positively associated with PCa risk. We carried out a two-pronged systematic review of (a) the effect of reducing body fatness on insulin biomarker levels and (b) the effect of insulin biomarkers on PCa risk, to determine whether a reduction in body fatness could reduce PCa risk via effects on the insulin signalling pathway. We identified seven eligible randomised controlled trials of interventions designed to reduce body fatness which measured insulin biomarkers as an outcome, and six eligible prospective observational studies of insulin biomarkers and PCa risk. We found some evidence that a reduction in body fatness improved insulin sensitivity although our confidence in this evidence was low based on GRADE (Grading of Recommendations, Assessment, Development and Evaluations). We were unable to reach any conclusions on the effect of insulin sensitivity on PCa risk from the few studies included in our systematic review. A reduction in body fatness may reduce PCa risk via insulin signalling, but more high-quality evidence is needed before any conclusions can be reached regarding PCa.
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