Search Results

You are looking at 1 - 10 of 184 items for :

  • neonatal adaptation x
Clear All
Free access

Malathi Srinivasan, Paul Mitrani, Gigani Sadhanandan, Catherine Dodds, Suhad Shbeir-ElDika, Shanthie Thamotharan, Hussam Ghanim, Paresh Dandona, Sherin U Devaskar and Mulchand S Patel

observation, we hypothesize that hypothalamic malprogramming predisposing to later onset of obesity occurs immediately in neonatal HC rats in response to the HC dietary modification as observed in the case of pancreatic islets and that these early adaptations

Free access

M G Gnanalingham, A Mostyn, J Wang, R Webb, D H Keisler, N Raver, M C Alves-Guerra, C Pecqueur, B Miroux, T Stephenson and M E Symonds

( Schwartz et al. 1996 , Friedman & Halaas 1998 , Ahima & Flier 2000 ). However, its exact role in the neonate has yet to be fully determined. In the human fetus, plasma leptin concentrations increase with gestational age ( Yuen et al. 1999 , Cetin et

Free access

Benoit Cox, Heleen Roose, Annelies Vennekens and Hugo Vankelecom

major regulatory pathways in the pituitary stem cell compartment during the different conditions of embryonic and neonatal development, homeostasis, adaptation and regeneration. In the second part, we discuss what is known about these pathways in

Open access

M A Hyatt, D H Keisler, H Budge and M E Symonds

accompanied by adaptations in its inflammatory and related responses ( Sharkey et al . 2009 b ). We hypothesised that gene expression of key regulators of adipose tissue function and composition would be increased in firstborn offspring during early postnatal

Free access

A J Forhead and A L Fowden

. (2013) 129 145 100 – – – Abnormal neonatal cardiovascular adaptations Breall et al . (1984) In fetal sheep, thyroidectomy reduces bodyweight, individual organ weights, and skeletal growth of the vertebrae and limbs ( Table 2 ). The

Free access

Luba Sominsky, Ilvana Ziko, Thai-Xinh Nguyen, Julie Quach and Sarah J Spencer

). During the early neonatal period when optimal nutrition is required to support an organism’s growth, leptin has an additional role, that of stimulating the development of satiety-signalling projections from the ARC to other hypothalamic nuclei ( Bouret

Restricted access

F Rivero, L Goya, C Aláez and A M Pascual-Leone

Abstract

The purpose of the present study was to investigate the influence of nutrients and insulin on IGFs and their binding proteins (IGFBPs) during the fetal and neonatal periods of three rat populations: (a) rats undernourished by a 35% reduction in the diet from day 16 of gestation, (b) streptozotocin-induced diabetic rats from the same day, or 4 days after birth, and (c) control rats. Fetuses from the diabetic population showed a decrease in insulinemia at 19 and 21 days, along with an increase in glycemia at all stages. Neither glycemia nor insulinemia changed in the fetuses of undernourished mothers, but body weight was decreased at birth. Serum IGF-II decreased at 18 and 19 days of gestation in fetuses from undernourished mothers, and increased at 18, 19 and 21 days in fetuses from diabetic mothers. Serum IGFBPs of low molecular weight (IGFBP-1 and IGFBP-2) increased in the three fetal populations studied, although no changes in serum IGFBPs were found from the effect of undernutrition or diabetes, but fetal liver IGFBP-1 mRNA expression was found to be decreased in undernourished and diabetic animals as compared with controls. In neonatal rats, body weight, insulinemia and serum GH decreased in both undernourished and diabetic rats vs controls, while glycemia decreased in the undernourished and increased in the diabetic group. Serum IGF-II decreased only in diabetic rats and serum IGF-I decreased in both groups. The neonatal serum 30 kDa complex (IGFBP-1 and -2) also increased in undernutrition and diabetes parallel to the expression of mRNA. But, taken together, the changes in IGFBP peptide levels and liver mRNA expression strongly suggest that the 30 kDa complex seems to be composed mostly of IGFBP-1 in the diabetic group and of both IGFBP-1 and -2 in the undernourished animals. The studies of liver mRNA expression of IGFs and IGFBPs confirm the different metabolic control mechanism for the availability of IGFs by the IGFBPs, depending on the animal's maturity. The different adaptation shown by the diabetic neonatal population was confirmed by correlation studies between body weight, glycemia, insulinemia, IGF-I and IGFBPs. The different mechanism of adaptation in diabetic vs undernourished rats seems to be probably due to the decisive role played by hyperglycemia in the diabetic population, and also shows the crucial influence of nutritional status on IGFs and IGFBPs.

Journal of Endocrinology (1995) 145, 427–440

Restricted access

A. ŚLEBODZIŃSKI

SUMMARY

(1) The interaction between thyroid hormone and thyroxine-binding globulin (TBG) has been studied in 39 pigs from eight litters, aged from 12 hr. to 11 days. In addition, single observations were made on six batches of 42 pigs from 1 day to 6 months old and in five newborn sheep.

(2) A rapid increase in the level of the unsaturated TBG capacity was found to occur from the 1st day after birth.

(3) Continuous changes in the unsaturated TBG capacity resulted in a decline in the plasma level of free thyroxine and in a decrease in the uptake of [131I]triiodothyronine by erythrocytes. Equilibrium between the hormonal iodine metabolism and its blood carrier is reached at the end of the 1st week of life.

(4) These findings suggest that in discussing thyroid metabolism in neonatal animals it is important to distinguish between the early neonatal adaptive period and the remainder of the period of thyroid hyperactivity. The physiological implications of the higher level of free thyroxine in the blood after birth for the adaptation to post-uterine life is discussed.

Free access

NB Holdstock, VL Allen, MR Bloomfield, CN Hales and AL Fowden

At birth, the endocrine pancreas must assume a glucoregulatory role if the neonate is to survive the transition from parenteral to enteral nutrition. In species like the horse, neonatal hypoglycaemia is common, which suggests that the glucoregulatory mechanisms are not always fully competent at birth. Hence, this study examined pancreatic beta cell function in newborn foals during nutritional adaptation over the first 10 days post partum. Over a 48 h period at three time intervals after birth (days 1-2, 5-6 and 9-10 post partum), the beta cell responses to suckling and to intravenous administration of glucose, arginine and saline were measured in seven normal pony foals. Basal plasma concentrations of proinsulin, but not insulin or glucose, increased significantly between days 1 and 10. Suckling caused a gradual increase in plasma glucose, which was accompanied by a significant increase in plasma insulin concentrations 15 min after the onset of suckling on days 5 and 9, but not day 1. There was no significant change in plasma proinsulin concentrations in response to suckling at any age. At all ages studied, glucose and arginine administration stimulated an increase in the plasma concentrations of insulin and proinsulin; these beta cell responses did not change significantly with postnatal age. The insulin responses to glucose were significantly greater than those of arginine at each time period. Glucose clearance was significantly slower on day 1 than subsequently. Proinsulin and glucose, but not insulin, concentrations decreased significantly after saline administration at all three ages. At each time period, there was a significant positive relationship between the plasma insulin and proinsulin concentrations, the slope of which was significantly shallower on days 1-2 than subsequently. These results show that equine beta cells are responsive to glucose and arginine and release both insulin and proinsulin during the immediate postnatal period. They also suggest that newborn foals may be insulin resistant on the first day after birth.

Free access

Hershel Raff and Lauren Jacobson

). Successful adaptation to neonatal hypoxia requires a coordinated physiological response, including an increase in the release of glucocorticoids from the adrenal cortex ( Hanukoglu et al. 1995 ). Understanding the mechanisms by which the resulting increase