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ANGELA FAIRNEY and A. A. WEIR

SUMMARY

Study of the offspring from parathyroidectomized and hypercalcaemic rats showed that both high and low levels of maternal plasma calcium produced abnormalities in the offspring. Both groups of offspring had hypocalcaemia at birth which reverted to normal by the 7th day of life. All the offspring grew poorly compared with controls. The growth defect in the offspring of the hypocalcaemic rats was reversed if the offspring were reared by normal rats, and in the offspring of the hypercalcaemic rats was accompanied by abnormalities of the fur, including focal alopecia, which reverted to normal when the offspring were weaned on to a normal diet. The calcium concentration in the milk of the hypercalcaemic rats was higher than that in the milk of normal and parathyroidectomized rats.

In the rat the plasma and milk calcium levels in the mother appeared to be important in the aetiology of neonatal hypocalcaemia and growth. It is suggested that the estimation of the plasma calcium in the mother should become a routine procedure in the investigation of cases of neonatal tetany in infants.

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C Nilsson, D Swolin-Eide, C Ohlsson, E Eriksson, HP Ho, P Bjorntorp and A Holmang

Leptin is involved in regulating food intake, energy balance and bone formation. Increasing evidence suggests that leptin is also involved in fetal growth and development. The aim of this study was to determine if increased maternal leptin is followed by changes in body composition, skeletal growth or hormonal regulation in the adult rat offspring. Pregnant rats were given injections of either human recombinant leptin (3.5 mg/kg, i.p.) or vehicle on days 8, 10 and 12 of gestation. Both genders of leptin-exposed offspring showed significantly reduced adipose tIssue weight at adult age. Skeletal growth and cortical bone dimensions were significantly reduced. Circulating testosterone levels were significantly increased in female leptin-exposed offspring, and male leptin-exposed offspring had significant testicular enlargement. No significant effects were seen on circulating leptin levels or hypothalamic protein levels of the leptin receptor. The results demonstrate that maternally administered leptin is involved in fetal growth and development, leading to lean offspring with reduced skeletal growth.

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D Swolin-Eide, J Dahlgren, C Nilsson, K Albertsson Wikland, A Holmang and C Ohlsson

Events occurring early in life or prenatally are able to play important roles in the pathogenesis of diseases in adult life. Different sorts of stress or hormonal influences, during particular periods of pregnancy, may result in persisting or transient changes in physiology. Glucocorticoids are used for the treatment of a variety of diseases, to promote organ maturation and to prevent preterm delivery. Glucocorticoids are also known to affect skeletal growth and adult bone metabolism. The aim of the present study was to investigate whether exposure to dexamethasone (Dex) during fetal life has any effect on skeletal growth and/or bone mineral density in adult rat offspring. Pregnant rats were given injections of either Dex (100 micro g/kg) or vehicle on days 9, 11 and 13 of gestation. Dex-exposed male but not female rat offspring showed transient increases in crown-rump length and tibia and femur lengths at 3-6 weeks of age. In contrast, the cortical bone dimensions were altered in 12-week-old female but not male Dex-exposed offspring. The areal bone mineral densities of the long bones and the spine, as determined by dual X-ray absorptiometry, and trabecular as well as cortical volumetric bone mineral density, as measured using peripheral quantitative computerized tomography, were unchanged in both male and female Dex-exposed offspring. In conclusion, prenatal Dex exposure affects skeletal growth in a gender-specific manner, while the mineralization of bones is unaffected in both male and female offspring.

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L. AERTS and F. A. VAN ASSCHE

At birth newborn rats from mothers with experimentally induced diabetes show hypertrophy and degranulation of the pancreatic islets. With birth the maternal hyperglycaemic stimulus is removed and during the lactation period the overstimulated B cells can restore their normal secretory activity. The increase of B-cell mass, however, remains retarded for several weeks. By adulthood the endocrine pancreas of offspring from mildly diabetic mothers seems to have recovered from the influence of the abnormal intra-uterine milieu, at least as judged by morphometric examination. In offspring from severely diabetic mothers an increased secretory activity of the individual B cells might be responsible for their sustained hypoglycaemia.

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CW Elton, JS Pennington, SA Lynch, FM Carver and SN Pennington

Maternal diet during pregnancy has been reported to alter the offspring's ability to respond to a glucose challenge. The current studies report changes in basal and insulin-stimulated, in vitro glucose uptake in red (soleus) and white (extensor digitorum longus) muscle fiber types, as well as whole body insulin responsiveness of adult rat offspring associated with their mother's dietary fat and alcohol content during pregnancy. The offspring of Harlan-derived Sprague-Dawley female rats, dosed during pregnancy with ethanol (ETOH) via a liquid diet (35% of calories as ETOH) with either 12% or 35% of calories as fat, were compared with offspring from litters whose mothers were pair-fed an isocaloric amount of the liquid diet without ETOH. Maternal access to the liquid diets was terminated on day 20 of the pregnancies (sperm plug=day 0). The offspring were surrogate fostered within 48 h of birth to mothers which had consumed commercial chow throughout their pregnancy. Following weaning at 21 days of age, the offspring consumed only commercial rat chow and they were examined over the next 14 months for changes in glucose homeostasis as a consequence of in utero exposure to maternal dietary fat and/or alcohol. The 35% maternal fat diet resulted in both in vivo and in vitro decreases in insulin sensitivity. Thus, compared with adults whose mother's diet contained 12% fat, significant, in vitro muscle and in vivo whole body insulin resistance (measured by hyperinsulinemic-euglycemic clamping) was observed in adult rats whose mothers consumed 35% of dietary calories as fat. The addition of ethanol to the maternal 35% fat diet further reduced the offspring's red muscle tissues in vitro response to insulin, but did not affect whole body insulin sensitivity. Muscle basal and insulin-stimulated receptor tyrosine kinase activity were significantly decreased (approximately -50%) by the 35% fat maternal diet but there was no compensatory increase in serum insulin or glucose levels. Based upon both in vivo and in vitro data, these studies suggested that in utero exposure to 35% fat has a sustained effect on the adult offspring's glucose uptake/insulin sensitivity and that the effect is paralleled, at least in part, by decreased insulin receptor tyrosine kinase activity. In utero ETOH exposure resulted in the loss of basal and insulin-stimulated, in vitro glucose uptake in red muscle fibers but maternal dietary ETOH had no detectable effect on either in vivo insulin sensitivity or muscle tyrosine kinase activity.

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EVELYN B. THOMAN, MYRNA SPROUL, BARBARA SEELER and S. LEVINE

SUMMARY

Mating and impregnation were not prevented by adrenalectomy in female rats; they carried their young to term, large litters of viable young were born and lactation was sufficient to maintain the young throughout the usual nursing period. By comparison with sham-operated mother rats, the adrenalectomized mothers gave birth to smaller litters, their pups weighed less and had increased levels of plasma corticosterone.

Prenatal and postnatal effects on the offspring were separated by crossfostering procedures. At 21 days of age there was no significant difference among the groups in the number of pups surviving; however, the pups weighed less if the biological or foster mother was adrenalectomized. These differences were less marked in multiparous mothers.

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V Sánchez-Margalet, E Ramos, J Mateo, J Oliván, R Pérez-Cano and R Goberna

Abstract

Pancreastatin is a regulatory peptide known to inhibit insulin secretion and insulin action with a glycogenolytic effect in the liver. This peptide is present in and secreted by many endocrine and chromaffin cells. Abnormalities of glucose, insulin and lipoprotein metabolism are common in patients with hypertension, as well as their first-degree relatives. We have recently studied a group of non-obese hypertensive subjects in which pancreastatin-like levels were increased compared with controls, and correlated with norepinephrine levels. We hypothesized that pancreastatin alongside the sympathoadrenal system might have a part in the insulin resistance of these patients, and this metabolic syndrome could play a role in the pathogenesis and complications of hypertension. In this article, we studied the normotensive offspring of these non-obese hypertensive patients and looked for metabolic abnormalities as well as plasma pancreastatin, glucagon and catecholamine levels. The subjects were separated into two groups: (1) offspring from non-insulin-resistant patients and (2) offspring from insulin-resistant patients. We found that after an intravenous glucose load, offspring from insulin-resistant patients were already hyperinsulinemic, although glucose clearance was normal, suggesting an early alteration in insulin sensitivity, whereas pancreastatin and catecholamine levels were normal compared with matched controls. However, offspring from non-insulin-resistant patients had no differences with controls. These results suggest that pancreastatin and catecholamines may not play an important role in triggering insulin resistance, although they may be important once the syndrome is established.

Journal of Endocrinology (1997) 153, 313–318

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T J Birdsey, S M Husain, H O Garland and C P Sibley

Abstract

The effect of maternal diabetes mellitus on renal calcium excretion in pregnant rats and their offspring has been examined in order to ascertain the role of the kidney in the disturbed calcium homeostasis of infants born to diabetic mothers. Diabetic pregnant (DP) rats exhibited severe hypercalciuria which greatly exceeded the urinary calcium losses (UCaV) in non-diabetic pregnant (CP) or non-pregnant diabetic (D) rats. Means ± s.e.m. for UCaV at day 21 (mmol/24 h) were: DP=1·12± 0·09 (n=7); CP=0·06±0·01 (n=7); D=0·63±0·06 (n=7) (P<0·001 DP vs CP and DP vs D). The profile for urinary calcium excretion in the three groups was different from that of other measured ions. The degree of natriuresis, for example, was comparable in DP and D rats at all stages studied. Although magnesium output was significantly greater in DP than D rats on days 14 and 21, this appeared to result from an additive effect of the magnesiuresis seen when pregnancy and diabetes were studied separately.

The marked renal calcium wasting of diabetic pregnancy will have implications for overall calcium balance in the mother. For example, an enhanced intestinal calcium absorption was seen in DP rats in the second half of gestation. Means ± s.e.m. for day 21 (mmol/24 h) were: DP=3·8±0·8 (n=7); CP=1·4±0·3 (n=7); D=1·6±0·3 (n=7) (P<0·05 DP vs CP and DP vs D). The hypercalciuria may also contribute to the disturbed calcium homeostasis of the neonate if it reduces the amount of calcium available for transfer to the fetus.

In contrast to their mothers, the offspring of DP rats did not show a raised UCaV compared with CP pups. Means ± s.e.m. at day 1 postpartum (nmol/2 h per pup) were: DP=47·2±15·7 (n=4 litters); CP=72·2±14·1 (n=7 litters) (not significant). Changes in neonatal renal function are therefore unlikely to contribute to their disturbed calcium balance. In fact, their slightly reduced urinary calcium output may be an attempt to compensate for their lowered total body calcium as reported elsewhere.

Journal of Endocrinology (1995) 145, 11–18

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K. Holemans, L. Aerts and F. A. Van Assche

ABSTRACT

We have previously demonstrated insulin resistance in the liver and peripheral tissues of the adult offspring of rats made diabetic with streptozotocin (SDF rats). In this study, a euglycaemic hyperinsulinaemic clamp was used to test the hypothesis that insulin resistance is further aggravated during pregnancy in SDF rats. Normal pregnancy was accompanied by a decrease in the sensitivity of the liver and peripheral tissues to insulin, with a normal responsiveness to insulin. In SDF rats no further decrease in the sensitivity of peripheral tissues to insulin occurred during pregnancy when compared with non-pregnant rats, and the dose–response curves of the glucose metabolic clearance rate during hyperinsulinaemia were similar in pregnant control and pregnant SDF rats. There was, however, a modest decrease in the sensitivity of the liver to insulin during pregnancy in SDF rats.

The normal increase in plasma insulin levels during pregnancy was blunted in SDF rats: this resulted in increased glucose levels in maternal and fetal rats and increased fetal insulin concentrations, features compatible with mild 'gestational diabetes'.

In conclusion, gestational diabetes develops in pregnant SDF rats, although there is no further deterioration in peripheral insulin resistance.

Journal of Endocrinology (1991) 131, 387–393

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I. Pollard

ABSTRACT

The effects of high-anxiety-producing stress administered to rats during pregnancy were studied. The birthweight of offspring of both sexes from the stressed group was found to be significantly lower compared to birthweights of rats from unstressed mothers. The subsequent growth rates, however, were not affected. Mortality rate was significantly higher in the stressed group, although litter size, gestation length and sex ratios were not affected. Mean plasma resting corticosterone levels of the young pups did not differ between the two groups although they rose significantly as they aged in all groups. The offspring of both sexes from stressed mothers responded differently from the controls when subjected to short-term stress (one session) in adulthood. Their increase in plasma corticosterone concentration was significantly below that of the controls. This difference in response was abolished with long-term stress (10 days) when the males, but not the females, had habituated to the stressor. The observed inability to respond adequately to a sudden environmental change suggests a defective emergency response.

Lingering effects due to stressing were also found. Male offspring of a second litter, conceived by the original mothers 8 weeks after the discontinuation of stress, had significantly lower birthweights than those of the controls. The subsequent growth rate of neither sex was affected nor was the response to short-term stress.

J. Endocr. (1984) 100, 301–306