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M R Wilson and S J Hughes


To test the hypothesis that poor foetal–neonatal nutrition predisposes adult animals to impaired glucose tolerance or diabetes, pregnant and lactating rats were fed a low (5%) protein diet and glucose tolerance and pancreatic islet function then assessed in the adult offspring. To expose any underlying defects the offspring were allowed access to a sucrose supplement (35%) or fed a high fat diet. Offspring born to low protein-fed females had significantly lower body weights than controls. In islets from previously malnourished rats, insulin release in batch incubations or perifusion was not significantly different to controls. In islets from previously malnourished animals fed sucrose, glucose-stimulated insulin release was reduced in perifusion by 66% (P<0·01) and batch incubations by 26–52% (6–16 mmol/l glucose, (P<0·01). Similarly, impaired secretory responses were found in islets from previously malnourished animals fed a high fat diet. These did not result from a reduced pool of releasable insulin, as arginine-stimulated secretion was not impaired. Rats previously malnourished showed a normal glucose tolerance. Glucose tolerance was impaired, however, in previously malnourished rats fed sucrose (area under the glucose tolerance test curve was increased by 42%, P<0·05) but despite the reduced islet secretory responses was not significantly different to sucrose-fed controls (area increased by 54%, P<0·05). Glucose tolerance was impaired in previously malnourished animals fed high fat diet (area increased by 48%, P<0·05) more so than in high fat fed-controls (28% increase, NS). These data support the hypothesis that poor foetal–neonatal nutrition leads to impaired pancreatic β-cell function which persists into adult life. Alone this is not sufficient to produce diabetes, but an inability to respond to a highly palatable fat diet may tip the balance towards impaired glucose tolerance.

Journal of Endocrinology (1997) 154, 177–185

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SM Woodall, BH Breier, BM Johnston, NS Bassett, R Barnard and PD Gluckman

Increasing evidence from human epidemiological studies suggests that poor growth before birth is associated with postnatal growth retardation and the development of cardiovascular disease in adulthood. We have shown previously that nutritional deprivation in the pregnant rat leads to intrauterine growth retardation (IUGR), postnatal growth failure, changes in the endocrine parameters of the somatotrophic axis, and to increased blood pressure in later life. In the present study, we investigated whether administration of insulin-like growth factor-I (IGF-I) or bovine growth hormone (GH) during pregnancy could prevent IUGR and/or alter long-term outcome. Dams from day 1 of pregnancy throughout gestation received a diet of ad libitum available food or a restricted dietary intake of 30% of ad libitum fed dams. From day 10 of gestation, dams were treated for 10 days with three times daily subcutaneous injections of saline (100 microl), IGF-I (2 micrograms/g body weight) or GH (2 micrograms/g body weight). Maternal weight gain was significantly increased (P<0.001) in ad libitum fed dams treated with GH, (98.9+/-4.73 g) compared with the IGF-I (80.5+/-2.17 g) and saline-treated (70.7+/-2.65 g) groups. There was a small increase in maternal weight gain (P<0.06) in 30% ad libitum fed dams following GH (16.3+/-2.47 g) and IGF-I (15.8+/-1.97 g) treatment compared with saline (9.2+/-1.96 g). Whole spleen, kidney and carcass weights were significantly (P<0.05) increased in ad libitum fed and 30% ad libitum fed dams with GH treatment. Circulating IGF-I was significantly increased (P<0.001) in ad libitum fed dams with both IGF-I (369.6+/-32.33 ng/ml) and GH (457.9+/-33.32 ng/ml) compared with saline treatment (211.7+/-14.02 ng/ml), and with GH (223.4+/-23.72 ng/ml) compared with saline treatment (112.0+/-7.33 ng/ml) in 30% ad libitum fed dams. Circulating GH binding protein (GHBP) levels were significantly reduced (P<0.05) in GH-treated (299.1+/-51.54 ng/ml) compared with saline-treated (503.9+/-62.43 ng/ml) ad libitum fed dams, but were not altered in 30% ad libitum fed dams. There was no significant effect of either IGF-I or GH treatment on fetal weight, placental weight, fetal organ weights or circulating IGF-I levels in both ad libitum fed and 30% ad libitum fed fetuses. Offspring of 30% ad libitum fed dams remained significantly growth retarded postnatally and showed elevated blood pressure in later life. The increased maternal weight gain following IGF-I or GH administration, without an effect on fetal and placental weights, suggests a modification in the mode of maternal nutrient repartitioning during mid to late pregnancy at the expense of the fetus.

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Alison Mostyn, Sylvain Sebert, Jennie C Litten, Katharine S Perkins, John Laws, Michael E Symonds and Lynne Clarke

offspring, suggesting that either leptin is broken down (a) from its intact form in the stomach, or does not pass through the gut wall or (b) through first pass metabolism in the pig in contrast to the rat ( Casabiell et al. 1997 ). However, leptin

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M. Peaker and M. C. Neville

Since methods for measuring hormone concentrations in biological fluids were developed during the 1960s and 70s the list of biologically active substances, including classical hormones, present in milk has grown ever longer. Postulated roles for these substances have reflected a remarkable imagination on the part of many investigators. As one example, in a recent report of benzodiazepine-like substances in human milk the authors ask whether these represent a phylogenetic relic from a time when babies had to keep quiet (Dencker & Johansson, 1990). A number of reviews of hormones in milk have been written, most recently and notably by Koldovsky (1989) on peptide hormones. It is not our intention to review that information again other than to point out that the list grows ever more wide-ranging. Rather, we address the question of whether the hormones in milk might have any biological role in the suckling ingesting that milk and the

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Takahiro Nemoto, Yoshihiko Kakinuma and Tamotsu Shibasaki

knowledge, no reports have addressed the pathophysiological role of the anterior pituitary in dysregulation of the negative feedback system of the HPA axis under stress in LBW offspring. Therefore, in this study, we used rats delivered from malnourished dams

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B. Kacsoh, J. S. Meyers, W. R. Crowley and C. E. Grosvenor


Serum GH levels increased in 2- or 8-day-old rat pups when sucking mammary glands whose main milk ducts were ligated. Although intragastric administration of rat milk has been shown to increase serum GH levels in neonatal rats, ingestion of milk during suckling did not increase serum GH values further. In another experiment, 2-day-old pups obtained no milk when they were suckled by anaesthetized mothers, and in this instance the serum GH concentration of the pups decreased. This decrease was prevented if the mothers were injected with oxytocin to counteract the depressant effect of the anaesthesia on milk ejection; nevertheless, GH levels in neonatal animals failed to increase following suckling. Thus some aspect of maternal activity appears to be involved in the suckling-induced increase of serum GH in rat pups. To elucidate which components of maternal activity might be involved, the effects of manipulations of ambient temperature as well as stimulation of the oral or anogenital regions were examined. Exposing rat pups to 37 °C (nest temperature) during the 6-h separation period before suckling prevented the separation-induced decrease in serum GH levels of 2-day-old pups. Moreover, exposure to 37 °C for 30 min following a 6-h separation at room temperature (22 °C) mimicked the effect of suckling in increasing serum GH levels in the pups. Suckling following separation at 37 °C was unable to increase serum GH values further. In other studies, stimulation of the oral zone (feeding from a soft cannula) or anogenital zone (inducing urination and defecation with a wet brush) of the pups significantly decreased neonatal serum GH values. The painful stimulus of administration of s.c. hyperosmotic saline was without effect on serum GH levels.

In summary: (1) suckling, even without milk removal, increases serum GH levels in neonatal rats; (2) some aspect of maternal activity is involved in the suckling-induced increase of serum GH concentration in the neonate; (3) provision of a warm ambient temperature by the mother is a critical component of this maternal activity; (4) the effects of milk and the maternal activity associated with suckling are not additive in increasing serum values of GH in neonatal rats; and (5) oral feeding is not a suitable approach for studying the effects of milk on serum GH in neonatal rats.

Journal of Endocrinology (1990) 124, 233–240

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It was observed in our laboratory that the age of onset of puberty of Long-Evans female rats differed according to their source. Animals from the University of California, Berkeley, California (U.C.B.) are reported to have an age of vaginal canalization of 39–45 days (J. Ehlert, personal communication), while animals from Simonsen Laboratories, Gilroy, California (S.L.) achieve puberty at 32–35 days (Simonsen Laboratories, personal communication). This difference of age is surprising since the S.L. rat colony was started from the U.C.B. colony in 1949. Simonsen Laboratories maintain semi-specific pathogen-free conditions, whereas no special precautions are taken in U.C.B. or San Francisco (U.C.M.C.S.F.).

This study was undertaken to determine if environmental influences affected the difference in the age of onset of puberty between rats from the two sources. Among these factors feed was considered to be important. Although the animals in both laboratories were fed on a common diet, powdered White Diet

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Jose Casasnovas, Yunhee Jo, Xi Rao, Xiaoling Xuei, Mary E Brown and Kok Lim Kua

Introduction Diabetes complicates 5.6–11.7% of all pregnancies ( Hunt & Schuller 2007 , DeSisto et al . 2014 ), with affected mothers and offspring vulnerable to adverse metabolic outcomes ( Ratner et al. 2008 , Fraser & Lawlor 2014

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Stefan O Krechowec, Mark Vickers, Arieh Gertler and Bernhard H Breier

resistance is linked to the development of obesity. Our previous work in rats suggests that prenatal exposure to maternal undernutrition leads to changes in the regulation of the insulin–leptin endocrine axes which appear to predispose offspring to

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Tod Fullston, Nicole O McPherson, Deirdre Zander-Fox and Michelle Lane

Introduction There is growing evidence from animal and human studies that demonstrate that acquired paternal traits can impair both a male’s fertility and the health of his offspring, including advanced age, smoking, stress, trauma, under