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Introduction
The past 10 years have witnessed the discovery of a new peptide family, the natriuretic peptides, which may rival the renin-angiotensin system in their contribution to cardiovascular homoeostasis. The first member to be identified and the most intensively studied is atrial natriuretic peptide (ANP) (DeBold et al. 1981: Flynn et al. 1983; Oikawa et al. 1984). More recently, brain natriuretic peptide (BNP) (Sudoh et al. 1988), C-type natriuretic peptide (CNP) (Sudoh et al. 1990) and urodilatin (Feller et al. 1989) have been isolated and their amino acid sequences determined (Fig. 1). The structural hallmark of this family is a 17-amino acid ring formed by a disulphide bond. From the functional viewpoint, their biological effects are mediated principally by receptors with integral guanylyl cyclase activity. The term 'natriuretic peptide family' is one of convenience ; recent studies suggest that CNP has little natriuretic activity and in some situations may even be
Adelaide Medical School, The University of Adelaide, Adelaide, Australia
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Nutrition and Health Program, Health and Biosecurity Business Unit, Commonwealth Scientific and Industrial Research Organisation, Adelaide, Australia
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Nutrition, Diabetes & Gut Health, Lifelong Health Theme, South Australian Health and Medical Research Institute (SAHMRI), Adelaide, Australia
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Nutrition, Diabetes & Gut Health, Lifelong Health Theme, South Australian Health and Medical Research Institute (SAHMRI), Adelaide, Australia
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Nutrition, Diabetes & Gut Health, Lifelong Health Theme, South Australian Health and Medical Research Institute (SAHMRI), Adelaide, Australia
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Adelaide Medical School, The University of Adelaide, Adelaide, Australia
Nutrition, Diabetes & Gut Health, Lifelong Health Theme, South Australian Health and Medical Research Institute (SAHMRI), Adelaide, Australia
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Adelaide Medical School, The University of Adelaide, Adelaide, Australia
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Adelaide Medical School, The University of Adelaide, Adelaide, Australia
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Adelaide Medical School, The University of Adelaide, Adelaide, Australia
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Circulating growth hormone (GH) concentrations increase during pregnancy in mice and remain pituitary-derived. Whether abundance or activation of the GH secretagogue ghrelin increase during pregnancy, or in response to dietary octanoic acid supplementation, is unclear. We therefore measured circulating GH profiles in late pregnant C57BL/6J mice and in aged-matched non-pregnant females fed with standard laboratory chow supplemented with 5% octanoic or palmitic (control) acid (n = 4–13/group). Serum total and acyl-ghrelin concentrations, stomach and placenta ghrelin mRNA and protein expression, Pcsk1 (encoding prohormone convertase 1/3) and Mboat4 (membrane bound O-acyl transferase 4) mRNA were determined at zeitgeber (ZT) 13 and ZT23. Total and basal GH secretion were higher in late pregnant than non-pregnant mice (P < 0.001), regardless of diet. At ZT13, serum concentrations of total ghrelin (P = 0.004), but not acyl-ghrelin, and the density of ghrelin-positive cells in the gastric antrum (P = 0.019) were higher, and gastric Mboat4 and Pcsk1 mRNA expression were lower in pregnant than non-pregnant mice at ZT23. In the placenta, ghrelin protein was localised mostly to labyrinthine trophoblast cells. Serum acyl-, but not total, ghrelin was lower at mid-pregnancy than in non-pregnant mice, but not different at early or late pregnancy. In conclusion, dietary supplementation with 5% octanoic acid did not increase activation of ghrelin in female mice. Our results further suggest that increases in maternal GH secretion throughout murine pregnancy are not due to circulating acyl-ghrelin acting at the pituitary. Nevertheless, time-dependent increased circulating total ghrelin could potentially increase ghrelin action in tissues that express the acylating enzyme and receptor.
