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      Nutritional effects on foetal growth

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      Animal Science
      Cambridge University Press (CUP)

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          Abstract

          The emphasis in nutritional studies on foetal growth has now moved from the last trimester of pregnancy, when most of the increase in foetal size takes place, to earlier stages of pregnancy that coincide with foetal organogenesis and tissue hyperplasia. At these stages absolute nutrient requirements for foetal growth are small but foetal metabolic activity and specific growth rate are high. It is thus a time when nutrient supply interacts with maternal factors such as size, body condition and degree of maturity to influence placental growth and set the subsequent pattern of nutrient partitioning between the gravid uterus and maternal body.

          Throughout pregnancy the maternal diet controls foetal growth both directly, by supplying essential nutrients and indirectly, by altering the expression of the maternal and foetal endocrine mechanisms that regulate the uptake and utilization of these nutrients by the conceptus. Nutritional effects on the endocrine environment of the embryo during the early stages of cell division can alter the subsequent foetal growth trajectory and size at birth; so too can current in vitro systems for oocyte maturation and embryo culture up to the blastocyst stage. There is increasing evidence that subtle alterations in nutrient supply during critical periods of embryonic and foetal life can impart a legacy of growth and developmental changes that affect neonatal survival and adult performance. Identifying the specific nutrients that programme these effects and understanding their mode of action should provide new management strategies for ensuring that nutritional regimens from oocyte to newborn are such that they maximize neonatal viability and enable animals to express their true genetic potential for production.

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          Glucocorticoids and the preparation for life after birth: are there long-term consequences of the life insurance?

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            Modulation of insulin activities by leptin.

            Leptin mediates its effects on food intake through the hypothalamic form of its receptor OB-R. Variants of OB-R are found in other tissues, but their function is unknown. Here, an OB-R variant was found in human hepatic cells. Exposure of these cells to leptin, at concentrations comparable with those present in obese individuals, caused attenuation of several insulin-induced activities, including tyrosine phosphorylation of the insulin receptor substrate-1 (IRS-1), association of the adapter molecule growth factor receptor-bound protein 2 with IRS-1, and down-regulation of gluconeogenesis. In contrast, leptin increased the activity of IRS-1-associated phosphatidylinositol 3-kinase. These in vitro studies raise the possibility that leptin modulates insulin activities in obese individuals.
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              Leptin and leptin receptor mRNA and protein expression in the murine fetus and placenta.

              Leptin is a 167-aa protein that is secreted from adipose tissue and is important in the regulation of energy balance. It also functions in hematopoiesis and reproduction. To assess whether leptin is involved in fetal growth and development we have examined the distribution of mRNAs encoding leptin and the leptin receptor (which has at least six splice variants) in the 14.5-day postcoitus mouse fetus and in the placenta using reverse transcription-PCR and in situ hybridization. High levels of gene expression for leptin, the leptin receptor, and the long splice variant of the leptin receptor with an intracellular signaling domain were observed in the placenta, fetal cartilage/bone, and hair follicles. Receptor expression also was detected in the lung, as well as the leptomeninges and choroid plexus of the fetal brain. Western blotting and immunocytochemistry, using specific antibodies, demonstrated the presence of leptin and leptin receptor protein in these tissues. These results suggest that leptin may play a role in the growth and development of the fetus, both through placental and fetal expression of the leptin and leptin receptor genes. In the fetus, leptin may be multifunctional and have both paracrine and endocrine effects.
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                Author and article information

                Journal
                applab
                Animal Science
                Anim. Sci.
                Cambridge University Press (CUP)
                1357-7298
                1748-748X
                March 1999
                August 2016
                : 68
                : 02
                : 315-331
                Article
                10.1017/S1357729800050323
                d5d27755-e9d3-4af0-af2b-e4ef3c3e2a57
                © 1999
                History

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