Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/23762
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dc.contributor.authorLappas, Martha-
dc.contributor.authorLim, Ratana-
dc.contributor.authorPrice, Sarah A-
dc.contributor.authorPrendergast, Luke A-
dc.contributor.authorProietto, Joseph-
dc.contributor.authorEkinci, Elif I-
dc.contributor.authorSumithran, Priya-
dc.date2020-
dc.date.accessioned2020-07-06T06:53:46Z-
dc.date.available2020-07-06T06:53:46Z-
dc.date.issued2020-
dc.identifier.citationInternational Journal of Women's Health 2020; 12: 455-462en_US
dc.identifier.issn1179-1411-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/23762-
dc.description.abstractCentral homeostatic regulation of fat stores is attenuated during pregnancy, to allow for adequate fat deposition to support fetal development and lactation. What factors particular to pregnancy facilitate fat accumulation, and why gestational weight gain (GWG) is so variable, are not clear. The aim of this cross-sectional study was to examine the associations between GWG and circulating hormones with known effects on appetite and growth. Women without obesity (body mass index, BMI <30 kg/m2), with a healthy singleton pregnancy, were recruited at the time of delivery by elective Caesarean section at a tertiary obstetric hospital. Women with preterm (<37 weeks) delivery and smokers were excluded. Maternal blood was collected at the time of delivery for measurement of fasting oestradiol, progesterone, prolactin, insulin, leptin, insulin-like growth factor 1 and insulin-like growth factor binding protein 3. Comparisons were made between women who gained weight within the range recommended by Institute of Medicine guidelines for normal weight women (11.5-16 kg; n=34) and those who gained excessive weight (>16 kg; n=35) during pregnancy. Analysis of covariance was carried out using multiple linear regression to test the effect of GWG group on biochemical parameters, accounting for pre-pregnancy BMI. The 69 participants had a mean age of 34.6 ± 4.3 years, and pre-pregnancy BMI of (23.3 ± 1.8 kg/m2), with no significant differences between groups in pre-pregnancy weight, BMI, age, birthweight or parity. Mean GWG was 14.0 ± 1.3 kg in the "recommended" group and 19.6 ± 3.2 kg in the "excessive" group. Leptin was significantly higher (43.4 ± 21.6 vs 33.4 ± 15.0 ng/mL, p=0.03) and prolactin tended to be lower (159.5 ± 66.1 vs 194.0 ± 85.6 ng/mL, p=0.07) at delivery in women with excessive (vs recommended) GWG. No other circulating factors were found to differ between groups. The between-group difference in leptin remained after adjustment for pre-pregnancy BMI in multiple linear regression and quantile regression analyses. In women without obesity, leptin remains a marker of adiposity during pregnancy. GWG was not associated with other circulating hormones with effects on appetite and growth.en_US
dc.language.isoeng-
dc.subjectappetiteen_US
dc.subjectgestational weight gainen_US
dc.subjectleptinen_US
dc.subjectpregnancyen_US
dc.titleExploring the Relationship Between Maternal Circulating Hormones and Gestational Weight Gain in Women Without Obesity: A Cross-Sectional Study.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleInternational Journal of Women's Healthen_US
dc.identifier.affiliationUniversity of Melbourne, Department of Obstetrics and Gynaecology, Melbourne, Australiaen_US
dc.identifier.affiliationLa Trobe University, Department of Mathematics and Statistics, Bundoora, Australiaen_US
dc.identifier.affiliationEndocrinologyen_US
dc.identifier.affiliationMedicine (University of Melbourne)en_US
dc.identifier.affiliationMercy Hospital for Women, Melbourne, Australiaen_US
dc.identifier.doi10.2147/IJWH.S241785en_US
dc.type.contentTexten_US
dc.identifier.orcid0000-0002-8773-3527en_US
dc.identifier.orcid0000-0001-7722-3171en_US
dc.identifier.orcid0000-0003-2372-395Xen_US
dc.identifier.orcid0000-0002-9576-1050en_US
dc.identifier.pubmedid32606997-
dc.type.austinJournal Article-
local.name.researcherEkinci, Elif I
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.grantfulltextnone-
item.openairetypeJournal Article-
crisitem.author.deptEndocrinology-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptEndocrinology-
crisitem.author.deptEndocrinology-
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