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Title: Fetal Leptin Is a Signal of Fat Mass Independent of Maternal Nutrition in Ewes Fed at or above Maintenance Energy Requirements
Contributor(s): Mulhausler, B S (author); Roberts, CT (author); McFarlane, James Robert (author)orcid ; Kauter, Kathleen (author); McMillen, I C (author)
Publication Date: 2002
DOI: 10.1095/biolreprod67.2.493
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Abstract: In adults, circulating leptin concentrations are dependent on body fat content and on current nutritional status. However, the relationships among maternal nutrient intake, fetal adiposity, and circulating leptin concentrations before birth are unknown. We investigated the effects of an increase in nutrient intake in the pregnant ewe on fetal adiposity and plasma leptin concentrations during late gestation. Between 115 and 139–141 days gestation (term = 147 ± 3 days gestation), ewes were fed a diet calculated to provide either maintenance (control, n = 6) or -155% of maintenance requirements (well-fed, n = 8). The fetal fat depots (perirenal and interscapular) were dissected, and the relative proportion of unilocular and multilocular adipocytes in each depot was determined. Maternal plasma glucose and leptin concentrations were significantly increased in well-fed ewes. Fetal plasma glucose concentrations were also higher in the well-fed group (115–139 days gestation: control, 1.65 ± 0.14 mmol/L; well-fed, 2.00 ± 0.14 mmol/L; F = 5.76, P < 0.04). There was no effect of increasing maternal feed intake on total fat mass, the relative mass of unilocular fat, or fetal plasma leptin concentrations (115–139 days gestation: control, 5.2 ± 0.8 ng/ml; well-fed, 4.7 ± 0.7 ng/ml). However, in both the control and well-fed groups fetal plasma leptin concentrations (y) were positively correlated with the relative mass of unilocular fat (x): y = 1.51x + 1.70; (R = 0.76, P < 0.01). Thus, fetal leptin may play a role as a signal of unilocular fat mass in the fetus when maternal nutrient intake is at or above maintenance requirements.
Publication Type: Journal Article
Source of Publication: Biology of Reproduction, 67(2), p. 493-499
Publisher: Society of the Study for Reproduction
Place of Publication: Madison, UK
ISSN: 1529-7268
Field of Research (FOR): 111601 Cell Physiology
Peer Reviewed: Yes
HERDC Category Description: C1 Refereed Article in a Scholarly Journal
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