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Programming of Adiposity in Offspring of Mothers With Type 1 Diabetes at Age 7 Years

OBJECTIVE: The goals of this study were to examine the influence of maternal type 1 diabetes during pregnancy on offspring adiposity and glucose tolerance at age 7 years and to assess whether metabolic factors at birth (neonatal leptin and insulin) predict adverse outcomes. RESEARCH DESIGN AND METHO...

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Autores principales: Lindsay, Robert S., Nelson, Scott M., Walker, James D., Greene, Stephen A., Milne, Gillian, Sattar, Naveed, Pearson, Donald W.
Formato: Texto
Lenguaje:English
Publicado: American Diabetes Association 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2858180/
https://www.ncbi.nlm.nih.gov/pubmed/20427684
http://dx.doi.org/10.2337/dc09-1766
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author Lindsay, Robert S.
Nelson, Scott M.
Walker, James D.
Greene, Stephen A.
Milne, Gillian
Sattar, Naveed
Pearson, Donald W.
author_facet Lindsay, Robert S.
Nelson, Scott M.
Walker, James D.
Greene, Stephen A.
Milne, Gillian
Sattar, Naveed
Pearson, Donald W.
author_sort Lindsay, Robert S.
collection PubMed
description OBJECTIVE: The goals of this study were to examine the influence of maternal type 1 diabetes during pregnancy on offspring adiposity and glucose tolerance at age 7 years and to assess whether metabolic factors at birth (neonatal leptin and insulin) predict adverse outcomes. RESEARCH DESIGN AND METHODS: We examined 100 offspring of mothers with type 1 diabetes (OT1DM) and 45 offspring of control mothers. Mothers had previously been recruited during pregnancy, and, where possible, birth weight, umbilical cord insulin, and leptin were measured. Children were classed as overweight and obese using age-specific reference ranges. RESULTS: OT1DM had similar height (control, 1.25 ± 0. 06 m; OT1DM, 1.24 ± 0.06 m; P = 0.81) but were heavier (control, 25.5 ± 3.8 kg; OT1DM, 27.1 ± 5.7 kg; P = 0.048) and had an increased BMI (control, 16.4 kg/m(2); OT1DM, 17.4 ± 2.6 kg/m(2), P = 0.005). Waist circumference (control, 56.0 ± 3.7 cm; OT1DM, 58 ± 6.8 cm; P = 0.02) and sum of skinfolds were increased (control, 37.5 ± 17.0 mm [n = 42]; OT1DM, 46.1 ± 24.2 mm [n = 91]; P = 0.02), and there was a marked increase in the prevalence of overweight and obese children (OT1DM, 22% overweight and 12% obese; control, 0% overweight and 7% obese; χ(2) P = 0.001). Glucose tolerance was not different compared with that in control subjects. BMI at age 7 years correlated with cord leptin (OT1DM, r = 0.25; n = 61, P = 0.047), weakly with adjusted birth weight (r = 0.19; P = 0.06) and hematocrit (r = 0.25; n = 50, P = 0.07), but not cord insulin (OT1DM, r = −0.08; P = 0.54). CONCLUSIONS: OT1DM are at increased risk of overweight and obesity in childhood. This risk appears to relate, in part, to fetal leptin and hematocrit but not insulin.
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spelling pubmed-28581802011-05-01 Programming of Adiposity in Offspring of Mothers With Type 1 Diabetes at Age 7 Years Lindsay, Robert S. Nelson, Scott M. Walker, James D. Greene, Stephen A. Milne, Gillian Sattar, Naveed Pearson, Donald W. Diabetes Care Original Research OBJECTIVE: The goals of this study were to examine the influence of maternal type 1 diabetes during pregnancy on offspring adiposity and glucose tolerance at age 7 years and to assess whether metabolic factors at birth (neonatal leptin and insulin) predict adverse outcomes. RESEARCH DESIGN AND METHODS: We examined 100 offspring of mothers with type 1 diabetes (OT1DM) and 45 offspring of control mothers. Mothers had previously been recruited during pregnancy, and, where possible, birth weight, umbilical cord insulin, and leptin were measured. Children were classed as overweight and obese using age-specific reference ranges. RESULTS: OT1DM had similar height (control, 1.25 ± 0. 06 m; OT1DM, 1.24 ± 0.06 m; P = 0.81) but were heavier (control, 25.5 ± 3.8 kg; OT1DM, 27.1 ± 5.7 kg; P = 0.048) and had an increased BMI (control, 16.4 kg/m(2); OT1DM, 17.4 ± 2.6 kg/m(2), P = 0.005). Waist circumference (control, 56.0 ± 3.7 cm; OT1DM, 58 ± 6.8 cm; P = 0.02) and sum of skinfolds were increased (control, 37.5 ± 17.0 mm [n = 42]; OT1DM, 46.1 ± 24.2 mm [n = 91]; P = 0.02), and there was a marked increase in the prevalence of overweight and obese children (OT1DM, 22% overweight and 12% obese; control, 0% overweight and 7% obese; χ(2) P = 0.001). Glucose tolerance was not different compared with that in control subjects. BMI at age 7 years correlated with cord leptin (OT1DM, r = 0.25; n = 61, P = 0.047), weakly with adjusted birth weight (r = 0.19; P = 0.06) and hematocrit (r = 0.25; n = 50, P = 0.07), but not cord insulin (OT1DM, r = −0.08; P = 0.54). CONCLUSIONS: OT1DM are at increased risk of overweight and obesity in childhood. This risk appears to relate, in part, to fetal leptin and hematocrit but not insulin. American Diabetes Association 2010-05 /pmc/articles/PMC2858180/ /pubmed/20427684 http://dx.doi.org/10.2337/dc09-1766 Text en © 2010 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.
spellingShingle Original Research
Lindsay, Robert S.
Nelson, Scott M.
Walker, James D.
Greene, Stephen A.
Milne, Gillian
Sattar, Naveed
Pearson, Donald W.
Programming of Adiposity in Offspring of Mothers With Type 1 Diabetes at Age 7 Years
title Programming of Adiposity in Offspring of Mothers With Type 1 Diabetes at Age 7 Years
title_full Programming of Adiposity in Offspring of Mothers With Type 1 Diabetes at Age 7 Years
title_fullStr Programming of Adiposity in Offspring of Mothers With Type 1 Diabetes at Age 7 Years
title_full_unstemmed Programming of Adiposity in Offspring of Mothers With Type 1 Diabetes at Age 7 Years
title_short Programming of Adiposity in Offspring of Mothers With Type 1 Diabetes at Age 7 Years
title_sort programming of adiposity in offspring of mothers with type 1 diabetes at age 7 years
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2858180/
https://www.ncbi.nlm.nih.gov/pubmed/20427684
http://dx.doi.org/10.2337/dc09-1766
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