Development of Early Adiposity in Infants of Mothers With Gestational Diabetes Mellitus
File(s)Article proof.pdf (799.44 KB)
Accepted version
Author(s)
Type
Journal Article
Abstract
OBJECTIVE
Infants born to mothers with gestational diabetes mellitus (GDM) are at greater
risk of later adverse metabolic health. We examined plausible candidate mediators;
adipose tissue (AT) quantity and distribution, and intrahepatocellular lipid
(IHCL) content, comparing infants of mothers with GDM and without GDM (control
group) over the first 3 postnatal months.
RESEARCH DESIGN AND METHODS
We conducted a prospective longitudinal study using MRI and spectroscopy to
quantify whole-body and regional AT volumes, and IHCL content, within 2 weeks
and 8–12 weeks after birth. We adjusted for infant size and sex, and maternal
prepregnancy BMI. Values are reported as the mean difference (95% CI).
RESULTS
We recruited 86 infants (GDM group 42 infants; control group 44 infants). Mothers
with GDM had good pregnancy glycemic control. Infants were predominantly
breast fed up to the time of the second assessment (GDM group 71%; control
group 74%). Total AT volumes were similar in the GDM group compared with the
control group at a median age of 11 days (228 cm3 [95% CI 2121, 65], P = 0.55), but
were greater in the GDM group at a median age of 10 weeks (247 cm3 [56, 439], P =
0.01). After adjustment for size, the GDM group had significantly greater total AT
volume at 10 weeks than control group infants (16.0% [6.0, 27.1], P = 0.002). AT
distribution and IHCL content were not significantly different at either time point.
CONCLUSIONS
Adiposity in GDM infants is amplified in early infancy, despite good maternal
glycemic control and predominant breast-feeding, suggesting a potential causal
pathway to later adverse metabolic health. Reduction in postnatal adiposity may
be a therapeutic target to reduce later health risks.
Infants born to mothers with gestational diabetes mellitus (GDM) are at greater
risk of later adverse metabolic health. We examined plausible candidate mediators;
adipose tissue (AT) quantity and distribution, and intrahepatocellular lipid
(IHCL) content, comparing infants of mothers with GDM and without GDM (control
group) over the first 3 postnatal months.
RESEARCH DESIGN AND METHODS
We conducted a prospective longitudinal study using MRI and spectroscopy to
quantify whole-body and regional AT volumes, and IHCL content, within 2 weeks
and 8–12 weeks after birth. We adjusted for infant size and sex, and maternal
prepregnancy BMI. Values are reported as the mean difference (95% CI).
RESULTS
We recruited 86 infants (GDM group 42 infants; control group 44 infants). Mothers
with GDM had good pregnancy glycemic control. Infants were predominantly
breast fed up to the time of the second assessment (GDM group 71%; control
group 74%). Total AT volumes were similar in the GDM group compared with the
control group at a median age of 11 days (228 cm3 [95% CI 2121, 65], P = 0.55), but
were greater in the GDM group at a median age of 10 weeks (247 cm3 [56, 439], P =
0.01). After adjustment for size, the GDM group had significantly greater total AT
volume at 10 weeks than control group infants (16.0% [6.0, 27.1], P = 0.002). AT
distribution and IHCL content were not significantly different at either time point.
CONCLUSIONS
Adiposity in GDM infants is amplified in early infancy, despite good maternal
glycemic control and predominant breast-feeding, suggesting a potential causal
pathway to later adverse metabolic health. Reduction in postnatal adiposity may
be a therapeutic target to reduce later health risks.
Date Issued
2016-05-12
Date Acceptance
2016-03-28
Citation
Diabetes Care, 2016, 39 (6), pp.1045-1051
ISSN
0149-5992
Publisher
American Diabetes Association
Start Page
1045
End Page
1051
Journal / Book Title
Diabetes Care
Volume
39
Issue
6
Copyright Statement
© 2016 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.
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.
Sponsor
Action Medical Research
Grant Number
GN2008
Subjects
Endocrinology & Metabolism
11 Medical And Health Sciences
Publication Status
Published