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Secondary analysis of gut hormone data from children with and without in utero exposure to gestational diabetes: Differences in the associations among ghrelin, GLP ‐1, and insulin secretion
Author(s) -
Zengul Ayse G.,
Hoover Sarah ET,
ChandlerLaney Paula C.
Publication year - 2021
Publication title -
pediatric obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.226
H-Index - 69
eISSN - 2047-6310
pISSN - 2047-6302
DOI - 10.1111/ijpo.12757
Subject(s) - ghrelin , medicine , endocrinology , gestational diabetes , insulin , type 2 diabetes , diabetes mellitus , hormone , glucose homeostasis , obesity , insulin resistance , pregnancy , gestation , biology , genetics
Summary Background Intrauterine exposure to gestational diabetes mellitus (GDM) increases risk for type 2 diabetes (T2D). Ghrelin and GLP‐1 have opposite functions in nutritional homeostasis and are associated with insulin secretion, but it is not known if individuals exposed to GDM exhibit dysregulation in these associations. Objective Test the hypothesis that children exposed to GDM in utero will exhibit dysregulation among ghrelin, GLP‐1, and C‐peptide (reflecting insulin secretion). Methods Data from N = 43 children aged 5 to 10 years were included in this secondary analysis of ghrelin, GLP‐1, and C‐peptide response to a liquid meal test. Repeated measures mixed model analyses were used to measure associations among hormones. Results The association of ghrelin and GLP‐1 was moderated by GDM group ( P < .01), such that ghrelin was inversely associated with GLP‐1 in children without GDM exposure, but not for those exposed to GDM. GLP‐1 was positively associated with C‐peptide in both groups, but the association was stronger in those exposed to GDM ( estimate = 1.06 vs 1.01). Conclusions Differences in the associations among ghrelin, GLP‐1, and C‐peptide displayed here suggest novel lines of research about whether the regulation of gut hormones and insulin secretion contribute to obesity and risk for T2D in children exposed to GDM.