ISSN 1662-4009 (online)

ESPE Yearbook of Paediatric Endocrinology (2020) 17 2.17 | DOI: 10.1530/ey.17.2.17

ESPEYB17 2. Antenatal and Neonatal Endocrinology Maternal Obesity and Long-Term Infant Consequences (3 abstracts)

2.17. Children exposed to maternal obesity or gestational diabetes mellitus during early fetal development have hypothalamic alterations that predict future weight gain

Page KA , Luo S , Wang X , Chow T , Alves J , Buchanan TA & Xiang AH



To read the full abstract: Diabetes Care. 2019 Aug;42(8):1473–1480. PMID: 31332028

Maternal obesity and gestational diabetes (GDM) increase the risk of offspring developing childhood obesity and type 2 diabetes. The underlying mechanisms and possible neuronal pathways are unknown but might involve changes in the hypothalamic structure and function. Novel non-invasive imaging techniques (such as pulsed arterial spin labeling (PASL) a type of functional MRI scan) allow the assessment of hypothalamic function in response to glucose by measuring changes in cerebral blood flow. These have been used in children and adults with reproducible results.

In this study, infants who had been exposed to maternal obesity and GDM (diagnosed at <26 week’s gestation) had significantly higher hypothalamic responses to glucose at age 7–11 years. On further follow up 1 year later, higher hypothalamic responses to glucose were predictive of greater gains in child’s adiposity. Maternal obesity was also was associated with child’s adiposity at 7–11 years of age and with increases in adiposity 1 year later. It is unclear why children aged 7–11 years were studied; presumably they were able to undergo the PASL assessments.

These observations of higher blood flow in the children’s hypothalamus in response to glucose represent a possible mechanism by which exposure to maternal metabolic disorders during fetal development increases the risk for obesity later in life. However, the imaging techniques used here provide indirect measures of neuronal activity and cannot distinguish between activation of hypothalamic areas involved in hunger versus areas involved in satiety. Therefore, a casual inference cannot be made regarding the role of altered brain pathways on the development of obesity in children. Furthermore, childhood obesity is a multifactorial disease process, and associations between maternal GDM and obesity and higher offspring obesity risk may be conveyed by many biological and behavioural mechanisms. However, the concept of assessing hypothalamic function in response to glucose by measuring changes in cerebral blood flow is interesting and exciting for future studies.

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