Exposure to gestational diabetes mellitus in utero impacts hippocampal functional connectivity in response to food cues in children

Zhao S; Semeia L; Veit R; Luo S; Angelo BC; Chow T; Birkenfeld AL; Preissl H; Xiang AH; et al Page KA

doi:10.1530/ey.22.11.5

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ESPE Yearbook of Paediatric Endocrinology (2025) 22 11.5 | DOI: 10.1530/ey.22.11.5

ESPEYB25 11. Obesity and Weight Regulation In Utero Programming of Hippocampal Connectivity (1 abstracts)

11.5. Exposure to gestational diabetes mellitus in utero impacts hippocampal functional connectivity in response to food cues in children

Zhao S , Semeia L , Veit R , Luo S , Angelo BC , Chow T , Birkenfeld AL , Preissl H , Xiang AH & Page KA et al

Author affiliations

Department of Internal Medicine, Division of Diabetology, Endocrinology and Nephrology, Eberhard Karls University Tübingen, Tübingen, Germany. [email protected]

Int J Obes (Lond) 2024, 48(12):1728-1734. PMID: 39198584. doi: 10.1038/s41366-024-01608-1. https://pubmed.ncbi.nlm.nih.gov/39198584/

Brief Summary: This study examined the impact of gestational diabetes mellitus (GDM) exposure in 90 children age 7–11 years on hippocampal functional connectivity (FC) in response to food-related cues, utilizing functional magnetic resonance imaging (fMRI). Hippocampal FC was compared between children with and without GDM exposure. Compared to children without intrauterine exposure to GDM, children with exposure showed increased hippocampal FC in response to food cues, particularly with regions involved in reward processing.

The hippocampus plays a central role in learning and memory and is thought to contribute to the regulation of food intake by integrating past experiences with internal bodily signals [1]. Prior structural MRI findings have demonstrated reduced left hippocampal thickness in children prenatally exposed to GDM compared to non-exposed peers [2]. These observations suggest that GDM may influence both hippocampal structure and function.

The findings reported here indicate a specific impact of intrauterine exposure to (GDM) on hippocampal connectivity, predominantly involving reward-processing regions, rather than being attributable to obesity at this early age. These results are consistent with prior animal research [3, 4, 5] and lend support to the hypothesis that prenatal diabetes exposure may induce alterations in neural pathways.

References: 1. Kanoski SE, Grill HJ. Hippocampus contributions to food intake control: mnemonic, neuroanatomical, and endocrine mechanisms. Biol Psychiatry. 2017;81:748–56.2. Lynch KM, Alves JM, Chow T, Clark KA, Luo S, Toga AW, et al. Selective morphological and volumetric alterations in the hippocampus of children exposed in utero to gestational diabetes mellitus. Hum Brain Mapp. 2021;42:2583–92.3. Vuong B, Odero G, Rozbacher S, Stevenson M, Kereliuk SM, Pereira TJ, et al. Exposure to gestational diabetes mellitus induces neuroinflammation, derangement of hippocampal neurons, and cognitive changes in rat offspring. J Neuroinflammation. 2017;14:80.4. Lotfi N, Hami J, Hosseini M, Haghir D, Haghir H. Diabetes during pregnancy enhanced neuronal death in the hippocampus of rat offspring. Int J Develop Neurosci Off J Int Soc Develop Neurosci. 2016;51:28–35.5. Golalipour MJ, Kafshgiri SK, Ghafari S. Gestational diabetes induced neuronal loss in CA1 and CA3 subfields of rat hippocampus in early postnatal life. Folia Morphologica. 2012;71:71–7.