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• W3118289388 endingPage "104919" @default.
• W3118289388 startingPage "104919" @default.
• W3118289388 abstract "Gestational diabetes mellitus (GDM) was associated with greater autism risk in epidemiological studies. Disrupted leptin signaling may contribute to their coincidence, as it is found in both disorders. Given this we examined leptin receptor (Lepr) deficient (BKS.Cg-Dock7m +/+ Leprdb/J diabetic (db)) heterozygous (db/+) mice for autism-relevant behaviors. BKS db/+ females are lean with normal blood glucose, but they develop GDM while pregnant. We hypothesized BKS db/+ offspring might exhibit physiological and behavior traits consistent with autism. Adolescent body weight, fasting blood glucose, serum corticosterone, social preferences, self-grooming, marble burying, social dominance and cognitive flexibility of BKS db/+ mice was compared to C57BLKS/J (BKS) and C57BL/6J (BL6) mice. Male db/+ weighed more and had higher blood glucose and corticosterone relative to BL6, but not BKS mice. Also, male db/+ lacked social interaction preference, explored arenas less, and buried more marbles than BL6, but not BKS males. Male and female db/+ were more dominant and made more mistakes in water T-mazes locating a sunken platform after its position was reversed than BL6, but not BKS mice. Overall BKS db/+, particularly males, exhibited some autism-like social deficits and restrictive-repetitive behaviors relative to BL6, but BKS strain contributions to BKS db/+ behaviors were evident. Since BKS db/+ and BKS behavioral and physiological phenotypes are already so similar, it will be difficult to use these models in studies designed to detect contributions of fetal GDM exposures to offspring behaviors." @default.
• W3118289388 created "2021-01-18" @default.
• W3118289388 creator A5012398838 @default.
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• W3118289388 date "2021-03-01" @default.
• W3118289388 modified "2023-10-14" @default.
• W3118289388 title "Assessment of autism-relevant behaviors in C57BKS/J leptin receptor deficient mice" @default.
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• W3118289388 doi "https://doi.org/10.1016/j.yhbeh.2020.104919" @default.
• W3118289388 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7965341" @default.
• W3118289388 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33428921" @default.
• W3118289388 hasPublicationYear "2021" @default.
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