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  Maternal diabetes compromises the organization of hypothalamic feeding circuits and impairs leptin sensitivity in offspring.

Steculorum, S. M., & Bouret, S. G. (2011). Maternal diabetes compromises the organization of hypothalamic feeding circuits and impairs leptin sensitivity in offspring. Endocrinology, (11), 4171-4179.

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Genre: Journal Article
Alternative Title : Endocrinology

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 Creators:
Steculorum, Sophie M.1, Author           
Bouret, Sebastien G., Author
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1Steculorum – Neurocircuit Wiring and Function, Max Planck Research Groups, Max Planck Institute for Metabolism Research, Max Planck Society, ou_3485597              

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Free keywords: Animals, Mice, Insulin/metabolism, Neurons/*metabolism, Female, Pregnancy, *Maternal Nutritional Physiological Phenomena, Adipose Tissue/metabolism/physiopathology, Diabetes Mellitus, Type 2/*metabolism/physiopathology, Diabetes, Gestational/*metabolism/physiopathology, Eating/physiology, Hypothalamus/*metabolism/physiopathology, Leptin/*metabolism, Nerve Net/*metabolism/physiopathology, Obesity/metabolism/physiopathology, Phosphorylation, STAT3 Transcription Factor/metabolism
 Abstract: Maternal diabetes is a common complication of pregnancy, and the offspring of diabetic mothers have a higher risk of developing obesity and type 2 diabetes later in life. Despite these observations, the precise biological processes mediating this metabolic programming are not well understood. Here, we explored the consequences of maternal diabetes on the organization of hypothalamic neural circuits involved in the regulation of energy balance. To accomplish this aim, we used a mouse model of maternal insulin deficiency induced by streptozotocin injections. Maternal diabetes was found to be associated with changes in offspring growth as revealed by a significantly higher pre- and postweaning body weight in the offspring of insulin-deficient dams relative to those of control mice. Mice born to diabetic dams also showed increased fasting glucose levels, increased insulin levels, and increased food intake during their adult lives. These impairments in metabolic regulation were associated with leptin resistance during adulthood. Importantly, the ability of leptin to activate intracellular signaling in arcuate neurons was also significantly reduced in neonates born to diabetic dams. Furthermore, neural projections from the arcuate nucleus to the paraventricular nucleus were markedly reduced in the offspring of insulin-deficient dams. Together, these data show that insulin deficiency during gestation has long-term consequences for metabolic regulation. They also indicate that animals born to diabetic dams display abnormally organized hypothalamic feeding pathways that could result from the attenuated responsiveness of hypothalamic neurons to the neurotrophic actions of leptin during neonatal development.

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 Dates: 2011
 Publication Status: Issued
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Title: Endocrinology
  Alternative Title : Endocrinology
Source Genre: Journal
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Publ. Info: -
Pages: - Volume / Issue: (11) Sequence Number: - Start / End Page: 4171 - 4179 Identifier: ISBN: 1945-7170 0013-7227