2023-03-20 ラトガース大学
ルトガース大学のMolecular Metabolismで発表された研究によると、母親から子供へのこのリンクをマウスで追跡しました。妊娠および授乳中に無制限の高脂肪食品を食べさせて肥満になったマウスと、無制限の健康的な食品を食べさせてスリムなマウスを維持したマウスを比較しました。肥満の母親から生まれたマウスは、健康的な食品に無制限にアクセスできる場合でも、痩せた母親から生まれたマウスよりも不健康な食品にアクセスできる場合に過剰摂取します。
この研究は、妊娠中および授乳中に母親が肥満だった人々がおやつの摂取を制限することに苦労する可能性がある一方で、健康的な食品を十分に食べることができることを示唆しています。また、この研究は、不健康な食べ物への渇望を減らす脳を変える薬剤の開発にも役立つ可能性があります。
<関連情報>
- https://www.rutgers.edu/news/excess-calories-during-development-alter-brain-and-spur-adult-overeating
- https://www.sciencedirect.com/science/article/pii/S2212877823000364
母親の過栄養は視床下部外側領域へのシナプス入力の変化と関連する Maternal overnutrition is associated with altered synaptic input to lateral hypothalamic area
Kuldeep Shrivastava, Thaarini Swaminathan, Alessandro Barlotta, Vikshar Athreya, Hassan Choudhry, Mark A. Rossi
Molecular Metabolism Available online:8 March 2023
DOI:https://doi.org/10.1016/j.molmet.2023.101702
Highlights
- •Maternal overnutrition yields hyperphagic and obesity-prone offspring.
- •Maternal overnutrition increases excitatory input in the BNST→LHA pathway
- •Early life growth rate predicts synaptic strength in the BNST→LHA pathway
Abstract
Objective
Maternal overnutrition is associated with adverse outcomes in offspring, including increased risk for obesity and diabetes. Here, we aim to test the effects of maternal obesity on lateral hypothalamic feeding circuit function and determine the relationship with body weight regulation.
Methods
Using a mouse model of maternal obesity, we assessed how perinatal overnutrition affected food intake and body weight regulation in adult offspring. We then used channelrhodopsin-assisted circuit mapping and electrophysiological recordings to assess the synaptic connectivity within an extended amygdala-lateral hypothalamic pathway.
Results
We show that maternal overnutrition during gestation and throughout lactation produces offspring that are heavier than controls prior to weaning. When weaned onto chow, the body weights of over-nourished offspring normalize to control levels. However, when presented with highly palatable food as adults, both male and female maternally over-nourished offspring are highly susceptible to diet-induced obesity. This is associated with altered synaptic strength in an extended amygdala-lateral hypothalamic pathway, which is predicted by developmental growth rate. Additionally, lateral hypothalamic neurons receiving synaptic input from the bed nucleus of the stria terminalis have enhanced excitatory input following maternal overnutrition which is predicted by early life growth rate.
Conclusions
Together, these results demonstrate one way in which maternal obesity rewires hypothalamic feeding circuits to predispose offspring to metabolic dysfunctio
