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Updated: Sep 9, 2025

Measuring Glucose Uptake in Drosophila Models of TDP-43 Proteinopathy
07:07

Measuring Glucose Uptake in Drosophila Models of TDP-43 Proteinopathy

Published on: August 3, 2021

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ハンチントン病の小児におけるグルコース代謝の調節障害に関する予備的な観察

Federica Graziola1, Federica Rachele Danti1, Martina Penzo2

  • 1Department of Pediatric Neuroscience, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.

Frontiers in neurology
|September 5, 2025
PubMed
まとめ

小児のハンティントン病 (PHD) は,特に基礎性ガンジリアにおいて,脳内のグルコース代謝の低下を示します. しかし,全身のグルコース輸送機能は正常であり,ケトーゲンダイエットのような代謝介入は,PHDの治療に現在推奨されていないことを示唆しています.

キーワード:
GLUT-1欠乏症症候群GLUT1 についてハンティントン病幼児発症のHD小児 ハンチントン病

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Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
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Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
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