Premium
Calorie restriction and glucose regulation
Author(s) -
Yamada Kelvin A.
Publication year - 2008
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2008.01847.x
Subject(s) - ketogenic diet , calorie restriction , endocrinology , ampk , medicine , hypoglycemia , calorie , epileptogenesis , leptin , glycolysis , protein kinase a , glucose uptake , insulin , glucose transporter , anticonvulsant , epilepsy , biology , kinase , neuroscience , metabolism , obesity , biochemistry , hippocampal formation
SummaryKetogenic diets (KDs) are effective treatments for epilepsy. The mechanisms of action are poorly understood. In some experimental seizure models, calorie restriction and hypoglycemia may augment the antiseizure effects of KDs. In addition, inhibiting glycolysis or diverting glucose from the glycolytic pathway inhibits seizures and possibly epileptogenesis, suggesting an interaction between energy regulation and the anticonvulsant actions of these interventions. Children on KDs frequently exhibit poor weight gain and have lower blood glucose levels compared to children on standard, balanced diets. Young rodents on a KD also exhibit slow weight gain, lower blood glucose and insulin levels, and elevated leptin levels. This review considers the possibility that calorie restriction, low serum glucose, and KDs share common cell signaling pathways to alter brain excitability. AMP‐activated protein kinase (AMPK) is an attractive candidate signaling protein that could link energy balance to gene expression in such a way so as to reduce brain excitability.