Ketogenic Diet (KD) is an isocaloric high-fat (80-90%), low carbohydrate (2-5%) diet applied effectively for treatment of refractory childhood epilepsy, pyruvate dehydrogenase complex deficiency and GLUT1 deficiency. KD induces ketone bodies production to support brain energy metabolism. We considered KD an unique model to evaluate in human the “overflow hypothesis” proposed by Bergman et al (Obesity. 2006;14:16S-19S) about the development of visceral adiposity, hyperinsulinemia, and insulin resistance after isocaloric high fat diet in the dog model. Body composition by anthropometry, subcutaneous (SAT) and visceral abdominal fat (VAT) by ultrasonography, glucose and lipid metabolism were evaluated before and after 12 weeks of KD in 7 children (mean age: 8,4±2,0). The table reports the time course of the main variables investigated In 12 weeks KD did not change BMI z-scores, VAT, SAT and total body fat whereas it significantly reduced fasting glucose, insulin and HOMA and increased QUICKI. No significant changes occurred on lipid metabolism. Thus, increasing fat in the diet without achieving an hypercaloric intake did not increase visceral and subcutaneous abdominal fat and did not cause peripheral insulin resistance in the short term in children. Longitudinal studies are needed to provide a conclusive answer on the adaptive metabolic changes on regional adiposity and insulin resistance occurring in humans during isocaloric high fat diet.
Regional Adiposity and Insulin Resistance: Insights from the Ketogenic Diet in Children / S. Bertoli, A. Battezzati, I. Giulini Neri, C. Trentani, A. Tagliabue. ((Intervento presentato al 73. convegno Scientific Sessions of American Diabetes Association tenutosi a Chicago nel 2013.
Regional Adiposity and Insulin Resistance: Insights from the Ketogenic Diet in Children
S. Bertoli;A. Battezzati;I. Giulini Neri;
2013
Abstract
Ketogenic Diet (KD) is an isocaloric high-fat (80-90%), low carbohydrate (2-5%) diet applied effectively for treatment of refractory childhood epilepsy, pyruvate dehydrogenase complex deficiency and GLUT1 deficiency. KD induces ketone bodies production to support brain energy metabolism. We considered KD an unique model to evaluate in human the “overflow hypothesis” proposed by Bergman et al (Obesity. 2006;14:16S-19S) about the development of visceral adiposity, hyperinsulinemia, and insulin resistance after isocaloric high fat diet in the dog model. Body composition by anthropometry, subcutaneous (SAT) and visceral abdominal fat (VAT) by ultrasonography, glucose and lipid metabolism were evaluated before and after 12 weeks of KD in 7 children (mean age: 8,4±2,0). The table reports the time course of the main variables investigated In 12 weeks KD did not change BMI z-scores, VAT, SAT and total body fat whereas it significantly reduced fasting glucose, insulin and HOMA and increased QUICKI. No significant changes occurred on lipid metabolism. Thus, increasing fat in the diet without achieving an hypercaloric intake did not increase visceral and subcutaneous abdominal fat and did not cause peripheral insulin resistance in the short term in children. Longitudinal studies are needed to provide a conclusive answer on the adaptive metabolic changes on regional adiposity and insulin resistance occurring in humans during isocaloric high fat diet.Pubblicazioni consigliate
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