Departments of Nutrition, Schools of Medicine and Engineering, Case Western Reserve University, 10900 Euclid Ave., W-G48, Cleveland, OH, 44106-4954, USA.
Departments of Biomedical Engineering, Schools of Medicine and Engineering, Case Western Reserve University, 10900 Euclid Ave., W-G48, Cleveland, OH, 44106-4954, USA.
Adv Exp Med Biol. 2013;789:323-328. doi: 10.1007/978-1-4614-7411-1_43.
The coupling of upstream oxidative processes (glycolysis, beta-oxidation, CAC turnover) to mitochondrial oxidative phosphorylation (OXPHOS) under the driving conditions of energy demand by the cell results in the liberation of free energy as ATP. Perturbations in glycolytic CAC or OXPHOS can result in pathology or cell death. To better understand whole body energy expenditure during chronic ketosis, we used a diet-induced rat model of ketosis to determine if high-fat-carbohydrate-restricted "ketogenic" diet results in changes in total energy expenditure (TEE). Consistent with previous reports of increased energy expenditure in mice, we hypothesized that rats fed ketogenic diet for 3 weeks would result in increased resting energy expenditure due to alterations in metabolism associated with a "switch" in energy substrate from glucose to ketone bodies. The rationale is ketone bodies are a more efficient fuel than glucose. Indirect calorimetric analysis revealed a moderate increase in VO2 and decreased VCO2 and heat with ketosis. These results suggest ketosis induces a moderate uncoupling state and less oxidative efficiency compared to glucose oxidation.
在细胞能量需求的驱动下，上游氧化过程（糖酵解、β-氧化、CAC 周转）与线粒体氧化磷酸化（OXPHOS）偶联，导致自由能以 ATP 的形式释放。糖酵解 CAC 或 OXPHOS 的扰动可导致病理或细胞死亡。为了更好地了解慢性酮症期间的全身能量消耗，我们使用饮食诱导的大鼠酮症模型来确定高脂肪-碳水化合物限制的“生酮”饮食是否会导致总能量消耗 (TEE) 的变化。与先前报道的小鼠能量消耗增加一致，我们假设喂养生酮饮食 3 周的大鼠由于与“切换”能量底物（从葡萄糖到酮体）相关的代谢改变而导致静息能量消耗增加。其原理是酮体比葡萄糖更有效率的燃料。间接量热分析显示酮症导致 VO2 适度增加，VCO2 和热量减少。这些结果表明酮症诱导的解偶联状态和氧化效率低于葡萄糖氧化。
