Abstract

The rampant growth of obesity worldwide has stimulated explosive research into human metabolism. Metabolic rate has been shown to be altered by diets differing in macronutrient composition, with low-carbohydrate, ketogenic diets eliciting a significant increase over other interventions. The purpose of this study was to determine the effects of the ketone β-hydroxybutyrate (βHB) on mitochondrial respiration and coupling status in adipose tissue. To explore this, we employed three distinct systems, namely cell, rodent, and human models. In every model, βHB robustly increased mitochondrial respiration. Furthermore, in cultured adipocytes and rodent adipose, we quantified the expression of genes involved in mitochondrial biogenesis and coupling status. We observed that genes involved in mitochondrial biogenesis and uncoupling were significantly higher in models exposed to ketone treatments. In conclusion, ketones increase mitochondrial respiration in cells and mammalian adipose tissue, but not ATP production, indicating greater mitochondrial uncoupling. These findings may partly explain the increased metabolic rate evident in states of elevated ketones and may facilitate the development of novel obesity interventions in the future.

Degree

College and Department

Life Sciences; Physiology and Developmental Biology

Rights

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