A ketogenic diet lowers myocardial fatty acid oxidation but does not affect oxygen consumption: a study in overweight humans

Author:

Luong Thien Vinh12ORCID,Pedersen Mette Glavind Bülow23,Abild Caroline Bruun24,Cunnane Stephen C.5,Croteau Etienne6,Lauritsen Katrine Meyer24,Kjærulff Mette Louise Gram12,Tolbod Lars Poulsen1,Møller Niels34,Søndergaard Esben2,Gormsen Lars Christian1

Affiliation:

1. Department of Nuclear Medicine and PET Center Aarhus University Hospital Aarhus N Denmark

2. Steno Diabetes Center Aarhus Aarhus University Hospital Aarhus N Denmark

3. Medical/Steno Aarhus Research Laboratory, Department of Clinical Medicine Aarhus University Denmark

4. Department of Endocrinology and Internal Medicine Aarhus University Hospital Aarhus N Denmark

5. Department of Medicine and Research Center on Aging Université de Sherbrooke Sherbrooke Quebec Canada

6. Sherbrooke Molecular Imaging Center Université de Sherbrooke Sherbrooke Quebec Canada

Abstract

AbstractObjectiveA ketogenic diet (KD) characterized by very low carbohydrate intake and high fat consumption may simultaneously induce weight loss and be cardioprotective. The “thrifty substrate hypothesis” posits that ketone bodies are more energy efficient compared with other cardiac oxidative substrates such as fatty acids. This work aimed to study whether a KD with presumed increased myocardial ketone body utilization reduces cardiac fatty acid uptake and oxidation, resulting in decreased myocardial oxygen consumption (MVO2).MethodsThis randomized controlled crossover trial examined 11 individuals with overweight or obesity on two occasions: (1) after a KD and (2) after a standard diet. Myocardial free fatty acid (FFA) oxidation, uptake, and esterification rate were measured using dynamic [11C]palmitate positron emission tomography (PET)/computed tomography, whereas MVO2 and myocardial external efficiency (MEE) were measured using dynamic [11C]acetate PET.ResultsThe KD increased plasma β‐hydroxybutyrate, reduced myocardial FFA oxidation (p < 0.01) and uptake (p = 0.03), and increased FFA esterification (p = 0.03). No changes were observed in MVO2 (p = 0.2) or MEE (p = 0.87).ConclusionsA KD significantly reduced myocardial FFA uptake and oxidation, presumably by increasing ketone body oxidation. However, this change in cardiac substrate utilization did not improve MVO2, speaking against the thrifty substrate hypothesis.image

Funder

Novo Nordisk Fonden

Publisher

Wiley

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