Introduction Obesity is associated with diminished myocardial energetic stores, as determined by PCr/ATP, and this is restored with weight loss. We have previously demonstrated that the creatine kinase rate constant (k f CK) is elevated in obesity, which may represent a compensatory mechanism preserving ATP delivery. We hypothesised that intentional weight loss would reduce the requirement for increased enzyme activity, and hence k f CK would fall.
Methods 31 obese individuals (53±13 years, 11 male, BMI 37±5 kg/m-2) underwent comprehensive metabolic phenotyping including MR (3 T, Siemens) for abdominal, hepatic and myocardial fat, and cardiac MR for structure and function. Triple Repetition time Saturation Transfer (TRiST) 31P magnetic resonance spectroscopy was used to measure k f CK. Participants then underwent repeat testing following a dietary weight loss intervention.
Results Mean BMI in the cohort fell from 37±5 kg/m-2 to 33±6 kg/m-2 (p<0.001), with 22 volunteers losing more than 10% body fat (mean −20±15%, p=0.004) and only 2 gaining weight. LV end-diastolic volume and mass fell (from 158±36 ml to 153±35 ml (p<0.001) and 115±31 g to 105±26 g (p=0.006) respectively. k f CK fell from 0.17±0.05s-1 to 0.12±0.05s-1 (p=0.001), a change which correlated with change in both fat mass (r=0.623, p=0.006), and visceral fat volume (r=0.565, p=0.010).
Conclusion We demonstrate that dietary weight loss in an obese population is associated with a fall in k f CK. It has previously been shown that weight loss in this population is associated with an increase in the PCr/ATP ratio. Our findings may reflect a recalibration of the required k f CK in the context of replenished substrate pool (i.e. higher PCr levels). The impact of weight loss in diseases with more profound myocardial energetic deficit must be investigated to establish its safety.
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