Key result
Obese subjects with MAFLD showed increased myocardial free fatty acid oxidation after exercise compared to a decrease in controls (4.8 vs 4.0 μmol·100 ml⁻¹ min⁻¹; p<0.048).
Why the study?
MAFLD is associated with dyslipidemia and may promote cardiac lipotoxicity, but whether exercise-induced myocardial FFA oxidation, VLDL-TG secretion, hepatic FFA utilization, and lactate production differ in obese subjects with vs without MAFLD was unclear.
Does exercise alter myocardial free fatty acid oxidation differently in obese subjects with MAFLD compared to those without MAFLD?
Observational (n=17)
Does exercise alter myocardial free fatty acid oxidation differently in obese subjects with MAFLD compared to those without MAFLD?
Absolute Event Rate: 4.8% vs 4%
p-value: p=<0.048
Obese subjects with MAFLD exhibit abnormal myocardial and hepatic fatty acid metabolism during exercise, failing to downregulate myocardial free fatty acid oxidation compared to controls.
Small mechanistic study in obese subjects; leaves open whether MAFLD alters exercise-related myocardial and hepatic metabolism.
Background and aims Metabolic dysfunction-associated fatty liver disease (MAFLD) is associated with dyslipidemia and may promote cardiac lipotoxicity. Myocardial free fatty acids (FFA) oxidation (MO FFA ) is normal in pre-diabetes, but reduced in heart failure. We hypothesized that during exercise MO FFA , very low-density lipoprotein triglycerides (VLDL-TG) secretion, hepatic FFA utilization, and lactate production differ among obese subjects with and without MAFLD. Methods Nine obese subjects with MAFLD and 8 matched subjects without MAFLD (Control) without a history of heart failure and cardiovascular disease were compared before and after 90-min exercise at 50% Peak oxygen consumption. Basal and exercise induced cardiac and hepatic FFA oxidation, uptake and re-esterification and VLDL-TG secretion were measured using [ 11 C]palmitate positron-emission tomography and [1– 14 C]VLDL-TG. Results In the heart, increased MO FFA was observed after exercise in MAFLD, whereas MO FFA decreased in Control (basal vs exercise, MAFLD: 4.1 (0.8) vs 4.8 (0.8) μmol·100 ml −1 min −1 ; Control: 4.9 (1.8) vs 4.0 (1.1); μmol·100 ml −1 min −1 , mean (SD), p < 0.048). Hepatic FFA fluxes were significantly lower in MAFLD than Control and increased ≈ two-fold in both groups. VLDL-TG secretion was 50% greater in MAFLD at rest and similarly suppressed during exercise. Plasma lactate increased significantly less in MAFLD than Control during exercise. Conclusions Using robust tracer-techniques we found that obese subjects with MAFLD do not downregulate MO FFA during exercise compared to Control, possibly due to diminished lactate supply. Hepatic FFA fluxes are significantly lower in MAFLD than Control, but increase similarly with exercise. VLDL-TG export remains greater in MAFLD compared to Control. Basal and post-exercise myocardial and hepatic FFA, VLDL-TG and lactate metabolism is abnormal in subjects with MAFLD compared to Control.
No takes yet. Share an insight, caveat, or question.
Risikesan et al. (2023) conducted an observational in Metabolic dysfunction-associated fatty liver disease (MAFLD) (n=17). Metabolic dysfunction-associated fatty liver disease (MAFLD) vs. Obese subjects without MAFLD was evaluated on Myocardial free fatty acid oxidation (MO FFA) during exercise (p=<0.048). Obese subjects with MAFLD showed increased myocardial free fatty acid oxidation after exercise compared to a decrease in controls (4.8 vs 4.0 μmol·100 ml⁻¹ min⁻¹; p<0.048).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: