Study demonstrates that dietary interventions such as calorie restriction, intermittent fasting, and ketogenic diet improve mitochondrial function in monocytes and reduce inflammation in obesity by modulating gut microbiota.
By Dr. Sanchari Sinha Dutta, Ph.D.Jul 23 2024 A randomized clinical trial involving obese individuals highlights the significance of dietary interventions in improving mitochondrial functions and the metabolic profile of monocytes, which are key aspects for controlling chronic inflammation in obesity.
Mitochondrial dysfunction in monocytes during obesity is known to contribute to low-grade chronic inflammation, a major hallmark of obesity. Recent evidence indicates that monocytes positively regulate fatty acid oxidation to reduce inflammatory responses in low-glucose environments. This suggests that dietary restrictions may influence monocyte bioenergetics.
Related StoriesThe participants subsequently received rifaximin, a non-absorbable antibiotic, and continued with the assigned diet for another month. Rifaximin was used to evaluate gut microbiota's role in modulating dietary interventions' effects on mitochondrial function in monocytes. This improvement in mitochondrial function was associated with a reduction in monocyte dependence on glycolysis for participants from the intermittent fasting and ketogenic diet groups.
Specifically, significant inverse correlations of serum LPS concentration were observed with the maximal respiration oxygen consumption rate, bioenergetic health index, and the bacterium Phascolarctobacterium faecium . A significant reduction in LPS-mediated intracellular signaling was observed in monocytes isolated from participants in the three dietary intervention groups. A significant reduction in body weight and visceral fat was also observed in these participants.
Obesity Chronic Clinical Trial Diet Fasting Glycolysis Intracellular Ketogenic Diet Mitochondria Monocyte Nutrition Oxygen Weight Loss
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