Study Finds Dietary Changes May Enhance Mitochondrial Function and Decrease Inflammation in Obesity

A randomized clinical trial involving obese individuals highlighted 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.

The study was published in the journal Clinical Nutrition.

Various dietary interventions, such as calorie restriction, intermittent fasting, and ketogenic diets, are popular for improving metabolic profiles and promoting weight loss in obese individuals. Mitochondria, essential for cellular energy, adapt to environmental signals to manage energy use. In obesity, mitochondrial dysfunction in monocytes contributes to chronic inflammation, a key feature of obesity. Monocytes regulate fatty acid oxidation to reduce inflammation in low-glucose conditions, suggesting dietary restrictions may impact monocyte bioenergetics.

In the randomized clinical trial, 44 obese individuals were randomly assigned to one of four dietary interventions: calorie restriction, intermittent fasting, a ketogenic diet, or an ad libitum habitual diet for one month. They then received the antibiotic rifaximin while continuing their assigned diets for another month to assess the gut microbiota's role in modulating the diets' effects on mitochondrial function in monocytes. Over four follow-up visits, researchers measured mitochondrial function in monocytes, serum anthropometric and biochemical parameters, and gut microbiota composition in fecal samples.

The results showed that calorie restriction, intermittent fasting, and ketogenic diet significantly increased the maximal respiration oxygen consumption rate in monocytes compared to an ad libitum habitual diet. A significant induction in the gut microbiota diversity was observed in response to both dietary intervention and rifaximin in the intermittent fasting and ketogenic diet groups.

This improved mitochondrial function was linked to reduced monocyte dependence on glycolysis in the intermittent fasting and ketogenic diet groups. These dietary interventions improved body composition and mitochondrial bioenergetic health in obese adults, shifting monocyte energy reliance from glycolysis to mitochondrial respiration. Additionally, positive changes in gut microbiota composition were observed.

The findings suggested that the improvement in mitochondrial function is associated with reduced serum LPS and LPS-mediated intracellular signalling in monocytes.

Reference: Martha Guevara-Cruz. 2024. Intermittent fasting, calorie restriction, and a ketogenic diet improve mitochondrial function by reducing lipopolysaccharide signaling in monocytes during obesity: A randomized clinical trial. Clinical Nutrition. https://www.sciencedirect.com/science/article/pii/S0261561424002280