Outcome

The study demonstrates that hyperbaric oxygen therapy (HBOT) administered at 2.0 atmospheres absolute with 100% oxygen significantly mitigates the detrimental effects of a high-fat diet on body weight and lipid metabolism in mice. HBOT effectively reduced weight gain fat tissue size and serum free fatty acid levels while improving the function of enzymes and proteins involved in fat metabolism such as hormone-sensitive lipase (HSL) and PPARα.

Introduction

Obesity and metabolic syndrome often driven by high-fat diets (HFD) represent significant global health challenges. Hyperbaric oxygen therapy (HBOT) has emerged as a promising intervention to counteract these issues. This study investigates the effects of HBOT administered at 2.0 atmospheres absolute with 100% oxygen on mice subjected to an HFD over four weeks. The results reveal that HBOT effectively mitigates weight gain reduces fat tissue size and normalizes lipid metabolism markers. Specifically HBOT treatment decreased adipocyte size serum free fatty acid levels and fat deposition while balancing L-carnitine levels and reversing biochemical changes induced by HFD. Additionally HBOT improved fat metabolism by enhancing the function of key enzymes and proteins such as hormone-sensitive lipase (HSL) uncoupling protein 1 (UCP1) and peroxisome proliferator-activated receptor-alpha (PPARα). These findings suggest that HBOT could be a powerful therapeutic tool for managing obesity and related metabolic disorders by improving overall metabolic health and addressing lipid metabolism dysfunction.

Results

Hyperbaric oxygen therapy (HBOT) demonstrated a significant mitigation of the negative effects imposed by a high-fat diet (HFD) on body weight and lipid metabolism in C57/B6 mice. Mice undergoing HBOT at 2.0 atmospheres absolute with 100% oxygen for four weeks exhibited notable reductions in weight gain and fat tissue mass specifically within both epididymal and inguinal white adipose tissues. Additionally HBOT alleviated the increase in adipocyte size in epididymal white adipose tissue (EWAT) and the size of fat droplets in brown adipose tissue (BAT).

A critical finding was HBOT’s effect on biochemical markers of lipid metabolism. The therapy significantly decreased serum free fatty acid levels which had been elevated by the HFD and positively regulated L-carnitine levels reversing dysregulation induced by the diet. Notably while HBOT mitigated the spike in serum L-carnitine levels it increased L-carnitine concentrations in skeletal muscles.

Molecular assessments underscored the therapeutic potential of HBOT in normalizing lipid-metabolism-related enzymes and proteins. HBOT reversed the HFD-induced decrease in the expression of hormone-sensitive lipase (HSL) in both EWAT and BAT. It also abolished the HFD-induced increases in the phosphorylation of HSL and the expression of uncoupling protein 1 (UCP1) in BAT which are crucial in lipid metabolism and energy expenditure.

Furthermore HBOT corrected the dysregulated expression of carnitine palmitoyltransferase 1B (CPT1b) and peroxisome proliferator-activated receptor-alpha (PPARα) in skeletal muscle tissues. Both CPT1b and PPARα are pivotal proteins for fatty acid oxidation and energy metabolism indicating that HBOT helps restore normal metabolic function disrupted by a high-fat diet.

These findings collectively suggest that HBOT has considerable potential in managing obesity and metabolic syndrome by addressing lipid metabolism dysfunction. The regulation of L-carnitine levels and PPARα expression appears to be particularly influential in mediating these beneficial effects. Therefore HBOT emerges as a promising non-invasive intervention for obesity and related metabolic disorders potentially paving the way for new therapeutic approaches.

Conclusion

In conclusion this study highlights the significant potential of hyperbaric oxygen therapy (HBOT) as a therapeutic intervention for obesity and metabolic syndrome induced by a high-fat diet (HFD). HBOT treatment at 2.0 atmospheres absolute with 100% oxygen effectively mitigated weight gain reduced adipocyte size and normalized serum free fatty acid and L-carnitine levels. These beneficial outcomes are linked to improved regulation of key metabolic enzymes and proteins such as hormone-sensitive lipase (HSL) and peroxisome proliferator-activated receptor-alpha (PPARα) which are crucial for lipid metabolism and energy homeostasis. The findings indicate that HBOT can address lipid metabolism dysfunction and offers a promising non-invasive treatment strategy for managing obesity and related metabolic disorders. Future research should explore the underlying mechanisms further and assess the long-term efficacy and safety of HBOT in diverse populations to validate its potential as a mainstream therapeutic option for metabolic health.