Outcome

Hyperbaric oxygen therapy (HBOT) significantly reduced body weight in obesity-prone MSG mice though it did not alter serum lipid levels. However increased oxidative stress was observed leading to liver damage and abnormal TNF-α expression. These findings suggest that while HBOT may be effective for weight management in metabolic syndrome it also poses risks of organ damage due to heightened oxidative stress.

Introduction

Hyperbaric oxygen therapy (HBOT) is often explored for its potential benefits across various medical conditions. This study delves into the effects of HBOT on obesity diabetes hyperlipidemia and nonalcoholic fatty liver disease using MSG mice an animal model for these conditions. The HBOT-treated group which received therapy in two phases (from 12 to 14 weeks and from 16 to 18 weeks) showed significantly lower body weight compared to the control group indicating a positive impact on obesity. However the therapy did not lead to significant changes in serum lipid levels. An unexpected outcome was the increased oxidative stress observed in the liver histology of HBOT-treated mice showing more severe cellular damage and abnormal TNF-α expression. This study highlights both the potential benefits of HBOT in weight management and its drawbacks such as increased oxidative stress and organ damage offering a nuanced view of its utility in treating metabolic syndromes.

Results

The study examined the impact of hyperbaric oxygen therapy (HBOT) on obesity diabetes hyperlipidemia and nonalcoholic fatty liver disease using MSG mice as a model. Nineteen male mice were divided into two groups: HBOT-treated and control. The HBOT group received treatment during two phases—12 to 14 weeks and 16 to 18 weeks of age.

The most significant finding was the substantial reduction in body weight in the HBOT-treated mice compared to the control group (P < 0.01). By the end of the study the HBOT group exhibited consistently lower body weight signifying the therapy’s noteworthy impact on managing obesity in this model.

Interestingly despite the significant weight loss serum lipid levels remained unchanged between the HBOT-treated and control groups. This indicates that HBOT’s effect on weight did not extend to altering lipid profiles in this particular setting.

A crucial observation was the increased oxidative stress associated with HBOT as evidenced by liver histology. The HBOT group showed more severe cellular damage and abnormal TNF-α expression suggesting a heightened oxidative stress response as a consequence of the treatment. These findings highlight a critical downside: while HBOT effectively reduces body weight it also contributes to liver damage through increased oxidative stress.

Overall the results underscore HBOT’s dual role in this model—demonstrating potential benefits in obesity management but also significant drawbacks due to oxidative stress-induced organ damage. This nuanced outcome stresses the importance of carefully weighing HBOT’s benefits against its risks when considering it as a treatment option for metabolic syndromes.

Conclusion

In conclusion this study has illuminated a dual-sided impact of hyperbaric oxygen therapy (HBOT) on obesity and associated metabolic disorders in MSG mice. The therapy demonstrated a significant reduction in body weight underscoring its potential as a weight management strategy. However the lack of improvement in serum lipid levels and the increased oxidative stress evidenced by liver damage and abnormal TNF-α expression reveal critical challenges. These findings indicate that while HBOT can effectively address obesity it concurrently poses risks of exacerbating organ damage through heightened oxidative stress. Future research should focus on strategies to mitigate these adverse effects potentially combining HBOT with antioxidants or exploring modified therapy protocols to harness its benefits while minimizing harm. This dual-focus approach could pave the way for more effective and safer use of HBOT in treating obesity and related metabolic conditions.