Journal of Obesity & Weight Loss Therapy
Open Access

Weight loss; Obesity; Obstructive Sleep Apnea

Introduction

Obesity has been identified as one of the main causal and perpetuating factors associated with sleep apnea.2 In an epidemiological study conducted in the city of So Paulo, where the prevalence of OSA was 32.8%, 60% of the volunteers were overweight. 3 Obstructive Sleep Apnea (OSA) is characterized by upper airway obstruction during sleep, resulting in periods of apnea, oxyhemoglobin desaturation, and frequent awakenings [1].

The mechanisms underlying OSA and obesity are still poorly understood. Imaging studies have shown that an increase in adipose tissue in the cervicofacial region reduces the volume of the upper airway. Another mechanism would be an increase in visceral fat, which would reduce the volume of the lung and the upper airway, which would support increased pharyngeal collapsibility and reduce caudal tracheal traction.

Literature Review

It is unclear how obesity and losing weight affect bone health in humans. Obesity, on the other hand, does not result in the same bone changes as weight loss does in rodents and humans. Obesity is usually linked to more bone mass in humans, which is made worse by getting older and going through menopause. In contrast, sex, age, and mechanical load all have an impact on the degree and duration of bone mass loss in obese rodents. In spite of these differences, rodents are frequently used as models for the human situation [2]. We focus on the applicability of findings from animal models in this review, which provides a summary of the existing knowledge regarding the effects of obesity and weight loss on bone mass in humans and rodents. Then, we talk about how human skeletal health, obesity, and weight loss can be better understood through the use of animal models. In particular, we draw attention to the aspects of the study design that ought to be taken into consideration in order to maximize the rodent models of obesity and weight loss's translatableness. Particularly, the animals' sex, age, and nutritional status ought to match those of interest to humans [3].

Importantly, ovariectomy is linked to an increase in body weight caused by hyperphagia, which is a type of DIO in and of itself. Since the obesity-induced decrease in bone mass may have already occurred prior to the change in diet, this may conceal a potential effect of HF feeding on bone mass. However, comparing ovariectomized rats fed sham controls and pair-fed ovariectomised rats fed ad libitum showed that there were no differences in bone mass between the two groups. Therefore, the less pronounced changes in bone mass observed in ovariectomized rats cannot be explained by the weight gain caused by hyperphagia.

The epidemic of obesity has increased the focus on developing new, more effective drugs to combat obesity. Therefore, the potential adverse effects of obesity and weight loss on bone health and the complexity of factors, such as age and sex that must be weighed when attempting to treat or prevent adverse bone outcomes are essential considerations [4]. As a result, research on these factors and the individual propensity for harmful skeletal changes is urgently required [5]. This kind of information might be useful in identifying people who are at "high risk," which would make it possible to provide preventative care or early intervention simultaneously [6,7].

Discussion

Discrepancies between human and rodent studies should be taken into consideration when evaluating the changes in bone health caused by obesity to maximize translatability. However, even in situations where translatability is low, animal models may still be useful for mechanistic research into things like hormonal interactions and changes in bone phenotype. Additionally, the goal of intervention studies using antiobesity drugs on obese animals is a return to normal bone mass, regardless of whether it is increased or decreased; consequently, the specific changes at baseline may not be important for translation.

Conclusion

Weight-bearing and non-weight-bearing bones may be affected differently by a reduction in body weight following calorie restriction. According to some studies, the weight-bearing bones in rats are primarily affected. Following calorie restriction, the femoral and tibial trabecular bone volume and cortical cross-sectional area decreased, while the lumbar vertebrae did not change when the bone properties were measured using histological methods. However, non-weightbearing bones showed more pronounced changes, according to others. In a similar vein, gastric surgery resulted in a greater volume loss of trabecular bone in the lumbar vertebrae than in the tibia . Weightbearing bones appear to be particularly affected by a decrease in body weight in mice, with the femur experiencing a greater reduction in trabecular bone mass than the lumbar vertebrae, regardless of whether the decrease in body weight was caused by food restriction or gastric surgery.

Acknowledgement

None

Conflict of Interest

None

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