Exploring the role of testosterone upon adiposity and cardiovascular risk markers in men with severe obesity

Abstract

A prominent endocrine disorder linked to unhealthy lifestyle behaviors and increased visceral adiposity is Male Obesity Secondary Hypogonadism (MOSH). The pathogenesis of MOSH remains under investigation. However, recent evidence supports a direct role of leptin in affecting Leydig cells, reducing testosterone production, and increasing appetite. Conversely, testosterone deficiency is associated with comorbidities like hypertension, diabetes, and nonalcoholic fatty liver disease. A recently published study entitled “Relationship between sex hormones, markers of adiposity and inflammation in male patients with severe obesity undergoing bariatric surgery” describes evidence supportive of an inverse association between testosterone and serum leptin as well as levels of c-reactive protein (CRP) and IL-6, as well as a correlation between body mass index and CRP. The same study also provides novel insight retrieved from their in vitro findings, which reveal that testosterone exposure influences the expression of genes associated with adiposity, like fatty acid binding protein 4, peroxisome proliferation-activated receptor γ (PPARγ), leptin, and adiponectin, as well as von Willebrand factor, in human-derived adipocytes. Overall, the latest evidence highlights the importance of early identification of hypogonadism in obese males and the potential benefits of testosterone supplementation in alleviating complications associated with obesity, particularly chronic inflammation. These observations underscore the need for a holistic approach to managing severe obesity, addressing hormonal and inflammatory factors to reduce its overall burden on health.