Obesity and male infertility: Mechanisms and management

Abstract

Obesity is characterised as an accumulation of excess body fat that has a detrimental impact on health outcomes and is clinically defined based on the body mass index (BMI), measured as weight (kg) divided by height (meters) squared (kg/m 2) (World Health Organization, 2000). The BMI is recommended by the World Health Organization (WHO) to clinically classify weight and determine clinical risk (Table 1) (McPherson & Lane, 2015). Within this system, obesity is defined as having a BMI of >30 kg/m 2 , while morbid obesity is defined as having a BMI of >35 kg/m 2 (Okorodudu et al., 2010). However, the type and distribution of body fat accumulation are of clinical importance in the assessment of the risk of obesity-related complications (Alberti et al., 2009). In fact, BMI does not consider lean body mass and fat mass proportions, nor the distribution of detrimental visceral adiposity (white adipose tissue) and protective subcutaneous adipose tissue. BMI is therefore considered to have a low sensitivity to appropriately determining adiposity and may underestimate or overestimate the risk of obesity in a significant proportion of the population (Okorodudu et al., 2010). The use of body fat percentage provides insight into the lean and fat mass ratios, differentiated between genders. The accepted consensus for increased risk of adiposity complications is >25% in males and >30% in females (Adler, Cassidy, Fricke, & Bonduriansky, 2013).

Dietary L‐carnitine affects the expression of genes involved in apoptosis and fatty acid metabolism in rooster testes

“…In addition, there is a positive correlation between the level of Bcl2 and the antioxidant status, which confirmed our findings regarding Bcl2 mRNA abundance (Hockenbery et al, 1993). homoeostasis, such that the expression of Bax is highly increased while Bcl2 expression is suppressed (Leisegang et al, 2020).…”

“…Uniquely, it was suggested that dysregulation of apoptosis induction in spermatogenic cells is a main causative factor of male infertility (Leisegang et al, 2020). How the testes are adjusted for apoptosis by nutrients supplementation has received much attention.…”

<p>The Impact of Obesity on Various Semen Parameters and Sex Hormones in Iranian Men with Infertility: A Cross-Sectional Study</p>

“…This eventually affects the release of gonadotropins from the pituitary, reduces steroidogenesis, and results in hypogonadotropic hypogonadism. 11 In addition, daily leptin administration to normal-weight rats has been shown to result in similar abnormalities in sperm parameters. Although the major pathways causing these abnormalities still remain unidentified, these adverse effects have been attributed to the leptin-induced increased oxidative stress and uncontrolled production of reactive oxygen species (ROS).…”

“…In human beings, increase in BMI reduces plasma sex hormone-binding globulin (SHBG) that results in lower testosterone and higher estrogen levels. 4,11,[31][32][33][34][35][36] Additionally, the state of obesity itself perpetuates high estrogen levels, due to a greater white adipose tissue. 37 Correspondingly, these hormonal changes were also observed in the present study.…”

“…It was reported that obesity can affect the GnRH-FSH/LH pulse; impair the functions of Sertoli and Leydig cells; and thereby affect the release of sex hormones, sperm production, and maturation. 10,11 Serum testosterone, gonadotropin, and sex hormonebinding globulin (SHBG) are also reported to decrease along with increasing body mass index (BMI), whereas estradiol increased with increasing BMI. 12 So, these endocrine dysregulations in obese males may be associated with an increased risk of alterations in semen quality.…”