Mechanisms of Obesity-induced Male Infertility

Karen P Phillips; Nongnuj Tanphaichitr


Expert Rev Endocrinol Metab. 2010;5(2):229-251. 

In This Article

Abstract and Introduction


Male infertility, characterized by hypogonadism, decreased semen quality or ejaculatory dysfunction, accounts for approximately 20% of infertility cases. Obesity and metabolic dysfunction have been identified, among other causal factors, to contribute to male infertility. In the context of the Western world's 'obesity epidemic', this article discusses three main biological mechanisms linking obesity to impaired male reproductive function: hypogonadism, testicular heat stress/hypoxia-induced apoptosis and endocrine disruption by 'obesogens'. Among these, obesity-induced hypogonadism is undoubtedly the most clinically significant and is easily assessed. Rapidly expanding areas of research in this area include leptin modulation of kisspeptins and hypothalamic–pituitary–testicular hormone pathways, and roles of other adipocytokines in male infertility, as well as the impact of exposure to obesogens on the quality of semen.


Approximately 30–40% of infertility cases can be attributed to problems with the male partner.[1] Obesity and related concomitant metabolic abnormalities are among the proposed causes of male infertility.[2] Metabolic syndrome has been characterized as a constellation of disorders, including Type 2 diabetes, coronary heart disease, obesity with visceral abdominal fat distribution, dyslipidemia, hypertension and impaired glucose metabolism/insulin resistance.[3–5] In the context of the 'obesity epidemic' in the Western world, this paper discusses three main biological mechanisms linking obesity to impaired male reproductive function. These mechanisms include hypogonadism, testicular heat-stress-/hypoxia-induced apoptosis and endocrine disruption by 'obesogens'.


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