Obesity and
metabolic syndrome (MetS) are global epidemics, driven by an obesogenic environment. This is mediated by complex underlying pathophysiology, in which chronic
inflammation is an important aetiological and mechanistic phenomenon. A shift towards a subclinical TH 1-lymphocyte mediated innate and chronic inflammatory response is well defined in
obesity and MetS, demonstrated in multiple systems including visceral adiposity, brain (hypothalamus), muscles, vasculature, liver, pancreas, testes, epididymis, prostate and seminal fluid. Inflammatory
cytokines disrupt the hypothalamic-pituitary-testes axis and steroidogenesis cascades (
hypogonadotropic hypogonadism), spermatogenesis (poor semen parameters, including DNA fragmentation and detrimental epigenetic modification) and results in subclinical
prostatitis and prostate
hyperplasia. This review aims to highlight the role of chronic
inflammation in
obesity and MetS,
cytokines in male reproductive physiology and pathophysiology, the impact on steroidogenesis and spermatogenesis, prostate pathology and
erectile dysfunction. Currently, it is recommended that clinical assessment of
male infertility and reproductive dysfunction in obese and MetS patients includes
inflammation assessment (highly sensitive
C-reactive protein), and appropriate advice and therapeutic options are incorporated in the management options. However, the mechanisms and therapeutic options remain poorly understood and require significant interdisciplinary research to identify potential novel therapeutic strategies.