The relationship of obesity and prostate cancer (review)

Obesity is a critical risk factor for prostate cancer (PCa). Adipose tissue plays an important role in tumor development, including growth, invasion, and metastasis. Diet and dietary components affect the progression of prostate cancer; however, the mechanisms underlying these associations remain unclear. Extraprostatic prostate tumor cells form a new microenvironment in the periprostatic adipose tissue, which alters these interactions and promotes tumor progression. Hyperinsulinemia leads to an increase in the level of free or biologically active insulin-like growth factor (IGF-1) due to a decrease in the production of IGF-binding proteins. Hypoandrogenism promotes the development of a more aggressive type of prostate cancer (higher Gleason scores). Adipokines of adipose tissue and cytokines (for example, interleukin-6 (IL-6) and tumor necrosis factor (TNF-α), angiogenic factors (for example, vascular endothelial growth factor (VEGF), apelin (AGTRL1) and other factors (for example, leptin and adiponectin) have multiple effects on prostate cancer cells. Tumor cells interact directly or indirectly with adipocytes. Yellow (inactive) bone marrow is adipose tissue with separate islands of reticular tissue. It is located in the medullary canals of the tubular bones and in parts of the cells of the cancellous bone. Bone tissue is the object of the most frequent metastasis in prostate cancer, and with age, the content of fat cells in it increases. Bone marrow adipose tissue interacts with tumor cells, osteoblasts and other stromal cells and participates in the organization of the tumor microenvironment. Adipokines are key molecules in the interaction between tumor cells and adipose tissue, which is carried out through various mechanisms. A better understanding of the role of adipose tissue in the induction and progression of prostate cancer will lead to effective therapeutic strategies for this disease

Metabolic changes in patients with prostate cancer with androgen deprivation therapy

Prostate cancer is the most common type of cancer among men. Androgen deprivation therapy (ADT) is the most effective treatment for this disease. The cornerstone of prostate cancer treatment is the inhibition of testosterone production, which interrupts testosterone-induced growth of the prostate tumour. A sharp decrease in testosterone, however, has several undesirable effects on the metabolic profile and bone metabolism and can also lead to fatigue, loss of libido, gynecomastia and anaemia, provoke vasomotor hyperaemia and generally affect the quality of life. To increase the good (long-term) survival of patients with prostate cancer, studying the side effects associated with treatment is important, and therefore, in every clinical situation, the benefits of ADT must be compared with the side effects associated with the treatment. This article focuses on the described metabolic complications of ADT, including obesity, diabetes, lipid changes, metabolic syndrome and cardiovascular diseases. It also contains practical recommendations for managing the side effects and complications based on the available guidelines issued by the medical professional community

Effect of Metabolic Syndrome in Patients with Prostate Cancer (Review)

The human prostate gland is an endocrine organ in which dysregulation of various hormonal factors plays a key role in the development of non-tissue transformation and leads to the formation of prostate cancer. Existing epidemiological data confirm the role of the components of the metabolic syndrome, namely obesity, hypercholesterolemia, diabetes, and hyperinsulinemia, in the development and/or progression of prostate cancer. Although the exact mechanisms underlying the relationship between metabolic syndrome and prostate cancer remain largely unknown, it has been shown that various "in vitro" and animal experiments with models of the metabolic syndrome contribute to survival, mitogenesis, metastasis, and treatment resistance pathways through various adaptive reactions, such as intracellular steroidogenesis and lipogenesis. Although the exact biopathophysiological mechanisms between metabolic syndrome and prostate cancer have yet to be studied, drugs that target specific components of the metabolic syndrome have also provided evidence for the relationship between metabolic syndrome, its components, and prostate cancer. The appearance of “in vitro” results and molecular genetic research data will bring us closer to using this knowledge to determine specific ways of cancer-specific survival and improve treatment outcomes in patients with this disease