Abstract. Carbohydrate metabolism disorders increase the risk of carcinogenesis. Diabetes mellitus alters numerous physiological processes that may encourage cancer growth. However, treating impaired glucose homeostasis may actually promote neoplasia; maintaining proper glucose plasma concentrations reduces metabolic stresses, however, certain medications may themselves result in oncogenic effects. A number of previous studies have demonstrated that metformin reduces the cancer risk. However, the use of sulfonylurea derivatives correlates with an increased risk of developing a malignancy. Another form of treatment, insulin therapy, involves using various forms of insulin that differ in pharmacodynamics, pharmacokinetics and efficacy. Previous studies have indicated that certain insulin variants also affect the cancer risk. The results from analyses that address the safety of long-lasting insulin types raise the most concern regarding the increased risk of malignancy. Rapid development of novel diabetic medications and their widespread use carries the risk of potentially increased rates of cancer, unnoticeable in limited, randomized, controlled trials. In the present review, the results of clinical and epidemiological studies are evaluated to assess the safety of anti-hyperglycemic medications and their effect on cancer risk and outcomes.
Abstract. the most important molecular mechanisms promoting carcinogenesis in patients with diabetes mellitus (DM) include oxidative stress, excessive generation of free radicals and nitrous oxide, damage to cellular membranes and Dna, overproduction of lactate, overabundance of protein glycosylation storage products, overexpression of pathological enzyme isoforms, and leakage of cytochromes from organelles. additionally, dysfunctional signal transduction pathways, especially in pathways involving phosphoinositide 3-kinase (Pi3K)/phosphatase and tensin homolog (Pten)/akt, raS/raf/erK, and mammalian target of rapamycin (mtor), have been implicated in malignant transformation and progression. obesity and metabolic disorders, such as DM, may contribute to a dysfunctional immune system with a suppressed immune response by inducing a chronic inflammatory state, abnormal humoral and cellular mediated immunity, and lower counts and activity levels of natural killer (nK) cells and natural killer t cells (nKt cells). recent advances in molecular biology will allow for better understanding of abnormal cellular pathways, as well as elucidating how metabolic disorders contribute to oncogenesis. Knowledge gained through these studies may lead to more efficacious oncologic therapies. Contents1. insulin resistance and hyperinsulinemia 2. abnormal glucose metabolism and colorectal cancer 3. abnormal glucose metabolism and pancreatic cancer 4. abnormal glucose metabolism and liver cancer 5. abnormal glucose metabolism and breast cancer 6. abnormal glucose metabolism and endometrial cancer 7. abnormal glucose metabolism and prostate cancer 8. abnormal glucose metabolism and lung cancer 9. DM, obesity, and the immune system 10. conclusions Insulin resistance and hyperinsulinemiainsulin is a peptide hormone produced by pancreatic β islet cells, it stimulates the transport of glucose, amino acids, and potassium from circulating blood serum into cells. Binding of the insulin molecule to the insulin receptor (ir) on muscle and liver cells stimulates the induction of glycogen synthesis, fatty acid esterification, lipolysis inhibition, protein catabolism, and gluconeogenesis. irs are present in two isoforms, ir a and B. as a result of glucose and amino acid transport
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