Abstract: Diabetes and Cancer are global chronic ailments with a significant impact on expectancy and quality of life. Metabolic disorders analysed during the progression and onset of diabetes may have a crucial function in the progression and initiation of carcinogenesis. Although there is growing evidence linking diabetes to some types of cancer, the fundamental processes of this possible relationship remain unclear. Insulin is a potent growth factor that either directly or indirectly stimulates cell division and carcinogenesis through the insulin-like growth factor 1 (IGF-1) pathway. To date, there is no critical data regarding the mechanism responsible for the relationship between diabetes and different types of cancer in humans. Although the latest evidence proposes that both hyperinsulinemia and hyperglycemia in diabetes could bring about pro-carcinogenic stress responses, for instance, lipotoxicity, glucotoxicity, and oxidative stress, which are involved in the process of transformation, increasing the chances of developing cancer. Because hyperinsulinemia inhibits IGF binding protein-1, it increases the bioactivity of IGF-1. Excess hyperglycemia may encourage the growth of cancer cells both directly and indirectly. Additionally, clinical studies have discovered that various anti-diabetic treatments may potentially cause the risk of cancer via undefined mechanisms. Natural compounds (p- and ricinoleic acid, epigallocatechin, coumaric acid, ricinine) targeting both ailments are described, along with their mechanisms of action. Thus, through this review, we targeted the pathophysiological and epidemiological aspects of diabetes, which further direct the process of cancer progression and initiation.
Apurva et al. (Tue,) studied this question.