[Investigation of glycaemic and nutritional status of patients suffering from cancer.] / Daganatos betegek glykaemiás és tápláltsági állapotának vizsgálata.

INTRODUCTION: Obesity, type 2 diabetes mellitus and cancers are equally endemic in our country. Their partially common metabolism may constitute the base of their similar epidemiology. OBJECTIVE: Proving metabolic relation between glycaemic and nutritional status and progression of cancers, as well as confirming the antitumor effect of non-insulin antidiabetics, primarily metformin. METHOD: We processed the data of 1224 patients treated at the Oncology Center in county Békés. We examined the progression of cancers depending on body mass index, blood glucose levels, the presence and therapy of type 2 diabetes, over and above analyzed changes in glycemic and nutritional status in relation to tumor stage, further more prevalence of diabetes mellitus. RESULTS: Despite of malignant cachexy, we found obesity or corresponding body mass index in relatively high rate (23.28%) more often associated with metastatic stage. We detected higher rate of type 2 diabetes (20.34%) compared to average population. We found even larger scale of diabetes among patients suffering from primary hepatocellular (60%, p<0.001), pancreatic (50%, p<0.001), urinary bladder (50%, p<0.001), prostate (50%, p<0.002), endometrial (50%, p<0.02) and postmenopausal breast cancer (30%, p<0.006), compared to other part of the studied population. Patients treated by non-insulin antidiabetics, taking metformin was accompanied by the lowest incidence of metastatic stage, the highest body mass index and blood glucose level. DISCUSSION: In our study, the order of malignant diseases most frequently associated with type-2 diabetes correspond to previously published literature data. Development of insulin resistance accompanied by tumor progression can be effectively delayed by antimetabolic medicines. The combined antimetastatic effect of metformin could achieve glucose and weight control independently. CONCLUSION: Based on our results, targeted screening for cancer among diabetic patients, and seeking and adequately treating glycometabolic disorders with concomitant malignant conditions, respectively , are suggested, mainly using metformin and new non-insulin antidiabetic medicines. Through these efforts, the fight against cancer can be more effective. Orv Hetil. 2023; 164(23) 900-910.

Oncodiabetology I. Metabolic and molecular relationships between cancer and diabetes / Onkodiabetológia I. Metabolikus és molekuláris összefüggések a rosszindulatú daganatok és a cukorbetegség között

In the recent decades, numerous studies have investigated the metabolic and molecular links between carbohydrate metabolic disorders and cancer, raising potential anti-tumor therapies. Based on epidemiological, preclinical, and clinical studies, now we know that advanced diabetes is a distinct risk factor of the development of many tumors, and even prediabetes may lead to the increased risk of developing cancer. Nowadays we can also state that the relationship is also present vice versa. It is a well-known fact that malignancies cause metabolic and molecular changes in the host over time resulting in an insulin-resistant state, characteristic of early diabetes. The tumor-induced insulin resistance may lead to the development of secondary diabetes in some patients with cancer. Furthermore, the diabetogenic ef-fect of the present anticancer therapies may worsen the metabolic condition. In recent years, research exploring the molecular causes of the correlation between malignancies and type 2 diabetes mellitus has highlighted the central role of RAS and PI3K signaling pathways. The altered function of these pathways significantly effects cell cycle, cellular metabolism, cell growth and proliferation, thus modifying cell survival, leading to tumorigenesis and tumor progres-sion and to insulin resistance as well. Without understanding the correlations between IGF receptors, RAS and PI3K signaling pathways the underlying molecular mechanism cannot be understood. Therefore, here we focus on these molecular mechanisms after a brief description of the most important metabolic connections between cancer and diabetes.