oxalates and Pancreatic-Neoplasms

Topics: Ethanol; Exocrine Pancreatic Insufficiency; Humans; Intestinal Absorption; Malabsorption Syndromes; Nutrition Disorders; Nutritional Physiological Phenomena; Oxalates; Pancreas; Pancreatic Diseases; Pancreatic Neoplasms; Pancreatitis; Triglycerides

Diabetes mellitus (DM) is a kind of metabolic disorder characterized by long-term hyperglycemia. Oxidative stress is involved in inducing the apoptosis of pancreatic β-cells and promoting the development of DM. Oxalomalate (OMA) is a competitive inhibitor of two classes of NADP+-dependent isocitrate dehydrogenase isoenzymes that are the main nicotinamide adenine dinucleotide phosphate (NADPH) producers to scavenge cellular reactive oxygen species (ROS). However, the role of OMA in DM remains unclear. The present study aimed to investigate the protective effects of OMA on streptozotocin (STZ)-induced β-cell damage and its underlying mechanisms. The viability of rat insulinoma cell line (INS-1) and the contents of ROS, nitric oxide and NAPDH were examined after cells being treated with STZ. After treatment with OMA in STZ-stimulated INS-1, the cell viability, apoptosis, and apoptosis-related proteins were measured. Meanwhile, the levels of oxidative stress-related factors and the changes of insulin secretion were determined. The results revealed that OMA significantly increased the cell viability (p < .05), reduced the apoptotic rate (p < .001), and altered the expression levels of Bcl-2, Bax, cleaved caspase3, and cleaved-caspase9 (p < .05 or p < .01) in STZ-induced INS-1 cells. Moreover, OMA enhanced the activities of superoxide dismutase, catalase, glutathione peroxidase (p < .01), whereas reduced the levels of ROS, malondialdehyde and lactic dehydrogenase (p < .001). Furthermore, OMA improved the ability of insulin secretion. These results indicated that OMA might have antioxidative stress and anti-apoptosis effects to protect INS-1 cells from STZ-induced cell damage.

Topics: Animals; Apoptosis; Cell Line, Tumor; Cell Survival; Insulin Secretion; Insulin-Secreting Cells; Insulinoma; Oxalates; Oxidative Stress; Pancreatic Neoplasms; Rats; Reactive Oxygen Species; Streptozocin

Patients with metastatic renal carcinoma frequently have pre-existing renal impairment and not infrequently develop worsening renal function as a complication of their treatment. The presence of pancreatic metastases in patients with metastatic renal carcinoma, often confers a more favourable prognosis and as a consequence this patient group may be exposed to such treatments for more prolonged periods of time. However, the development of renal failure may also be a consequence of the cancer itself rather than its treatment.. We present an 84-year-old patient receiving the tyrosine kinase inhibitor (TKI) pazopanib for metastatic renal carcinoma who developed oxalate nephropathy as a consequence of pancreatic exocrine insufficiency resulting from pancreatic metastases.. This case demonstrates the importance of investigating unexpected toxicities and highlights the potential consequences of pancreatic insufficiency and its sequelae in patients with pancreatic metastases.

Topics: Acetates; Aged, 80 and over; Calcium Compounds; Carcinoma, Renal Cell; Exocrine Pancreatic Insufficiency; Gastrointestinal Agents; Humans; Indazoles; Kidney Failure, Chronic; Kidney Neoplasms; Male; Oxalates; Pancreatic Neoplasms; Pancrelipase; Protein Kinase Inhibitors; Pyrimidines; Renal Dialysis; Sulfonamides; Treatment Outcome

Topics: Blood Protein Disorders; Cold Temperature; Diagnosis, Differential; Fibrinogen; Humans; Male; Middle Aged; Neoplasm Metastasis; Oxalates; Pancreatic Neoplasms; Phlebitis; Pulmonary Embolism; Thrombophlebitis