the Silesia region (Poland). The exclusion criteria were as follows: microvascular diabetic complications, history of stroke, depression, or other psychiatric disorders, and alcohol abuse.Telemedicine consultation A semi -structured telephone interview was used in all patients, and this was based on the 5 topic areas: current glycemic control, comorbidities, provision of medicines and food products, compliance with individual protection against severe acute respiratory syndrome coronavirus 2 (SARS -CoV -2) infection, and anxiety associated with the current pandemic. Patients answered specific questions related to currently used medications, fasting, and postprandial glucose levels self -measured on the day of the interview or the day before. Anxiety was examined based on questions about the patient's sense of threat associated with SARS -CoV -2 infection and assessed on a scale of 1 to 4 where 1 meant anxiety experienced all the time, and 4-no anxiety present. Severe acute respiratory syndrome coronavirus 2 infection was not diagnosed in the study group.The study was performed in accordance with the guidelines of the 2013 Declaration of Helsinki on human experimentation. Data confidentiality and patient anonymity were maintained at all times. Patient -identifying information had been deleted before the database was analyzed. Individual patients cannot be identified either in this article or in the database. Due to the anonymous nature and mandatory collection of information included in the dataset, informed patient consent was not necessary.Statistical analysis Statistical analysis was performed using the Statistica 13.3 software for
Insulin resistance (IR) may be associated with oxidative stress and leads to cardiovascular disorders. Current research focuses on interplay between insulin-resistance indices and oxidant-antioxidant markers in elderly individuals with or without insulin-resistance. The assessment involved anthropometric data (weight, height, BMI, percentage of body fat (FAT)) and biochemical tests (glucose, lipids, serum insulin and plasma oxidant-antioxidant markers: Thiobarbituric Acid-Reacting Substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1) and total antioxidant status). Insulin resistance index (IR) assuming a cut-off point of 0.3 allows to divides groups into: insulin sensitive group (InsS) IR < 0,3 ( n = 35, median age 69.0 years) and insulin-resistant group (InsR) IR ≥ 0.3 ( n = 51, median age 71.0 years). Lipids and antioxidant defense system markers did not differentiate the investigated groups. In the InsR elderly group, the FAT was increased ( P < 0.000003) and TBARS ( P = 0.008) concentration decreased in comparison with InsS group. A positive correlation for SOD-1 and total antioxidant status ( P < 0.05; r = 0.434) and a negative correlation for TBARS and age ( P < 0.05 with r = −0.421) were calculated in InsR individuals. In elderly individuals, oxidative stress persists irrespective of insulin-resistance status. We suggest that increased oxidative stress may be consequence of old age. An insulin action identifies those at high risk for atherosclerosis, via congruent associations with oxidative stress and extra- and intra-cellular antioxidant defense systems. Thus, we maintain that insulin-resistance is not the cause of aging. Impact statement Insulin resistance is associated with oxidative stress leading to cardiovascular diseases. However, little research has been performed examining elderly individuals with or without insulin-resistance. We demonstrate that antioxidant defense systems alone is not able to abrogate insulin action in elderly individuals at high risk for atherosclerosis, whereas the combined oxidant-antioxidant markers (thiobarbituric acid-reacting substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1), and total antioxidant status (TAS)) might be more efficient and perhaps produce better clinical outcome. In fact, a decrease in oxidative stress and strong interaction between antioxidant defense can be seen only among insulin-resistant elderly individuals. This is, in our opinion, valuable information for clinicians, since insulin-resistance is considered strong cardiovascular risk factor.
ExpErt opinionas well as MATE1 and MATE2-K located in the renal tubular cells. Polymorphism of genes encoding metformin transport membrane proteins or the influence of other drugs on these proteins (e.g. inhibition of the MATE protein by cimetidine) may have a direct impact on the pharmacokinetics of metformin, the variability of the drug response, and the toxic effect of the drug in a particular patient [2,3]. In impaired renal function with decreased creatinine clearance, renal clearance of metformin is also decreased, leading to a prolonged metformin half-life and increased plasma levels. This mechanism may lead to the development of lactic acidosis in patients taking metformin and suffering from acute or chronic kidney disease with significantly reduced glomerular filtration rates [1,3].One of the mechanisms of action of metformin is to inhibit hepatic gluconeogenesis by blocking mitochondrial glycerophosphate dehydrogenase (mGDP), an enzyme that links carbohydrate and lipid metabolic pathways. The action of metformin on the mGDP enzyme hinders the conversion of glycerol-3-phosphate to dihydroxyacetone phosphate (DHAP) and thus blocks gluconeogenesis from glycerol. Due to the influence of metformin on this part of the metabolic pathway, the concentration of oxidized nicotine adenine dinucleotide (NAD+) is decreased, which leads to impaired
Evaluating tools to support a new practical classification of diabetes: excellent control may represent misdiagnosis and omission from disease registers is associated with worse control.
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