For many years metformin has been the gold standard in the treatment of type 2 diabetes. According to recommendations of the most important diabetes associations, this is the first-choice drug for use as monotherapy in patients with newly diagnosed type 2 diabetes. Metformin is also recommended in combined treatment when monotherapy is no longer effective. It is then combined with a sulfony­lurea, an incretin, flozin, or insulin, irrespective of the number of insulin injections per day. Besides its properties used in the treatment of diabetes, metformin has been treated for some time as a drug of a so-called pleiotropic activity, as each year brings new reports about its favourable effect in different conditions. At present, the scope of reimbursed indications of this drug has been expanded to include prediabetes, insulin resistance syndromes, and polycystic ovary syndrome. Metformin does not stimulate insulin secretion by the beta cells of the pancreas, and thus it is a drug that does not cause hypoglycaemia. The blood glucose-lowering effect of the drug is a consequence of hepatic glucose production inhibition, and of peripheral tissue (muscle tissue, fatty tissue) sensitisation to the effect of insulin of both endogenous and exogenous origin. The exact mechanism of metformin action at the cellular level remained unknown for a long time. Studies performed in recent years have provided a great deal of information that enables better understanding of the mechanism of action of the drug as well as the clinical effects resulting from its use. Metformin, besides improvement of glycaemia, is neutral to body weight, is cardioprotective, improves lipid profile, and has a probable anti-cancer effect. Metformin accumulation in the intestinal mucosa may interfere with FDG (18F-deoxyglucose) PET-CT image assessment. The aim of this article is a detailed discussion of metformin properties, its mechanisms of action, and clinical effects. For many years metformin has been the gold standard in the treatment of type 2 diabetes. According to recommendations of the most important diabetes associations, this is the first-choice drug for use as monotherapy in patients with newly diagnosed type 2 diabetes. Metformin is also recommended in combined treatment when monotherapy is no longer effective. It is then combined with a sulfony­lurea, an incretin, flozin, or insulin, irrespective of the number of insulin injections per day. Besides its properties used in the treatment of diabetes, metformin has been treated for some time as a drug of a so-called pleiotropic activity, as each year brings new reports about its favourable effect in different conditions. At present, the scope of reimbursed indications of this drug has been expanded to include prediabetes, insulin resistance syndromes, and polycystic ovary syndrome. Metformin does not stimulate insulin secretion by the beta cells of the pancreas, and thus it is a drug that does not cause hypoglycaemia. The blood glucose-lowering effect of the drug is a consequence of hepatic glucose production inhibition, and of peripheral tissue (muscle tissue, fatty tissue) sensitisation to the effect of insulin of both endogenous and exogenous origin. The exact mechanism of metformin action at the cellular level remained unknown for a long time. Studies performed in recent years have provided a great deal of information that enables better understanding of the mechanism of action of the drug as well as the clinical effects resulting from its use. Metformin, besides improvement of glycaemia, is neutral to body weight, is cardioprotective, improves lipid profile, and has a probable anti-cancer effect. Metformin accumulation in the intestinal mucosa may interfere with FDG (18F-deoxyglucose) PET-CT image assessment. The aim of this article is a detailed discussion of metformin properties, its mechanisms of action, and clinical effects.

BACKGROUND:New-onset diabetes after transplantation (NODAT) is a serious complication after a solid organ transplant. NODAT occurs in 2% to 53% of all solid organ transplant recipients. The identification of high-risk patients and the implementation of measures to limit the development of NODAT can improve the long-term patient prognosis. MATERIAL AND METHODS:Our study group consisted of 336 patients undergoing heart transplant. Patients with prior diabetes (60 patients) were excluded from analysis. The remaining 276 patients were divided in 2 groups: with NODAT (n=109) and without NODAT (n=167). Logistic regression analysis was used for NODAT risk factor assessment. RESULTS:NODAT occurred in 109 (32%) out of 336 patients without diagnosed diabetes before heart transplantation. Risk factors for post-transplant diabetes mellitus, which was shown by the analysis of the collected data, were BMI at discharge (OR=1.082, CI 1.011-1.158, p=0.0233), history of diagnosed CMV infection (OR=1.464, CI 1.068-2.007, p=0.0179), and age over 51 years (OR=1.634, CI 1.274-2.095, p=0.0001). CONCLUSIONS:1. New-onset diabetes after transplantation (NODAT) or long-lasting hypoglycemia (over 2 years after transplantation) was diagnosed in 32% patients after heart transplantation developed. 2. The risk factors of NODAT were BMI at discharge and history of diagnosed CMV infection, and age over 51 years was an independent risk factor.

Diabetes mellitus is a major, global problem. Among the numerous complications of diabetes, there is increasing concern over the coexisting heart failure. Metformin is the most frequently used oral antidiabetic drug that is considered to be safe and effective in the management of type 2 diabetes mellitus. Since the publication of the UK Prospective Diabetes Study, it has been suggested that metformin might improve cardiovascular prognoses. Results from available studies have shown that metformin therapy in patients with type 2 diabetes mellitus and heart failure was associated with improved clinical outcomes when compared with other oral antidiabetic agents, insulin, or lifestyle management. However, there have been no randomized controlled trials evaluating the influence of metformin use on clinical outcomes in patients with type 2 diabetes mellitus and heart failure. New evidence from large cardiovascular outcome trials that showed a reduction in heart failure hospitalization for SGLT2 inhibitors caused changes in recommendations on the management of hyperglycaemia. Currently, the European Society of Cardiology recommends sodium-glucose co-transporter 2 inhibitors in patients with type 2 diabetes mellitus and heart failure or at high risk for heart failure, as a first choice in drug naïve patients, or as a second drug if the patient is already on metformin. The aim of our study is to review the current state of knowledge about the position of metformin in the treatment of patients with type 2 diabetes mellitus and heart failure. Diabetes mellitus is a major, global problem. Among the numerous complications of diabetes, there is increasing concern over the coexisting heart failure. Metformin is the most frequently used oral antidiabetic drug that is considered to be safe and effective in the management of type 2 diabetes mellitus. Since the publication of the UK Prospective Diabetes Study, it has been suggested that metformin might improve cardiovascular prognoses. Results from available studies have shown that metformin therapy in patients with type 2 diabetes mellitus and heart failure was associated with improved clinical outcomes when compared with other oral antidiabetic agents, insulin, or lifestyle management. However, there have been no randomized controlled trials evaluating the influence of metformin use on clinical outcomes in patients with type 2 diabetes mellitus and heart failure. New evidence from large cardiovascular outcome trials that showed a reduction in heart failure hospitalization for SGLT2 inhibitors caused changes in recommendations on the management of hyperglycaemia. Currently, the European Society of Cardiology recommends sodium-glucose co-transporter 2 inhibitors in patients with type 2 diabetes mellitus and heart failure or at high risk for heart failure, as a first choice in drug naïve patients, or as a second drug if the patient is already on metformin. The aim of our study is to review the current state of knowledge about the position of metformin in the treatment of patients with type 2 diabetes mellitus and heart failure.

(1) Background: The aim was to assess whether combined aerobic and resistance training performed under hypoxic and normoxic conditions had an impact on diabetes control, VO₂max (maximum oxygen consumption), and echocardiological and anthropometric parameters in men with long-term type 1 diabetes. (2) Methods: Sixteen male participants (mean age: 37 years, mean HbA1c (glycated hemoglobin): 7.0%) were randomly assigned to two groups: training in normoxic conditions or training in conditions of altitude hypoxia. All subjects participated in 60 min combined aerobic and resistance training sessions twice a week for 6 weeks. At baseline and in the 6th week, echocardiography, incremental exercise test, and anthropometric and diabetes control parameters were assessed. (3) Results: After 6 weeks, there was no significant change in HbA1c value in any group. We noted a more stable glycemia profile during training in the hypoxia group (p > 0.05). Patients in the hypoxia group required less carbohydrates during training than in the normoxia group. A comparable increase in VO₂max was observed in both groups (p > 0.05). There were no significant differences in cardiological and anthropometric parameters. (4) Conclusions: Combined aerobic and resistance training improved VO₂max after 6 weeks regardless of the conditions of the experiments. This exercise is safe in terms of glycemic control in patients with well-controlled diabetes.