Chronic wounds are becoming an increasingly common clinical problem due to an aging population and an increased incidence of diabetes, atherosclerosis, and venous insufficiency, which are the conditions that impair and delay the healing process. Patients with diabetes constitute a group of subjects in whom the healing process is particularly prolonged regardless of its initial etiology. Circulatory dysfunction, both at the microvascular and macrovascular levels, is a leading factor in delaying or precluding wound healing in diabetes. The prolonged period of wound healing increases the risk of complications such as the development of infection, including sepsis and even amputation. Currently, many substances applied topically or systemically are supposed to accelerate the process of wound regeneration and finally wound closure. The role of clinical trials and preclinical studies, including research based on animal models, is to create safe medicinal products and ensure the fastest possible healing. To achieve this goal and minimize the wide-ranging burdens associated with conducting clinical trials, a correct animal model is needed to replicate the wound conditions in patients with diabetes as closely as possible. The aim of the paper is to summarize the most important molecular pathways which are impaired in the hyperglycemic state in the context of designing an animal model of diabetic chronic wounds. The authors focus on research optimization, including economic aspects and model reproducibility, as well as the ethical dimension of minimizing the suffering of research subjects according to the 3 Rs principle (Replacement, Reduction, Refinement).

Obstructive sleep apnea syndrome (OSAS) is often associated with impaired glucose metabolism. Data on the effects of OSAS treatment with continuous positive airway pressure (CPAP) on blood glucose and insulin resistance are conflicting. The study aimed at assessing the immediate effect of CPAP on glucose control measured with a continuous glucose monitoring system (CGMS). Nine non-diabetes subjects with OSAS (mean age 53.0 ± 8.0 years; body mass index 34.8 ± 5.3 kg/m2) underwent 2 overnight polysomnographic examinations: a diagnostic study and one with CPAP treatment. Continuous glucose monitoring system (CGMS) was applied overnight on both occasions. Glucose metabolism was assessed with a 75-g oral glucose tolerance test, plasma insulin and homeostatic model assessment of insulin resistance (HOMA-IR) index. The mean (± SD) apnoea-hypopnea index (AHI) at diagnostic polysomnography was 54.3 ± 29.3 (range 16–81). Fasting plasma insulin levels in patients with OSAS was 84.3 ± 43.4 pM at baseline, and the HOMA-IR was 3.6 ± 2.2. CPAP treatment in the subjects with OSAS resulted in a significant reduction in the AHI to 4.5 ± 7.1. All of the major saturation parameters improved significantly on CPAP. CGMS showed mean glucose values significantly higher during the CPAP night than during the diagnostic night: 80 ± 11 mg/dL versus 63 ± 7 mg/dL (P < .01). Fasting insulin and HOMA-IR measured after the CPAP night tended to be higher than at baseline (98.4 ± 51.0 pmol vs 84.3 ± 43.4 pmol and 3.9 pmol ± 2.6 vs 3.6 ± 2.2 pmol, respectively, P > .05). CPAP treatment in nondiabetic obese patients with OSAS may have an immediate elevating effect on blood glucose.

The risk of several types of cancer is increased in type 2 diabetes mellitus. The earliest possible diagnosis of cancer – difficult within regular outpatient diabetes care - is of utmost importance for patients’ survival. The aim of this multicenter, retrospective (years 1998–2015), case-control study was to identify risk factors associated with malignancy in subjects with diabetes treated in a typical outpatient setting. In the databases of 3 diabetic and 1 primary care clinics 203 patients (115 women) with type 2 diabetes mellitus who developed malignancy while treated for diabetes were identified. The control group consisted of 203 strictly age- and gender matched subjects with type 2 diabetes without cancer. Factors associated with diabetes: disease duration, antidiabetic medications use and metabolic control of diabetes were analyzed. Also other variables: BMI (body mass index), smoking habits, place of residence and comorbidities were included into analysis. The most prevalent malignancies in men and women together were breast cancer (20.7 %) and colorectal cancer (16.3 %). HbA1c (hemoglobin A1c) level ≥8.5 %, obesity and insulin treatment in dose-dependent and time-varying manner demonstrated significant association with increased risk of malignancy, while metformin use was associated with a lower risk of cancer. Diabetes duration, comorbidities, smoking habits, place of residence and aspirin use did not show significant association with risk of malignancy. In the outpatient setting the obese patients with poorly controlled insulin treated type 2 diabetes mellitus should be rigorously assessed towards malignancies, particularly breast cancer in women and colorectal cancer in men.

Obstructive sleep apnea (OSA) is a recognized independent risk factor for metabolic disorders, type 2 diabetes mellites (DM2) in particular. Therefore, the study aimed to assess the influence of nocturnal oxygen saturation parameters on the onset of DM2 among OSA patients. The study consisted of 549 participants, who underwent polysomnography examination. Based on apnea hypopnea index (AHI), 465 patients were diagnosed with OSA. One hundred and seven individuals had comorbid DM2. Cox regression models were used to assess the effect of oxygen saturation parameters on the onset of DM2. Classification and regression trees (CART) analysis was used to assess the onset of the DM2 in the study group in context of oxygen saturation variables. One-way Cox regression showed higher risk of earlier DM2 for increased values of BMI, AHI, decreased basal O₂ and O₂ nadir value, while lowered mean O₂ desaturation has not shown statistical significance. In the CART analysis, the following cut-off points 92.2%, 81.7%, 87.1% were determined for basal O₂, O₂ nadir and mean O₂ desaturation, respectively, with the first two parameters being statistically significant. Therefore, basal O₂ is independent from AHI, BMI and age is a risk factor of DM2 among OSA patients.

Background The main cause of chronic pancreatitis (CP) is excessive alcohol consumption. On the other hand, only 5–10% of heavy drinkers develop chronic pancreatitis. We have only limited information regarding the pathogenic mechanism by which alcohol leads to the disease. Mutations of the PRSS1 and SPINK 1 have been mostly implicated in hereditary and idiopathic CP, but their presence in other types of this disease have also been reported. Aims The aim of the study was to determine the frequency of PRSS1 and SPINK1 mutations in patients with chronic alcoholic (ACP) and idiopathic pancreatitis (ICP) as well as to investigate their relation to the clinical course of the disease. Methods The study included 33 ACP and 14 ICP patients as well 46 healthy subjects. The diagnosis of CP was based on clinical data, ultrasound, and computed tomography. After isolation of DNA from peripheral blood two trypsinogen mutations were detected N29I and R122H by allelo-specific amplification polymerase chain reaction (ASA-PCR) and by the PCR-restriction fragment length polymorphism (RFLP). Beside this N34S mutation of SPINK1 was analyzed by PCR restriction fragment length polymorphism (PCR-RFLP). Results PRSS1 mutations have been detected in 11 (33%) patients with ACP. The frequency of the PRSS1 mutations was higher in patients with ACP than in controls (4.3%) (p < 0.001). The frequency of PRSS1 mutation was present in 21.4% of ICP patients, which was significantly higher (p < 0.05) than in controls. Overall, six (18%) SPINK1 mutations in ACP group have been detected. Among 14 patients with ICP, in four (28.6%) of them SPINK1 has been detected. The same mutations have also been found in three (6.5%) control subjects. The frequency of the N34S mutation was higher in patients with ICP than in the controls (p < 0.05), but the frequency of N34S mutation did not differ between ACP and the control group. No relations have been detected between PRSS1 and SPINK1 mutations presence and clinical course and complications of CP. Conclusions Those preliminary data suggest the high prevalence of SPINK1 and PRSS1 mutations in the Polish population, generally, as well as in CP patients. It may be speculated that those mutations contribute to the development of chronic pancreatitis, especially in patients with alcohol overindulgence.