This study aims to establish relationships between inflammatory status, ferrokinetics and lipid metabolism in patients with diabetes mellitus. Subclinical inflammation was assessed by levels of high-sensitive C-reactive protein, tumor necrosis factor-α and erythrocyte sedimentation rate. Iron metabolism parameters included complete blood count, serum iron, transferrin and ferritin. Metabolic status assessment included lipid profile, glycated hemoglobin and microalbuminuria measurement. As a result of the study it was possible to establish both general (universal) and diabetes mellitus (DM) type-dependent relationships between the parameters of lipid profile and metabolic control in DM. High-density lipoprotein cholesterol (HDL-C) levels negatively correlated with microalbuminuria (r = −0.293; p ˂ 0.05 for type 1 diabetes and r = −0.272; p ˂ 0.05 for type 2 diabetes). Ferritin concentration positively correlated with triglyceride level (r = 0.346; p ˂ 0.05 for type 1 diabetes and r = 0.244; p ˂ 0.05 for type 2 diabetes). In type 1 diabetes, a negative correlation was discovered between estimated glomerular filtration rate (eGFR) and LDL-C (r = −0.480; p ˂ 0.05), very low-density-lipoprotein cholesterol (VLDL-C) (r = −0.490; p ˂ 0.05) and triglycerides (r = −0.553; p ˂ 0.05), and a positive one between C-reactive protein concentration and triglyceride level (r = 0.567; p ˂ 0.05). Discovered relationships between lipid profile indices, inflammatory status and microalbuminuria confirmed mutual influence of hyperlipidemia, inflammation and nephropathy in diabetes patients. Obtained results justify the strategy of early hypolipidemic therapy in patients with diabetes mellitus to prevent the development and progression of microvascular complications.

Introduction. Carrying out studies on the supply of vitamin D in the Russian population is an important task in order to demonstrate the global nature of the problem of vitamin D deficiency.Objective of  the  study. To conduct a study of the level of vitamin D at different age periods and to assess the relationship of the 25(OH)D supply with the seasons of the year.Materials and methods. The study included 10707 people, 78.8% (n = 2323) women and 21.2% (n = 2266) men, mean age 49.86 ± 21.925 years (Me 56.00).Results. Only 17.1% (n = 1833) of the examined had an adequate level of 25(OH)D, 31.4% (n = 3362) people had an insufficient level of 25 (OH) D, 43.7% (n = 4681) of the examined – a deficiency of 25(OH)D and among 7.8% (n = 831) a severe deficiency of 25(OH)D was revealed. An adequate level of 25(OH)D was found only in the group of children under 3 years of age (mean value 40.55 ng/ml). From 4 to 7 years of age, there is a pronounced 2-fold decrease in the concentration of 25(OH)D in all seasons of the year. A consistently low content of 25(OH)D is observed in the period 8-10 years – 20.91 ng / ml, and in the period 11-18 years – 18.30 ng/ml. The lowest average values of 25(OH)D were found at the age of 11-18 years (18.30 ng/ml) and from 19 to 22 years (19.15 ng/ml), as well as in senile (76 years and above) age (19.05 ng/ml). The lowest median concentration of 25(OH)D is recorded in spring (17.70 ng/ml) and winter (18.80 ng/ml), with a slight positive trend in summer (20.40 ng/ml) and autumn (22.00 ng/ml) season.Conclusions. The optimal level of 25(OH)D was found in every fifth (17.1%) subject, vitamin D deficiency (20.01–30.00 ng/ml) was observed in every third (3362 people out of 10707 examined, 31.4%), a moderate calcidiol deficiency is recorded among 4681 people (43.7%), a severe deficiency of 25 (OH) D among the surveyed is 7.8%.

Hepcidin, a hormone regulating iron metabolism, has received attention for its role in the pathogenesis of dysregulations in carbohydrate metabolism. Hepcidin disorders in patients with diabetes mellitus are bi-directional: manifesting as iron overload syndrome in cases of decreased hepcidin production and as anaemia of chronic disease in cases of hepcidin hypersecretion. However, till date, detailed analyses of mechanisms underlying hepcidin dysregulation have not been conducted nor have the interactions of ferrocinetic and carbohydrate-metabolic disorders been examined. An association between diabetes mellitus and neurodegenerative diseases as well as the role of iron metabolism in Alzheimer or Parkinson diseases is a subject of ongoing research. This review provides a summary of the current understanding of hepcidin regulation and its disorders in various diseases, including diabetes mellitus and neurodegenerative diseases. In addition, we provide an overview of the available therapies that address ferrocinetic disorders resulting from the dysregulation of hepcidin.

Background: Enteropancreatic hormonal system disorder is a possible reason for β-cell dysfunction and carbohydrate metabolism disorder among pregnant women. However, no information is available about the state of enteroinsulin hormones [glucagon, glucose-dependent insulinotropic peptide (GIP), glucagon-like peptide1 (GLP-1) and GLP-2] during pregnancy. The role of enteroinsulin hormones in the development of carbohydrate metabolism disorder during pregnancy is poorly understood. Aim: To quantify and compare incretin hormone secretion in groups of pregnant women with and without gestational diabetes mellitus (GDM). Materials and methods: The study included 80 patients, 50 of whom had GDM, and the control group consisted of 30 pregnant women without GDM. All patients underwent an oral glucose tolerance test; glycated haemoglobin (HbA1c) estimation; ferritin, transferrin, basal and postprandial glucagon estimation; GLP-1 and GLP-2 estimation. Results: Basal glucagon and GLP-1 levels were significantly higher (p 0. 05) in the group of women with GDM than in the control group. The most significant differences in GLP-1, basal and postprandial glucagon levels were observed during the first trimester of pregnancy. Conclusion: High GLP-1 levels in the group of women with GDM may reflect a state of ‘incretin resistance’, which is similar to hyperinsulinemia in the early stages of type 2 diabetes mellitus.

Iron affects the pathogenesis and clinical course of several chronic metabolic diseases such as obesity, atherosclerosis, non-alcoholic fatty liver disease and type 2 diabetes mellitus. High pro-oxidant iron activity is physiologically controlled by mechanisms regulating entry, recycling, and loss of body iron. These mechanisms include the interplay of iron with ferritin, transferrin, hepcidin, insulin, as well as with adipokines and proinflammatory molecules. An imbalance of these regulatory mechanisms results in both systemic and parenchymal siderosis. Iron overload has a toxic effect on the major tissues involved in lipid and glucose metabolism — pancreatic β cells, liver, muscle, and adipose tissue — as well as the organs affected by chronic hyperglycemia — brain, retina and kidneys. Hyperferremia leads to a decrease in insulin secretion, the formation of insulin resistance and increased liver gluconeogenesis. Molecular mechanisms for these effects are diverse. Elucidating them will implicate both for carbohydrate metabolism disorders prevention and for the pathogenesis of other diseases that are, like diabetes mellitus type 2, associated with nutrition, aging and iron. The literature review presents data from world studies on the mutual influence of glucose metabolism and iron overload, and discusses the differences between hereditary and acquired disorders of iron metabolism from the standpoint of their influence on carbohydrate metabolism.