The worldwide prevalence of obesity more than doubled between 1980 and 2014. The most frequent cause, which leads to the obesity development, is an imbalance between energy intake and expenditure. In this complex process, genetic susceptibility, environmental and lifestyle factors are involved. The gut microbiota is a part of a complex network. Numerous studies have shown that the gut microbiota interacts with the host metabolism and plays an important role in various processes. The core gut microbial profile mainly embodies bacteria, belonging to the Gram-positive Firmicutes and the Gram-negative Bacteroidetes. An increase in gut Firmicutes/Bacteroidetes ratio is detected in obese patients and during high-fat diet consumption in human and animal stu­dies. Strains belonging to the genera Lactobacillus and Bifidobacterium are commonly used as probiotics and are most studied for the treatment and prevention of obesity-associated disorders. Moreover, several potential bacterial candidates, such as Akkermansia muciniphila, Faecalibacterium prausnitzii, Prevotella copri, Roseburia or Ruminococcus, have been identified and novel mechanisms of action intervening their positive effects for obesity have been elucidated. Consequently, the gut microbiota is gaining significant research interest in relation to obesity and associated metabolic disorders in an attempt to better understand the etiology of obesity and potentially new methods of its prevention and treatment. However, traditional culture methods are very limited for identifying microbes. With the application of molecular biologic technologies, especially metagenomic next-generation sequen­cing, progress has been made in the study of the human intestinal microbiome.

Background. Recently, vitamin D deficiency has been considered one of the factors in the development of type 2 diabetes mellitus (DM) and nonalcoholic fatty liver disease (NAFLD). The purpose was to establish the effectiveness of Decap (cholecalcife­rol) in patients with its deficiency who suffered from type 2 DM and NAFLD. Materials and methods. Fifty-two people with NAFLD and type 2 DM on the background of established D-deficiency were treated, they were evenly divided into two groups. Patients in the comparison group (n = 26) received only traditional antidiabetic therapy, and the main group (n = 26) additio­nally took vitamin D — Decap, which was prescribed at a dose of 4,000 IU/day for 6 months. Results. Vitamin D use was associated with a statistically significant reduction in fasting blood glucose after 6 months of treatment — by 4.2 % (p = 0.041). The level of glycated hemoglobin in the main group of patients decreased on ave­rage by 0.38 % (p = 0.121) after 3 months, and remained almost at the same level after 6 months — by 0.44 % (p = 0.088). In parallel with the improvement of glycemic control parameters in the main group, there was a tendency to a decrease in the HOMA-2-IR by 0.28 (–0.11; 0.86; p = 0.152) and to a better insulin sensitivity by 1.39 (–10.04; 6.01; p = 0.621) compared to the baseline. The use of vitamin D (Decap) is associated with a decrease in steatosis indices FLI and TyG. The baseline values for FLI was 74.11 ± 18.71 and for TyG — 5.21 ± 0.29, and after a six-month course of vitamin D treatment, they decreased by 4.4 % (p = 0.029) and 2.68 % (p = 0.031), respectively, compared to baseline. Conclusions. It was found that the use of Decap in patients with vitamin D deficiency at a dose of 4,000 IU/day for a course of at least six months improved glycemic control and metabolic profile in those with type 2 DM and NAFLD.