The review considers the problem of sarcopenia, a muscle weakness and loss of mass, quality and strength of skeletal muscles, which often accompanies type 2 diabetes, especially in the elderly. Recently, sarcopenia has been considered as one of the complications of diabetes, which is associated with an increase in the frequency of cardiovascular complications, the need for hospitalization, and patient mortality. The molecular mechanisms of muscle atrophy in sarcopenia are associated with a violation of the anabolic-catabolic balance in muscles and their energy supply, fatty infiltration and shifts in proteostasis (decreasing the synthesis of muscle proteins and increasing their degradation), mitochondrial dysfunction. Insulin resistance, oxidative stress, accumulation of abdominal and ectopic fat, local inflammation play a key role in the pathogenesis of both sarcopenia and dysmetabolic diabetic complications, i.e., there is a bidirectional relationship between these pathological conditions, which mutually reinforce each other’s negative consequences. According to clinical observations, the risk of sarcopenia in patients with diabetes is 3–4 times higher than in people without diabetes, while the presence of sarcopenia increases the risk of reduced work capacity, disability, mortality, and worsening of diabetes control. These data indicate the feasibility of screening for signs of sarcopenia in patients with type 2 diabetes, especially in the older age group, using dynamic tests, as well as bone monitoring, to prevent the risk of falls and fractures. Antidiabetic therapy for such patients should include drugs that help preserve muscle and bone tissue (have an anabolic effect), do not increase the risk of hypoglycemia and gastrointestinal disorders. According to the literature, the safest preparations include the biguanide metformin, dipeptidyl peptidase inhibitors, and insulin. Sulfonylurea derivatives, thiazolidinediones, glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter-2 inhibitors are not recommended, as they can cause undesirable effects in weakened elderly people. Timely diagnosis of sarcopenia is important to prevent the deterioration of muscle function (through the rehabilitation of the musculoskeletal system using adaptive physical exercises and diet modification) and to improve the quality of life of patients with type 2 diabetes. In turn, improving the prevention and treatment of diabetes in the early stages can also help prevent the development of sarcopenia and its complications.
The bone hormone osteocalcin is formed by osteoblasts and is partially released into the bloodstream during bone resorption, being a biomarker of bone remodeling. Osteocalcin also plays an important role in the endocrine regulation of metabolic and energy processes in the body and in their coordination. Osteocalcin uses a feedback mechanism to regulate insulin secretion, insulin sensitivity of peripheral tissues, and adipokine levels. In general, the secretion of osteocalcin and insulin are important factors in the formation of hormonal-metabolic phenotype, body composition, determination of regional distribution and metabolic activity of both bone and adipose tissue.The aim of this study was to establish the relationship between osteocalcin concentration and hormonal changes in men with type 2 diabetes with and without obesity on the background of involutive changes. Results. 64 men with type 2 diabetes, older than 50 years, were divided into 2 groups by BMI: 1) non-obese, BMI <30 kg / m2 (n = 31); 2) -obese, BMI ≥ 30 kg / m2 (n = 33). Lower levels of insulin secretion (lower serum C-peptide and insulin levels) were observed in non-obese patients in the absence of a compensatory increase in proinsulin levels. It can be assumed that the increase in the concentration of osteocalcin in group 1 is compensatory, although it does not have a significant effect on blood glucose levels. However, it may have a protective effect on the severity of insulin resistance syndrome and related metabolic disorders. Lower levels of osteocalcin in the obese group were associated with a higher degree of insulin resistance and insulin secretion. There was no significant difference between the two groups in serum proinsulin levels, as well as in androgen supply, which was assessed by the levels of total testosterone, testosteronestradiol-binding globulin, and free testosterone index. Conclusion. Lower levels of osteocalcin may be a marker of an increased risk of adverse metabolic changes in obese patients with type 2 diabetes, followed by complications compared to non-overweight patients
Background. Clinical trials showed a number of additional phenotypes of metabolic syndrome. All of them differ in the type of metabolic disorders and the composition of subcutaneous and visceral adipose tissue. Some of phenotypes have a number of clinical and metabolic similarities with endogenous or exogenous hypercorticism syndromes. The purpose was to characterize the functional activity of the adrenal glands in type 2 diabetes depending on the phenotypic features: the degree of general obesity and the level of visceral fat. Material and methods. Our trial included 89 patients with type 2 diabetes (46 men and 43 women) aged 32 to 85 years. The examination included evaluation of anthropometric parameters, body composition by the bioelectrical impedance method, assessment of the lipid and carbohydrate metabolism, the level of cortisol, dehydroepiandrosterone sulfate (DHEAS) in blood serum, and the activity of 11-beta-hydroxysteroid dehydrogenase (11β-HSD) enzyme. Results. Insulin and C-peptide levels were significantly lower in the non-obese group. The cortisol/DHEAS ratio was elevated in both subgroups with high levels of visceral fat as possible marker of imbalance of anabolic and catabolic hormones. In addition, the concentration of the cortisol, measured in the blood serum of the patients after waking up, was within the normal range. However, the average value in both groups was closer to its upper ranges. This may suggest the presence of subclinical hypercortisolism caused by an increased activity of 11β-HSD, which contributes to the local production of cortisol in visceral adipose tissue. Conclusions. The hormonal and metabolic changes that we found in our groups of patients with type 2 diabetes may indicate anabolic-catabolic imbalance, which is manifested both in the features of the topography of adipose tissue and in changes of metabolic processes, i.e. form the special metabolic phenotype with a catabolic or anabolic axis. Detection the subgroups at high risk allows to develop pathogenetic approaches to the most targeted comprehensive correction of existing violations.
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