Time in range is a tool for assessing the quality of glycemic control in diabetes

The presence of continuous glucose monitoring (CGM) systems has expanded diagnostic capabilities. The implementation of this technology into clinical practice allowed to determine the patterns and tendencies of excursions in glucose levels, to obtain reliable data concerning short-term glycemic control. Taking into consideration the large amount of obtained information using CGM systems, more than 30 different indicators characterizing glycemic variability were proposed. However, it is very difficult for a practitioner to interpret the data obtained due to the variety of indicators and the lack of their target values. The first step in the standardization of indices was the creation of the International Guidelines for CGM in 2017, where the Time in Range (TIR) (3,9–10,0 mmol/l, less often 3,9–7,8 mmol/l) was significant. To complement the agreed parameters and simplify the interpretation of obtained data using CGM, in 2019 the recommendations were prepared for the International Consensus on Time in Range, where TIR was validated as an additional component of the assessment of glycemic control along with HbA1c. In the literature review the issues of the association of TIR with the development of micro- and macrovascular complications in type 1 and 2 diabetes are considered. The relationship with other indicators of the glycemic control assessment was also analyzed and the dependence of insulin therapy on TIR was shown. TIR is a simple and convenient indicator, it has a proven link with micro- and macrovascular complications of diabetes and can be recommended as a new tool for assessing the glycemic control. The main disadvantage of TIR usage is the insufficient apply of CGM technology by the majority of patients with diabetes

The role of micrornas in the regulation of artificially induced liver fibrosis

MicroRNAs are small non‑coding RNA molecules with a length of 19—24 nucleotides. By RNA interference, inhibition of initiation, or lengthening of translation, each microRNA is able to inhibit gene expression of a large number of target transcripts. In recent years, it has been shown that altered microRNA patterns after chronic liver diseases have a significant effect on the progression of fibrosis due to their ability to target the expression of extracellular matrix proteins and the synthesis of mediators of profibrogenic pathways. The article presents modern ideas about the role of microRNAs in liver fibrosis. On the example of a number of microRNAs, intracellular pathways that implement protection against fibrous processes in the liver are demonstrated. It is demonstrated that the main way to suppress liver fibrosis using microRNA is inactivation of perisinusoidal liver cells. In experiments with induction of liver fibrosis with carbon tetrachloride in mice and cultivation of perisinusoidal cells, it was found that with the genetic deletion of microRNA‑223, liver fibrosis increased, and with the introduction of microRNAs of this family, the process of accumulation of extracellular matrix, on the contrary, slowed down. Other studies have shown that the process of liver fibrosis was slowed down due to the influence of microRNA‑101 by transferring activated perisinusoidal cells to a resting state. This was evidenced by the suppression of proliferation and migration of perisinusoidal cells, as well as the loss of activation markers and the strengthening of resting markers. microRNA‑16 has been shown to inhibit the expression of CD1, an important regulator of the cell cycle pathway. It was noted that the expression levels of miR‑16 and cyclin D1 were inversely correlated with activation of perisinusoidal cells. Overexpression of this microRNA in activated perisinusoidal cells led to the accumulation of cells in the G0/G1 phase of the cell cycle.МикроРНК представляют собой небольшие некодирующие молекулы РНК длиной 19–24 нуклеотида. Путем РНК‑интерференции, ингибирования инициации или удлинения трансляции каждая микроРНК способна ингибировать экспрессию генов большого количества целевых транскриптов. В последние годы было показано, что измененные паттерны микроРНК после хронических заболеваний печени оказывают значительное влияние на прогрессирование фиброза благодаря их способности нацеливаться на экспрессию белков внеклеточного матрикса и синтез медиаторов профиброгенных путей. В статье изложены современные представления о роли микроРНК в фиброзе печени. На примере ряда микроРНК продемонстрированы внутриклеточные пути, реализующие защиту от фиброзных процессов в печени. Демонстрируется, что основным способом подавления фиброза печени при помощи микроРНК является инактивация перисинусоидальных клеток печени. В экспериментах с индукцией фиброза печени четыреххлористым углеродом у мышей и культивированием перисинусоидальных клеток было выяснено, что при генетической делеции микроРНК‑223 фиброз печени усиливался, а при введении микроРНК этого семейства, процесс накопления внеклеточного матрикса, напротив, замедлялся. В других исследованиях было показано, что процесс фиброза печени замедлялся за счет влияния микроРНК‑101 путем перевода активированных перисинусоидальных клеток в состояние покоя. Об этом свидетельствовало подавление пролиферации и миграции перисинусоидальных клеток, а также потеря ими маркеров активации и усиление маркеров покоя. Было показано, что микроРНК‑16 ингибировала экспрессию CD1, важного регулятора пути клеточного цикла. Отмечалось, что уровни экспрессии miR‑16 и циклина D1 обратно коррелировали при активации перисинусоидальных клеток. Сверхэкспрессия этой микроРНК в активированных перисинусоидальных клетках приводила к накоплению клеток в G0/G1‑фазе клеточного цикла

Analysis of time in range depending on the method of assessing the glucose level

Introduction. In recent years, there has been an increase in the prevalence and incidence diabetes type 1. The high-quality glycemic control is critical in reducing the risk of developing and progression of vascular complications and adverse outcomes of diabetes. Self-monitoring blood glucose (SMBG) and professional continuous glucose monitoring (PCGM) provide the data set which must be interpreted using multiple indicators of glycemic control. A number of researchers have demonstrated the relationship between the time in range (TIR) and the risk of developing both micro- and macrovascular complications of diabetes. Considering the insufficient amount of data on TIR differences depending on the glucose level assessment method and the significant potential of using this indicator for the stratification of the risk of both micro- and macrovascular complications of diabetes, the study of TIR differences based on the data of PCGM and SMBG is relevant at present.Aims. To estimate the time range according to professional continuous glucose monitoring and self-monitoring of blood glucose levels in the patients with diabetes type 1 among the adult population to improve the control of the disease course.Materials and methods. An interventional open-label multicenter study in the patients with diabetes type 1 was conducted. The patients with diabetes type 1 aged 18 and older, with the disease duration of more than 1 year receiving the therapy with analog insulin was enrolled into the study. The calculation of the indicators of the time spent in the ranges of glycemia was carried out on the basis of the data of PCGM and SMBG.Results and discussion. We examined 218 patients who met the inclusion criteria and did not have exclusion criteria. The presented differences in the indicators of time in ranges indicate the comparability of the SMBG and PCGM methods.Conclusions. When assessing the indicators of time in the ranges of glycemia obtained on the basis of the data of PCGM and SMBG, clear correlations and linear dependence were demonstrated, which indicates the comparability of these parameters regardless of the measurement method