Obesity is a high-risk factor for such comorbidities as cardiovascular disease, several types of cancer, and type 2 diabetes; however not all individuals with obesity have such complications. Approximately 20% of individuals with obesity are metabolically healthy. This study focused on differences between obese individuals with and without type 2 diabetes (T2D+ and T2D–, respectively) on the transcriptome level. Subjects included were 35 T2D– patients with obesity and 35 T2D+ patients with obesity with the same body mass index (BMI). The study was based on the transcription analysis of mRNA and microRNAs (miRs) by RNAseq. In the first step, we performed RNAseq of miRs, in the second step, we analyzed only those mRNA, which appeared targets for significant miRs from the first step. All RNAseq results were validated by qPCR. There were seven miRs differently expressed with adjusted p-value <0.1, which were confirmed by qPCR. Five among them: miR-204-5p, miR125b-5p, miR-125a-5p, miR320a, miR-99b—were upregulated in T2D+ patients with obesity, while only two miRs, miR-23b-3p, and miR197-3p, were increased in T2D– patients with obesity. These seven miRs target two groups of genes: matrix metalloproteinases and TGFβ signal pathway genes. According to the results of transcriptome analysis, the main difference between T2D+ and T2D– patients with obesity was in adipogenesis and fibrosis regulation by matrix metalloproteinases and SMAD4-RUNX2 signal cascade. Based on the data about transcription profiles of both groups, we suggested that the process of fibrosis in T2D+ patients with obesity is more pronounced than in T2D– patients with obesity.

ЦЕЛЬ: пандемия коронавирусной инфекции внесла крайне негативный вклад в аспекты ведения пациентов с сахарным диабетом (СД), ставших «мишенью» вируса как в плане более тяжелого течения COVID-19, так и повышения риска неблагоприятных исходов. Оценка исходов течения в данной популяции представляет важнейшее значение для анализа факторов риска развития летального исхода. Целью исследования является анализ уровня и факторов летальности у пациентов с СД в РФ, перенесших COVID-19.МАТЕРИАЛЫ И МЕТОДЫ: объект исследования -база данных Федерального регистра СД (http://diaregistry.ru), 84 региона РФ. В анализ были включены 156 950 пациентов с СД (7751 пациент с СД 1 типа (СД1) и 149 199 -с СД 2 типа (СД2) с указанием в регистре о перенесенной ОРВИ/пневмонии вследствие COVID-19 в период с 01.02.2020 г. и исхода заболевания (смерть/выздоровление), выгрузка данных от 20.05.2021. Риск летальности оценивался по отношению шансов (ОШ), с повышением риска при ОШ >1, 95% доверительному интервалу (ДИ), критерий значимости<0,05.

Russian Society of Cardiology, National Society of Preventive Cardiology

The acute effects of protein loading (1.5 g kg-1) on glomerular filtration rate (GFR) and urinary albumin excretion (UAE) were investigated in 23 type-I diabetic patients with no clinical nephropathy, and in 7 healthy subjects (controls). The results were compared with renal morphology data. In controls and in 14 diabetic patients (group 1) GFR increased by 27 and 37%, respectively, corresponding to normal renal reserve, but in 9 patients (group 2) GFR decreased by 20%, indicating the absence of a renal reserve. Microalbuminuria was found in none of the patients in group 1 and in 50% of patients in group 2. Two hours after the load UAE increased in all groups, but the increase was most marked in group 2, despite the fall in GFR. The two groups of patients did not differ with regard to the duration and control of diabetes, but differed markedly in terms of baseline GFR (131 vs. 195 ml min-1, P less than 0.01, in groups 1 and 2, respectively). Renal morphology showed minimal non-specific glomerular injury in group 1, and signs of glomerulosclerosis in group 2. We conclude that the impaired renal response to protein load precedes other subclinical manifestations of diabetic renal injury, and may be useful in the diagnosis of latent diabetic nephropathy.

The acute effect of a protein loading test (1.5 g kg-1) on glomerular filtration rate (GFR) was examined in 10 Type 1 diabetic patients without clinical nephropathy to evaluate the renal functional reserve. GFR was measured before (baseline) and after (test) ingestion of the protein load. Two groups of diabetic patients were distinguished: those who exhibited normal renal reserve equal to that in healthy individuals (change in GFR 35 +/- 17 (+/- SD)%) and those who had no renal reserve (change in GFR -20 +/- 20%). These groups did not differ in the duration and control of diabetes nor in the level of urinary albumin excretion. However baseline GFR was 120 +/- 34 and 209 +/- 46 ml min-1 in diabetic patients with and without renal reserve, respectively. Renal morphology revealed hilar glomerular lesions composed of severely expanded mesangium only in diabetic patients without renal reserve. Minimal structural nephropathy was observed in those who exhibited normal renal reserve. We suggest that the impaired response of GFR to protein loading precedes other subclinical manifestations of renal lesions in diabetic patients.