Increased body weight as well as type 2 diabetes (T2D) are found to be associated with increased incidence of hypertension, although the mechanisms facilitating hypertension in T2D or nondiabetic individuals are not clear. Therefore, in this study we compared the levels of insulin resistance (IR:OGIS), plasma insulin (PI:RIA) levels, and pro-inflammatory cytokines (IL-6 and TNF-α: ELISA), being risk factors previously found to be associated with hypertension, in T2D patients showing increased body weight (obese and overweight, BMI ≥ 25 kg/m2) with hypertension (group A, N = 30), or without hypertension (group B, N = 30), and in nonobese (BMI < 25 kg/m2), normotensive controls (group C, N = 15). We found that OGIS index was the lowest (A: 267 ± 35.42 vs. B: 342.89 ± 32.0, p < 0.01) and PI levels were the highest (A: 31.05 ± 8.24 vs. B: 17.23 ± 3.23, p < 0.01) in group A. In addition, IL-6 levels were higher in group A (A: 15.46 ± 5.15 vs. B: 11.77 ± 6.09; p < 0.05) while there was no difference in TNF-α levels. Our results have shown that appearance of hypertension in T2D patients with increased body weight was dependent on further increase in IR which was associated with the rise in pro-inflammatory IL-6 cytokine. The results imply that lifestyle intervention aimed to decrease IR might be beneficial in reducing the risk for hypertension in those T2D individuals.
This study aimed to analyse the impact of obesity in type 2 diabetes (T2D) on adipocytokines (adiponectin, leptin and resistin) and inflammatory markers (TNF-α, IL-6 and hsCRP) as cardiovascular risk factors. A cross-sectional study comparing the basal levels of adipocytokines and inflammatory markers was done in 18 obese (BMI ≥ 30 kg/m2) (group A), 21 overweight (25 kg/m2 ≤ BMI < 30 kg/m2) (group B), 25 non-obese T2D patients (group C) and 15 non-obese controls (group D). The lowest levels of adiponectin and the highest levels of leptin, resistin, TNF-α, IL-6 and hsCRP were found in group A. Adiponectin levels were significantly lower, and resistin, TNF-α, and hsCRP levels were elevated in group C vs. D. However, leptin and IL-6 levels differed significantly between groups A and B, but not between groups C and D. Moreover, we found a significant negative correlation between adiponectin and TNF-α, but not with other markers, which was independent of the presence of obesity. In contrast, leptin and resistin correlated with the inflammatory markers, and this correlation was obesity-dependent. Our results suggest that obesity influences cardiovascular risk primarily through changes in leptin and resistin and less efficiently at the level of adiponectin.
Background
Hyperglycemia has detrimental effect on ischemic myocardium, but the impact of acute hyperglycemia on the myocardium in asymptomatic diabetic patients has not been fully elucidated. Thus, this follow-up study was aimed to investigate the effects and reversibility of acute hyperglycemia on regional contractile function of left ventricle (LV) in diabetic patients without cardiovascular disease.
Methods
The two-dimensional speckle tracking echocardiography (2D-STE), including multilayer strain analysis, was used for evaluation of global and regional LV function in asymptomatic, normotensive patients with uncomplicated diabetes, with acute hyperglycemia ( ≥ 11.1 mmol/l) (Group A, n = 67), or with optimal metabolic control (fasting plasma glucose < 7 mmol/l and HbA1c < 7%) (Group B, n = 20), while 20 healthy individuals served as controls (Group C). In group A, after 72 h of i.v. continuous insulin treatment (at the time euglycemia was achieved) (second examination) and after 3 months following acute hyperglycemia (third examination) 2D-STE was repeated.
Results
Global longitudinal strain (GLS) (− 19.6 ± 0.4%) in Group A was significantly lower in comparison to both groups B (− 21.3 ± 0.4%; p < 0.05) and C (− 21.9 ± 0.4%; p < 0.01) at baseline, while we could not detect the differences between groups B and C. Peak systolic
longitudinal
endocardial (Endo), mid-myocardial (Mid) and epicardial (Epi) layer strain were significantly lower in group A at baseline compared to both groups B and C. Deterioration in peak systolic
circumferential
strain was observed at basal LV level, in all three layers (Endo, Mid and Epi) and in mid-cavity LV level in Epi layer in group A in comparison to group C. Moreover, in group A, after euglycemia was achieved (at second and third examination) GLS, as well as peak longitudinal and circumferential strain remain the same.
Conclusion
Acute hyperglycemia in asymptomatic diabetic patients has significant negative effects on systolic LV myocardial mechanics primarily by reducing GLS and multilayer peak systolic longitudinal and circumferential strain which was not reversible after three months of good glycemic control.
The aim of this study was to estimate the possibility of predicting the course of type 1 diabetes. We analyzed the importance of islet cell antibody levels and residual β cell function in 46 newly diagnosed patients with diabetes. Islet cell antibodies (ICAs; Juvenile Diabetes Foundation [JDF] units) were determined at the time of diagnosis by the indirect immunofluorescent method. β cell function was estimated by C peptide levels (nmol/L) before and after glucagon stimulation at the time of clinical remission. Of the 46 patients, 13 were ICA negative (group A). Among ICA‐positive patients, ICAs were < 20 JDF units (group B) in 15, between 20 and 80 JDF in 9 (group C), and > 80 JDF in 9 (group D). In group A, 9 patients had clinical remission for 7.5 ± 1.7 months. Their basal C peptide level was 0.26 ± 0.05 nmol/L and it increased after stimulation to 44.5 ± 2.5%. Ten patients in group B had remission for 6.2 ± 1.5 months. Their basal C peptide levels (0.28 ± 0.07 nmol/L) were similarly increased after stimulation (47.5 ± 2.5%). In group C, all patients had remission and it was of the longest duration (14.7 ± 1.5 months). They had the highest basal C peptide levels (0.45 ± 0.12 nmol/L) with increases to 57.5 ± 3.5%. Seven patients in group D with ICA levels > 80 JDF had a short remission (3.2 ± 1.2 months) despite good basal C peptide levels (0.42 ± 0.05 nmol/L) and excellent increases after stimulation (92.5%). Our results suggest that moderate levels of ICA are associated with good residual β cell function and longer remission. Very high ICA levels (> 80 JDF) at the time of diagnosis despite better β cell function are associated with short clinical remission. Therefore, high ICA levels could be a marker of strong autoimmune reaction and accelerated depletion of β cell function.
This study was aimed at investigating daily fluctuation of PAI-1 levels in relation to insulin resistance (IR) and daily profile of plasma insulin and glucose levels in 26 type 2 diabetic (T2D) patients with coronary artery disease (CAD) (group A), 10 T2D patients without CAD (group B), 12 nondiabetics with CAD (group C), and 12 healthy controls (group D). The percentage of PAI-1 decrease was lower in group A versus group B (4.4 ± 2.7 versus 35.0 ± 5.4%; P < 0.05) and in C versus D (14.0 ± 5.8 versus 44.7 ± 3.1%; P < 0.001). HOMA-IR was higher in group A versus group B (P < 0.05) and in C versus D (P < 0.01). Simultaneously, AUCs of PAI-1 and insulin were higher in group A versus group B (P < 0.05) and in C versus D (P < 0.01), while AUC of glucose did not differ between groups. In multiple regression analysis waist-to-hip ratio and AUC of insulin were independent determinants of decrease in PAI-1. The altered diurnal fluctuation of PAI-1, especially in T2D with CAD, might be strongly influenced by a prolonged exposure to hyperinsulinemia in the settings of increased IR and abdominal obesity, facilitating altogether an accelerated atherosclerosis.
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