scholarly journals Serum levels of endothelial monocyte activating polypeptide-II in type 1 diabetes patients with microangyopathy and arterial hypertention.

2016 ◽  
Vol 19 (4) ◽  
pp. 309-314 ◽  
Author(s):  
Liliya A. Mogylnytska ◽  
Boris N. Mankovsky

Aim. Тo determine the serum level of EMAP-II in type 1 diabetic patients with microangyopathy and arterial hypertention.Materials and methods We examined 23 type 1 diabetic patient with microangyopathy and arterial hypertention, 10 type 1 diabetic patient with microangyopathy without hypertention and 28 control subjects. Serum levels of EMAP-II were determined by immunoenzyme assay. The data were presented as means±SD.  Results. We found an increased serum level of EMAP-II in type 1 diabetic patients with microangyopathy and arterial hypertention compared to control group (5,23±1,66 ng/ml and 1,25±0,76 ng/ml respectively, р0,01), and in type 1 diabetic patients with microangyopathy and arterial hypertension compared to group without hypertension (5,23±1,66 ng/ml and 3,63±1,9 ng/ml respectively, р0,01). Also, the level of EMAP-II correlated with key markers of carbohydrate and lipid metabolism, inverse correlated with endothelium-dependent dilatation (p0,05).Conclusion. The revealed change of EMAP-II could reflect an endothelial dysfunction in patients with type 1 diabetes with microangyopathy and arterial hypertension. Arterial hypertension, hyperglycemia, dyslipidemia appears to be significant factor to contributing elevation of EMAP-II.Keywords: Endothelial monocyte activating polypeptide II, endothelial dysfunction, type 1 diabetes, arterial hypertension.

Pharmacia ◽  
2021 ◽  
Vol 68 (2) ◽  
pp. 313-319
Author(s):  
Jehan A. Mohammad ◽  
Zainab H. Fathi ◽  
Thikra Ali Allwash

Type 1 diabetes (T1DM) is well recognized risk factor cardiovascular disease (CVD). Insulin therapy is recommended for all patients with type 1 diabetes. Previous findings showed that diabetes impairs endothelial function and increased glucose level reduces nitric oxide (NO) output and increases myeloperoxidase (MPO) activity. However, adiponectin (APN) decreases serum glucose levels. The current study evaluated effects of insulin therapy on circulating levels of oxidative stress and CVD biomarkers like NO, APN, MPO, AIP and lipid profile in type 1 diabetic patients. Fifty patients with T1DM and 18 healthy people were enrolled in this study. The recruited people with T1DM were classified into two groups: 22 newly diagnosed (untreated) type 1 diabetic patients and 28 insulin treated patients. In all groups, circulating NO, APN, MPO, AIP and lipids levels were measured. Compared to control, untreated diabetes revealed a significant increase in the serum levels of APN, MPO, TG, VLDL, TC, LDL and AIP, with a marked reduction in NO and HDL levels. However, insulin therapy significantly lowered MPO, TC and LDL, with no significant changes in the other biochemical parameters. As expected, oxidative stress and CVD-associated markers were significantly increased in untreated diabetes. Insulin therapy exhibited a relatively positive effect on oxidative stress and CVD biomarkers. Accordingly, insulin plus antioxidant supplementation required to normalize these parameters.


2001 ◽  
Vol 281 (5) ◽  
pp. E1029-E1036 ◽  
Author(s):  
Raymond R. Russell ◽  
Deborah Chyun ◽  
Steven Song ◽  
Robert S. Sherwin ◽  
William V. Tamborlane ◽  
...  

Insulin-induced hypoglycemia occurs commonly in intensively treated patients with type 1 diabetes, but the cardiovascular consequences of hypoglycemia in these patients are not known. We studied left ventricular systolic [left ventricular ejection fraction (LVEF)] and diastolic [peak filling rate (PFR)] function by equilibrium radionuclide angiography during insulin infusion (12 pmol · kg−1 · min−1) under either hypoglycemic (∼2.8 mmol/l) or euglycemic (∼5 mmol/l) conditions in intensively treated patients with type 1 diabetes and healthy nondiabetic subjects ( n = 9 for each). During hypoglycemic hyperinsulinemia, there were significant increases in LVEF (ΔLVEF = 11 ± 2%) and PFR [ΔPFR = 0.88 ± 0.18 end diastolic volume (EDV)/s] in diabetic subjects as well as in the nondiabetic group (ΔLVEF = 13 ± 2%; ΔPFR = 0.79 ± 0.17 EDV/s). The increases in LVEF and PFR were comparable overall but occurred earlier in the nondiabetic group. A blunted increase in plasma catecholamine, cortisol, and glucagon concentrations occurred in response to hypoglycemia in the diabetic subjects. During euglycemic hyperinsulinemia, LVEF also increased in both the diabetic (ΔLVEF = 7 ± 1%) and nondiabetic (ΔLVEF = 4 ± 2%) groups, but PFR increased only in the diabetic group. In the comparison of the responses to hypoglycemic and euglycemic hyperinsulinemia, only the nondiabetic group had greater augmentation of LVEF, PFR, and cardiac output in the hypoglycemic study ( P < 0.05 for each). Thus intensively treated type 1 diabetic patients demonstrate delayed augmentation of ventricular function during moderate insulin-induced hypoglycemia. Although diabetic subjects have a more pronounced cardiac response to hyperinsulinemia per se than nondiabetic subjects, their response to hypoglycemia is blunted.


2020 ◽  
Vol 9 (7) ◽  
pp. 2155
Author(s):  
Francesca Iannantuoni ◽  
Aranzazu M. de Marañon ◽  
Zaida Abad-Jiménez ◽  
Francisco Canet ◽  
Pedro Díaz-Pozo ◽  
...  

Type 1 diabetes has been associated with oxidative stress. This study evaluates the rates of oxidative stress, mitochondrial function, leukocyte–endothelium interactions and adhesion molecules in type 1 diabetic patients. The study population consisted of 52 diabetic patients and 46 body-composition and age-matched controls. We assessed anthropometric and metabolic parameters, oxidative stress and mitochondrial function by evaluating reactive oxygen species (ROS) production, mitochondrial ROS production, mitochondrial membrane potential and superoxide dismutase (SOD) and catalase (CAT) expression in polymorphonuclear leukocytes from type 1 diabetic patients. In addition, we evaluated interactions between leukocytes and human umbilical vein endothelial cells (HUVEC), and serum expression of adhesion molecules (P-selectin, VCAM-1 and ICAM-1), proinflammatory cytokines (IL-6 and TNFα) and myeloperoxidase (MPO). HbA1C and glucose levels were higher in diabetic patients than in control subjects, as expected. Mitochondrial function was altered and leukocyte–endothelium interactions were enhanced in diabetic patients, which was evident in the increase in total and mitochondrial ROS production, higher mitochondrial membrane potential, enhanced leukocyte rolling and adhesion, and decreased rolling velocity. Furthermore, we observed an increase in levels of adhesion molecules P-selectin, VCAM-1, and ICAM-1 in these subjects. In addition, type 1 diabetic patients exhibited an increase in proinflammatory mediators TNFα and MPO, and a decreased expression of SOD. The enhancement of leukocyte–endothelium interactions and proinflammatory markers correlated with glucose and HbA1Clevels. Mitochondrial alteration, oxidative stress, and enhanced leukocyte–endothelium interactions are features of type 1 diabetes and may be related to cardiovascular implications.


2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Agnieszka Polkowska ◽  
Izabela Elżbieta Pasierowska ◽  
Marta Pasławska ◽  
Elżbieta Pawluczuk ◽  
Artur Bossowski

Introduction. The increasing knowledge of adropin, afamin, and neudesin and the regulation of glucose metabolism and insulin resistance allows for the assessment of the differences in their concentrations between the groups with varied duration of diabetes mellitus (DM). Aim of the Study. Assessment of serum levels of adropin, afamin, and neudesin in children with type 1 diabetes, with respect to the disease duration. Materials and Methods. The study consisted of 138 patients aged 5–18 years (M 40.58%). Children with type 1 diabetes (n = 68) were compared to the control group (n = 70). The diabetic group was divided into 4 subgroups: (I) newly diagnosed patients, after an episode of ketoacidosis (n = 14), (II) duration no longer than 5 years (n = 18), (III) 5 to 10 years (n = 27), and (IV) longer than 10 years (n = 9). Serum concentrations of adropin, afamin, and neudesin were assessed and compared between the groups of patients. The criterion for statistical significance was p<0.05. Results. The concentrations of adropin and afamin across all subgroups were lower than that in the control group, while neudesin levels were higher in diabetic patients compared to the control group. The differences were statistically significant. Conclusions. Adropin, afamin, and neudesin may play a major role in the regulation of glucose metabolism and have a significant potential as novel biomarkers to predict future metabolic disorders. However, further multicentre studies on a larger cohort of patients are necessary to specify the role of these substances in the course and treatment of type 1 diabetes.


1991 ◽  
Vol 37 (10) ◽  
pp. 1696-1699 ◽  
Author(s):  
C D Agardh ◽  
E Agardh ◽  
A Isaksson ◽  
B Hultberg

Abstract Urinary N-acetyl-beta-glucosaminidase (NAG) and its isoenzymes (NAG A and NAG B) in samples from 87 type 1 diabetic patients and 40 apparently healthy reference subjects were studied with enzyme immunoassays. The diabetic patients had higher concentrations of urinary NAG than did the control subjects (P less than 0.01), but the isoenzyme pattern did not differ. There was a positive correlation between metabolic control (Hb A1c concentrations) and total NAG (P less than 0.01), NAG A (P less than 0.01), and NAG B (P less than 0.001). The diabetic patients were divided into three groups, depending on the degree of retinopathy. Subjects with severe forms of retinopathy did not have increased concentrations of urinary NAG unless they had concomitant nephropathy. The isoenzyme pattern was similar irrespective of degree of retinopathy or nephropathy. The results indicate that concentrations of urinary NAG are positively correlated to the degree of nephropathy, whereas there is no such correlation to the degree of retinopathy.


2018 ◽  
Vol 34 (10) ◽  
pp. 1731-1738 ◽  
Author(s):  
Charlyne Carpentier ◽  
Séverine Dubois ◽  
Kamel Mohammedi ◽  
Narimène Belhatem ◽  
Béatrice Bouhanick ◽  
...  

Abstract Background Hyperglycaemia impairs tubulo-glomerular feedback. We tested whether variable tubulo-glomerular feedback during hyperglycaemia contributes to renal risk heterogeneity seen in Type 1 diabetes. Methods During the period 1990–92, we studied the tubulo-glomerular feedback in Type 1 diabetic patients at high or low renal risk [21 of 54 with glomerular hyperfiltration and/or microalbuminuria against 11 of 55 with normal glomerular filtration rate (GFR) and urinary albumin despite uncontrolled diabetes]. The GFR, effective renal plasma flow, mean arterial pressure and fractional reabsorptions of glucose, osmols, sodium and lithium were measured sequentially during normo- and hyperglycaemia. All patients were followed up until 2016 for incident proteinuria, estimated GFR &lt;60 mL/min/1.73 m2, doubling of serum creatinine, end-stage renal disease or all-cause death. Results Glycaemia increased from 6.1 ± 1.3 to 15.1 ± 1.9 mmol/L in both high-risk and low-risk patients. Glycosuria was lower in the high- versus low-risk patients: 0.34 ± 0.25 versus 0.64 ± 0.44 mmol/min (P = 0.03). Both groups displayed similar kidney function during normoglycaemia. Hyperglycaemia increased more importantly GFR and fractional reabsorptions, and pre-glomerular vasodilatation in the high- than in the low-risk patients (all P &lt; 0.05). Over 21 years, 31.5% high- versus 12.7% low-risk patients developed endpoints (adjusted P = 0.006). In a multi-adjusted survival analysis of patients having undergone renal tests, each 0.10 mmol/min glycosuria during hyperglycaemia reduced the outcome risk by 0.72 (95% confidence interval 0.49–0.97, P = 0.03). Conclusions Reduced tubulo-glomerular feedback and glycosuria during hyperglycaemia indicate high renal risk for Type 1 diabetic patients. Inter-individual variability in tubulo-glomerular feedback activity determines renal risk in Type 1 diabetes.


2006 ◽  
Vol 154 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Lars Melholt Rasmussen ◽  
Lise Tarnow ◽  
Troels Krarup Hansen ◽  
Hans-Henrik Parving ◽  
Allan Flyvbjerg

Objective: The bone-related peptide osteoprotegerin (OPG) has recently been found in increased amounts in the vasculature in diabetes. It is produced by vascular smooth muscle and endothelial cells, and may be implicated in the development of vascular calcifications. OPG is present in the circulation, where increased amounts have been observed in patients with diabetes. In this study, we examined whether plasma OPG is associated with the glycaemic and vascular status of patients with type 1 diabetes. Methods: Two gender-, age- and duration-comparable groups of type 1 diabetic patients either with (n = 199) or without (n = 192) signs of diabetic nephropathy were studied. Plasma OPG was determined by an ELISA. Results: The plasma OPG concentration was significantly higher in patients with nephropathy than those without (3.11 (2.49–3.99) vs 2.57 (2.19–3.21) (median (interquartiles), ng/ml), P < 0.001). Plasma OPG correlated with haemoglobin A1c (HbA1c), systolic blood pressure and age in both groups and, in addition, with kidney function in the nephropathic group. These correlations remained significant in multivariate models. In addition, we found that plasma OPG concentrations were increased among patients with cardiovascular diseases (CVD), both in the normoalbuminuric and the nephropathic groups. The differences between nephropathic and normoalbuminuric, as well as subgroups with and without CVD, could largely be ascribed to changes in HbA1c, age, systolic blood pressure and creatinine. Conclusion: OPG is associated with glycaemic control and CVD in patients with type 1 diabetes, compatible with the hypothesis that OPG is associated with the development of diabetic vascular complications.


1998 ◽  
pp. 44-48 ◽  
Author(s):  
CC Chang ◽  
CN Huang ◽  
LM Chuang

OBJECTIVE: Type 1 diabetes mellitus is frequently associated with autoimmune thyroid disease (ATD). Genetic susceptibility to autoantibody formation in association with ATD and type 1 diabetes mellitus has been described with varying frequencies, but there is still debate about the situation in the Chinese population. We have, therefore, investigated the prevalence of anti-thyroid peroxidase (anti-TPO) in type 1 diabetic patients, and compared the effect of anti-glutamate decarboxylase (anti-GAD) on the thyroid autoimmunity in patients with type 1 diabetes mellitus in Taiwan. SUBJECTS AND METHODS: Two hundred and forty-three subjects with type 1 diabetes mellitus and seventy unrelated normal controls were recruited for the detection of anti-TPO. Two hundred and seventeen sera from two hundred and forty-three type 1 diabetic patients were tested for anti-GAD. RIA and immunoprecipitation were used for anti-TPO and anti-GAD detection respectively. RESULTS: The intra-assay and interassay coefficients of variation of anti-TPO detected by the RIA method ranged from 5.5% to 11.1%. Among 243 type 1 diabetic patients, 53 (21.8%) were positive for anti-TPO. Compared with those without thyroid autoimmunity, there was a female preponderance for the type 1 diabetic patients with thyroid autoimmunity (female:male, 99:91 vs 37:16 respectively). Among the type 1 diabetic patients with thyroid autoimmunity, anti-TPO tended to occur in those of older age or with long-standing disease. The frequency of anti-GAD was 45.6%, (99 of 217), without gender preponderance (males:females, 18.0% vs 27.61%). Compared with those with negative anti-GAD, no significant difference of anti-TPO positivity for the type 1 diabetic patients with positive anti-GAD was found. CONCLUSION: Our data indicated that the RIA method for anti-TPO detection is sensitive and precise for routine clinical use. The presence of anti-TPO in 21.8% of our type 1 diabetic patients confirmed the strong association of ATD and type 1 diabetes mellitus without ethnic differences. The absence of correlation between anti-TPO and anti-GAD in our type 1 diabetic patients suggested genetic heterogeneity in the role of autoimmunity of type 1 diabetes mellitus and ATD among races.


2010 ◽  
Vol 95 (1) ◽  
pp. 194-200 ◽  
Author(s):  
Domenico Cozzolino ◽  
Raffaello Furlan ◽  
Domenico Gruosso ◽  
Cristiana Di Maggio ◽  
Emanuele Miraglia del Giudice ◽  
...  

Abstract Context: Food intake induces relevant cardiovascular changes together with parallel increases in cardiac sympathetic activity and insulin plasma levels in man. Objective: We evaluated hemodynamics, neurohormones, and cardiac autonomic control after eating in patients with type 1 diabetes, a disease characterized by the absence of basal and stimulated insulin production. Design and Setting: Fifteen type 1 diabetic patients and 15 healthy controls underwent blood sampling, electrocardiogram, blood pressure and respiration recordings, and heart rate variability analysis while recumbent, during the 70° head-up tilt, and 20 min after a mixed meal; on another occasion, diabetic patients were also studied 20 min after a mixed meal preceded by their scheduled bolus of exogenous insulin. Spectrum analysis of RR interval provided the indices of sympathetic (LFRR) and vagal (HFRR) modulation of the sinoatrial node. Results: At baseline, no significant differences were found between groups, except for metabolic parameters. Compared with baseline, heart rate, plasma catecholamines, and LFRR significantly (P &lt; 0.005) increased, whereas HFRR significantly (P &lt; 0.0001) decreased during the tilt in all subjects. Compared with baseline, plasma norepinephrine, heart rate, and LFRR significantly (P &lt; 0.05) increased, whereas HFRR significantly (P &lt; 0.02) decreased after eating in controls but not in diabetic patients (with and without insulin administered before eating). In both controls and diabetic patients, no relationship between postprandial changes of insulin and LFRR and HFRR was found. Conclusions: Hemodynamic, neurohormonal, and cardiac neural responses to eating are abnormal in type 1 diabetic patients, independently of insulin.


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