scholarly journals Assessment the effects of insulin on adiponectin, nitric oxide, myeloperoxidase and lipid profile in type 1 diabetic patients

Pharmacia ◽  
2021 ◽  
Vol 68 (2) ◽  
pp. 313-319
Author(s):  
Jehan A. Mohammad ◽  
Zainab H. Fathi ◽  
Thikra Ali Allwash
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Type 1 Diabetes ◽  
Insulin Therapy ◽  
Lipid Profile ◽  
Serum Levels ◽  
Serum Glucose ◽  
Diabetic Patients ◽  
Type 1 Diabetic Patients

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.

scholarly journals Mitochondrial Alterations and Enhanced Human Leukocyte/Endothelial Cell Interactions in Type 1 Diabetes

2020 ◽  
Vol 9 (7) ◽  
pp. 2155
Author(s):  
Francesca Iannantuoni ◽  
Aranzazu M. de Marañon ◽  
Zaida Abad-Jiménez ◽  
Francisco Canet ◽  
Pedro Díaz-Pozo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 1 Diabetes ◽  
Adhesion Molecules ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Diabetic Patients ◽  
Ros Production ◽  
Mitochondrial Ros ◽  
Type 1 Diabetic Patients

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.

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
Keyword(s):  
Type 1 Diabetes ◽  
Endothelial Dysfunction ◽  
Serum Level ◽  
Arterial Hypertension ◽  
Diabetic Patient ◽  
Serum Levels ◽  
Diabetic Patients ◽  
Emap Ii ◽  
Type 1 Diabetic Patients

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.

scholarly journals Evaluation the effects of insulin on oxidant/antioxidant status in type 1 diabetic patients

Pharmacia ◽  
2021 ◽  
Vol 68 (3) ◽  
pp. 699-704
Author(s):  
Ammar A. Y. Almulathanon ◽  
Jehan A. Mohammad ◽  
Thikra Ali Allwash
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Insulin Therapy ◽  
Antioxidant Status ◽  
Serum Glucose ◽  
Diabetic Patients ◽  
Insulin Regimen ◽  
Control Serum ◽  
Healthy Control

Earlier works have revealed increased generation of reactive oxygen species (ROS) and decreased antioxidant levels in type 1 diabetes mellitus (T1DM). The current study aimed to investigate the effect of mixed insulin therapy on oxidative stress and antioxidant status in patients with T1DM. This study involved 75 participants who were divided into three groups: 20 healthy subjects as a control, 25 newly diagnosed patients with T1DM (without treatment) and 30 patients with T1DM treated with insulin (regular and Human Neutral Protamine Hagedorn (NPH)) twice daily. Fasting serum glucose (FSG), serum concentrations of insulin, malondialdehyde (MDA), catalase (CAT), reduced glutathione (GSH), and vitamins (C and E) were measured in all participants. Compared with the healthy control, serum glucose and MDA concentrations were observed to be significantly higher, while significantly lower concentrations of CAT, GSH, and vitamins (C and E) were found in both the treated and untreated diabetic groups. Although insulin therapy caused a significant decrease in blood sugar with a marked elevation in the levels of insulin, CAT, GSH and vitamin E compared to the untreated patients, the changes in the levels of MDA and vitamin C between diabetic groups were not significant. Moreover, the level of insulin resistance was significantly increased in insulin-treated patients as compared to the control and untreated diabetic groups. In conclusion, twice daily treatment with regular and NPH insulin can ameliorate hyperglycemia and improve antioxidant levels in patients with T1DM. However, the insulin regimen used in this study did not reveal a beneficial effect on oxidative stress and insulin resistance. Hence, exogenous antioxidants (vitamins C and E) can be used in combination with insulin to control these parameters.

scholarly journals Nitric Oxide Gene Polymorphism is a Risk Factor for Diabetic Nephropathy and Atherosclerosis in Type 1 Diabetic Patients

2019 ◽  
Vol 7 (19) ◽  
pp. 3132-3138
Author(s):  
Soha M. El Dayem ◽  
Ahmed A. Battah ◽  
Abo El Maged El Bohy ◽  
Solaf Ahmed ◽  
Mona Hamed ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Risk Factor ◽  
Diabetic Nephropathy ◽  
Serum Level ◽  
Lipid Profile ◽  
Diabetic Patients ◽  
Creatinine Ratio ◽  
Albumin Creatinine Ratio ◽  
Type 1 Diabetic Patients

AIM: To assess the risk factor for diabetic atherosclerosis nephropathy and diabetic nephropathy in type 1 diabetic patients. PATIENTS AND METHODS: Thirty healthy volunteers age and sex-matched and Sixty-five type 1 diabetic patient were in rolled in the study. The mean age of patients was 17.99 ± 2.59 years, mean age of onset of diabetes was 7.00 ± 3.28 years, mean duration of diabetes was 10.91 ± 3.54 years. Glycosylated sex-matched (HbA1c) was assessed in blood samples, serum lipid profile was determined, and serum level of oxidised low-density lipoprotein (OxLDL), and nitric oxide was evaluated by enzyme-linked immunosorbent assay (ELISA) technique. Nitric oxide 894G > T genotype was analysed by (PCR-RFLP) method and confirmed by Sequencing. Assessment of the albumin / creatinine ratio was done in urine samples. Renal Doppler and Carotid intima-media thickness (cIMT) via ultrasound was also performed. RESULTS: OxLDL, lipid profile, albumin/creatinine ratio, cIMT and resistivity index were significantly higher in diabetic patients while nitric oxide was significantly lower. Nitric oxide genotype shows no significant difference between diabetic’s patients and controls. Diabetic patients with homozygous NO had a significantly lower serum level of Nitric oxide, a significantly higher OxLDL, albumin / creatinine ratio and lipid profile. CONCLUSION: diabetic patients are liable for the occurrence of early diabetic nephropathy and atherosclerosis as a result of the presence of low level of nitric oxide. Nitric oxide gene polymorphism 894G > T in diabetic patients is a risk factor for diabetic nephropathy and atherosclerosis.

Cardiac responses to insulin-induced hypoglycemia in nondiabetic and intensively treated type 1 diabetic patients

2001 ◽  
Vol 281 (5) ◽  
pp. E1029-E1036 ◽  
Author(s):  
Raymond R. Russell ◽  
Deborah Chyun ◽  
Steven Song ◽  
Robert S. Sherwin ◽  
William V. Tamborlane ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Radionuclide Angiography ◽  
Left Ventricular ◽  
Cardiac Response ◽  
Left Ventricular Ejection ◽  
Diabetic Patients ◽  
Plasma Catecholamine ◽  
Ventricular Ejection Fraction ◽  
Type 1 Diabetic Patients

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.

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