Association of Sympathovagal Imbalance with Cognitive Deficit, Insulin Resistance and Oxidative Stress in Newly Diagnosed Hypertension

We analysed endothelial function and oxidative stress in patients with abnormal glucose metabolism, the effect of glucose load, and the impact of nateglinide. 109 participants were grouped into newly diagnosed diabetes, prediabetes, and control. Fasting plasma glucose (FPG), postprandial plasma glucose (PPG), glycosylated haemoglobin (HbA1c), and glycated albumin (GA) varied significantly among the study groups (P<0.01). Nitric oxide (NO) and insulin resistance index (HOMA-IRI) levels were markedly different between the newly diagnosed diabetes and the control (P<0.01). Glucose loading lowered flow-mediated endothelium-dependent dilation (FMEDD), NO, and superoxide dismutase (SOD) (P<0.01). Fasting and glucose loading FMEDD, FPG, PPG,HbA1c, and GA were negatively correlated (r=-0.4573, −0.4602, −0.3895, −0.3897, andr=-0.4594, −0.4803, −0.4494, −0.3885;P<0.01), whereas NO, SOD, and HOMA-βwere positively correlated (r=0.2983, 0.3211, 0.311, andr=0.1954, 0.361, 0.2569;P<0.05). After the treatment with nateglinide, significant decreases in FPG, PPG, GA, HbA1C, endothelin-1(ET-1), malondialdehyde (MDA), and HOMA-IRI were observed, whereas FMEDD, NO, and SOD increased (P<0.01). Thus, the study demonstrated the adverse effect of glucose load on endothelial function and oxidative stress. Nateglinide lowers blood glucose, reduces insulin resistance and oxidative stress, and improves endothelial function in newly diagnosed diabetes.

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Serum and hepatic sphingolipids relate to insulin resistance, hepatic mitochondrial capacity and oxidative stress in non-alcoholic fatty liver disease

Diabetologie und Stoffwechsel ◽

10.1055/s-0037-1601637 ◽

2017 ◽

Vol 12 (S 01) ◽

pp. S1-S84

Author(s):

M Apostolopoulou ◽

R Gordillo ◽

C Koliaki ◽

S Gancheva ◽

T Jelenik ◽

...

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Liver Disease ◽

Fatty Liver ◽

Fatty Liver Disease ◽

Alcoholic Fatty Liver ◽

And Oxidative Stress ◽

Alcoholic Fatty Liver Disease ◽

Mitochondrial Capacity

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Low nourishment of B-vitamins is associated with hyperhomocysteinemia and oxidative stress in newly diagnosed cardiac patients

Experimental Biology and Medicine ◽

10.1177/1535370215596860 ◽

2015 ◽

Vol 241 (1) ◽

pp. 46-51 ◽

Cited By ~ 8

Author(s):

Mostafa I. Waly ◽

Amanat Ali ◽

Amira Al-Nassri ◽

Mohamed Al-Mukhaini ◽

John Valliatte ◽

...

Keyword(s):

Oxidative Stress ◽

B Vitamins ◽

Cardiac Patients ◽

Newly Diagnosed ◽

And Oxidative Stress

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4324Effects of the glucagon like peptide-1 receptor agonist on arterial stiffness, LV myocardial deformation and oxidative stress in newly diagnosed type 2 diabetes after 6-month treatment

European Heart Journal ◽

10.1093/eurheartj/ehy563.4324 ◽

2018 ◽

Vol 39 (suppl_1) ◽

Author(s):

I Ikonomidis ◽

G Pavlidis ◽

V Lambadiari ◽

F Kousathana ◽

H Triantafyllidi ◽

...

Keyword(s):

Oxidative Stress ◽

Type 2 Diabetes ◽

Arterial Stiffness ◽

Receptor Agonist ◽

Myocardial Deformation ◽

Newly Diagnosed ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1 ◽

And Oxidative Stress

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Liraglutide protects cardiac function in diabetic rats through the PPARα pathway

Bioscience Reports ◽

10.1042/bsr20180059 ◽

2018 ◽

Vol 38 (2) ◽

Cited By ~ 1

Author(s):

Qian Zhang ◽

Xinhua Xiao ◽

Jia Zheng ◽

Ming Li ◽

Miao Yu ◽

...

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Cardiac Dysfunction ◽

Diabetic Rats ◽

Left Ventricular ◽

Serum Adiponectin ◽

Diabetic Rat ◽

Lv Function ◽

High Dose ◽

And Oxidative Stress

Increasing evidence shows that diabetes causes cardiac dysfunction. We hypothesized that a glucagon-like peptide-1 (GLP-1) analog, liraglutide, would attenuate cardiac dysfunction in diabetic rats. A total of 24 Sprague–Dawley (SD) rats were divided into two groups fed either a normal diet (normal, n=6) or a high-fat diet (HFD, n=18) for 4 weeks. Then, the HFD rats were injected with streptozotocin (STZ) to create a diabetic rat model. Diabetic rats were divided into three subgroups receiving vehicle (diabetic, n=6), a low dose of liraglutide (Llirag, 0.2 mg/kg/day, n=6), or a high dose of liraglutide (Hlirag, 0.4 mg/kg/day, n=6). Metabolic parameters, systolic blood pressure (SBP), heart rate (HR), left ventricular (LV) function, and whole genome expression of the heart were determined. Diabetic rats developed insulin resistance, increased blood lipid levels and oxidative stress, and impaired LV function, serum adiponectin, nitric oxide (NO). Liraglutide improved insulin resistance, serum adiponectin, NO, HR, and LV function and reduced blood triglyceride (TG), total cholesterol (TC) levels, and oxidative stress. Moreover, liraglutide increased heart nuclear receptor subfamily 1, group H, member 3 (Nr1h3), peroxisome proliferator activated receptor (Ppar) α (Pparα), and Srebp expression and reduced diacylglycerol O-acyltransferase 1 (Dgat) and angiopoietin-like 3 (Angptl3) expression. Liraglutide prevented cardiac dysfunction by activating the PPARα pathway to inhibit Dgat expression and oxidative stress in diabetic rats.

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Abstract 357: Hepatic ERK2 Suppresses Endoplasmic Reticulum Stress, Leading to Protection from Oxidative Stress and Endothelial Dysfunction

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.33.suppl_1.a357 ◽

2013 ◽

Vol 33 (suppl_1) ◽

Author(s):

Takehiko Kujiraoka ◽

Yasushi Satoh ◽

Makoto Ayaori ◽

Yasunaga Shiraishi ◽

Yuko Arai-Nakaya ◽

...

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Endoplasmic Reticulum ◽

Fatty Acid ◽

Endothelial Dysfunction ◽

Er Stress ◽

Vascular Complications ◽

Metabolic Remodeling ◽

And Oxidative Stress

Background Insulin signaling comprises 2 major cascades, the IRS/PI3K/Akt and Ras/Raf/MEK/ERK pathways. Many studies on the tissue-specific effects of the former pathway had been conducted, however, the role of the latter cascade in tissue-specific insulin resistance had not been investigated. High glucose/fatty acid toxicity, inflammation and oxidative stress, all of which are associated with insulin resistance, can activate ERK. Liver plays a central role of metabolism and hepatosteatosis (HST) is associated with vascular diseases. The aim of this study is to elucidate the role of hepatic ERK2 in HST, metabolic remodeling and endothelial dysfunction. Methods Serum biomarkers of vascular complications in human were compared between subjects with and without HST diagnosed by echography for regular medical checkup. Next, we created liver-specific ERK2 knockout mice (LE2KO) and fed them with a high-fat/high-sucrose diet (HFHSD) for 20 weeks. The histological analysis, the expression of hepatic sarco/endoplasmic reticulum (ER) Ca 2+ -ATPase 2 (SERCA2) and glucose-tolerance/insulin-sensitivity (GT/IS) were tested. Vascular superoxide production and endothelial function were evaluated with dihydroethidium staining and isometric tension measurement of aorta. Results The presence of HST significantly increased HOMA-IR, an indicator of insulin resistance or atherosclerotic index in human. HFHSD-fed LE2KO revealed a marked exacerbation in HST and metabolic remodeling represented by the impairment of GT/IS, elevated serum free fatty acid and hyperhomocysteinemia without changes in body weight, blood pressure and serum cholesterol/triglyceride levels. In the HFHSD-fed LE2KO, mRNA and protein expressions of hepatic SERCA2 were significantly decreased, which resulted in hepatic ER stress. Induction of vascular superoxide production and remarkable endothelial dysfunction were also observed in them. Conclusions Hepatic ERK2 revealed the suppression of hepatic ER stress and HST in vivo , which resulted in protection from vascular oxidative stress and endothelial dysfunction. HST with hepatic ER stress can be a prominent risk of vascular complications by metabolic remodeling and oxidative stress in obese-related diseases.

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Relationship Between Oxidative Stress, ER Stress, and Inflammation in Type 2 Diabetes: The Battle Continues

Journal of Clinical Medicine ◽

10.3390/jcm8091385 ◽

2019 ◽

Vol 8 (9) ◽

pp. 1385 ◽

Cited By ~ 48

Author(s):

Burgos-Morón ◽

Abad-Jiménez ◽

Marañón ◽

Iannantuoni ◽

Escribano-López ◽

...

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Type 2 Diabetes ◽

Er Stress ◽

Mitochondrial Dysfunction ◽

Current Knowledge ◽

Β Cells ◽

The Relationship ◽

And Oxidative Stress

Type 2 diabetes (T2D) is a metabolic disorder characterized by hyperglycemia and insulin resistance in which oxidative stress is thought to be a primary cause. Considering that mitochondria are the main source of ROS, we have set out to provide a general overview on how oxidative stress is generated and related to T2D. Enhanced generation of reactive oxygen species (ROS) and oxidative stress occurs in mitochondria as a consequence of an overload of glucose and oxidative phosphorylation. Endoplasmic reticulum (ER) stress plays an important role in oxidative stress, as it is also a source of ROS. The tight interconnection between both organelles through mitochondrial-associated membranes (MAMs) means that the ROS generated in mitochondria promote ER stress. Therefore, a state of stress and mitochondrial dysfunction are consequences of this vicious cycle. The implication of mitochondria in insulin release and the exposure of pancreatic β-cells to hyperglycemia make them especially susceptible to oxidative stress and mitochondrial dysfunction. In fact, crosstalk between both mechanisms is related with alterations in glucose homeostasis and can lead to the diabetes-associated insulin-resistance status. In the present review, we discuss the current knowledge of the relationship between oxidative stress, mitochondria, ER stress, inflammation, and lipotoxicity in T2D.

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