scholarly journals Hyperglycemia- and Hyperlipidemia-Induced Inflammation and Oxidative Stress through Human T Lymphocytes and Human Aortic Endothelial Cells (HAEC)

2021 ◽  
Author(s):  
Frankie B. Stentz
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
T Cells ◽  
Endothelial Cells ◽  
Fatty Acid ◽  
T Lymphocytes ◽  
Palmitic Acid ◽  
Insulin Receptors ◽  
And Oxidative Stress

Approximately 65% of patients with T2DM die as a result of cardiovascular disease with hyperglycemia and hyperlipidemia being important risk factors for cardiovascular diseases. Both T2DM and atherosclerosis are considered to be inflammatory processes Human T-lymphocytes (T-cells) and aortic endothelial cells (HAEC) have been shown to be components of plaque formation in atherosclerosis. T cells and HAEC are unique in that in their naive state they have no insulin receptors responsive to insulin but become activated in vitro hyperglycemia and in vivo hyperglycemic conditions such as diabetic ketoacidosis and non-ketotic hyperglycemic conditions. Our studies show that T-cells and HAEC in the presence of high concentrations of glucose /and or the saturated fatty acid (SFA) palmitic acid become activated and express insulin receptors, reactive oxygen species (ROS), cytokine elevation, and lipid peroxidation in a time and concentration-dependent manner. Whereas, the unsaturated fatty acid α-linoleic, was not able to activate these cells and had a salutary effect on the activation by glucose and palmitic acid. We have demonstrated that unsaturated fatty acids (UFA) may provide a protective mechanism against the prooxidant effects of hyperglycemia and high SFA such as palmitic acid. Therefore, diet alternations may be beneficial for decreasing hyperglycemia and cardiovascular risks. Studies have shown that lifestyle changes of diet and exercise can reduce the risk of developing diabetes by 58%. Hyperglycemia and hyperlipidemia are important risk factors of developing diabetes and cardiovascular disease. Therefore, we studied the effects of a High Protein diet versus a High Carbohydrate diet in obese non-diabetic, prediabetic and diabetic subjects for effects on weight loss, blood sugar, lipid levels, inflammation, and oxidative stress.

scholarly journals Hyperglycemia and Hyperlipidemia Induced Inflammation and Oxidative Stress in Human T Lymphocytes and Salutary Effects of ω- 3 Fatty Acid.

2020 ◽  
pp. 1-9
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Fatty Acids ◽  
T Cells ◽  
Fatty Acid ◽  
T Lymphocytes ◽  
Palmitic Acid ◽  
Linolenic Acid ◽  
High Glucose ◽  
Human T Lymphocytes

Abstract Type 2 Diabetes conditions are associated with hyperglycemia and hyperlipidemia; however, the role of Saturated Fatty Acids (SFA) vs. Unsaturated Fatty Acids (UFA) and high glucose on human T lymphocytes (T cells) is not known. We investigated the salutary effect of the UFA ω-3 fatty acid, α- linolenic acid, on glucose and SFA, palmitic acid, induced activation on T cells as a cause of the inflammatory process with high glucose and SFA foods. These cells in the presence of palmitic acid and/or high glucose but not linolenic acid exhibited a concentration and time-dependent emergence of insulin receptors (INSR), expression, generation of ROS, lipid peroxidation, cytokines and NF-kB p65 translocation to the nucleus. Whereas, activation of the cells by elevated levels of glucose and palmitic acid were additive, addition of linolenic acid in a dose-related manner inhibited activation of cells by glucose and palmitic acid and reduced markers of oxidative stress, lipid peroxidation and cytokines. We propose that UFAs such as α-linolenic acid may serve as a protective mechanism against the deleterious effects of hyperglycemia and hyperlipidemia of high sugar and SFA foods as in diabetes.

scholarly journals New Perspectives of S-Adenosylmethionine (SAMe) Applications to Attenuate Fatty Acid-Induced Steatosis and Oxidative Stress in Hepatic and Endothelial Cells

Molecules ◽  
2020 ◽  
Vol 25 (18) ◽  
pp. 4237 ◽  
Author(s):  
Laura Vergani ◽  
Francesca Baldini ◽  
Mohamad Khalil ◽  
Adriana Voci ◽  
Pietro Putignano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Fatty Acid ◽  
Lipid Accumulation ◽  
Endothelium Dysfunction ◽  
Beneficial Effects ◽  
Mitochondrial Fatty Acid ◽  
Oxidant Production ◽  
Pleiotropic Functions ◽  
And Oxidative Stress

S-adenosylmethionine (SAMe) is an endogenous methyl donor derived from ATP and methionine that has pleiotropic functions. Most SAMe is synthetized and consumed in the liver, where it acts as the main methylating agent and in protection against the free radical toxicity. Previous studies have shown that the administration of SAMe as a supernutrient exerted many beneficial effects in various tissues, mainly in the liver. In the present study, we aimed to clarify the direct effects of SAMe on fatty acid-induced steatosis and oxidative stress in hepatic and endothelial cells. Hepatoma FaO cells and endothelial HECV cells exposed to a mixture of oleate/palmitate are reliable models for hepatic steatosis and endothelium dysfunction, respectively. Our findings indicate that SAMe was able to significantly ameliorate lipid accumulation and oxidative stress in hepatic cells, mainly through promoting mitochondrial fatty acid entry for β-oxidation and external triglyceride release. SAMe also reverted both lipid accumulation and oxidant production (i.e., ROS and NO) in endothelial cells. In conclusion, these outcomes suggest promising beneficial applications of SAMe as a nutraceutical for metabolic disorders occurring in fatty liver and endothelium dysfunction.

Abstract P136: Cardiometabolic Burden in Adolescents is Associated with DNA Methylation in Genes Related to Cardiovascular Disease Risk

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Fan He ◽  
Arthur Berg ◽  
Edward O Bixler ◽  
Julio Fernandez-Mendoza ◽  
Yuka Imamura Kawasawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Dna Methylation ◽  
Glucose Tolerance ◽  
Endothelial Function ◽  
Model Assessment ◽  
Cvd Risk ◽  
And Oxidative Stress

Background: Metabolic syndrome is related to increased cardiovascular disease (CVD) risk. Although continuous metabolic syndrome score (cMets) is a marker of cardiometabolic burden in adolescence, the relationship between cardiometabolic burden and DNA methylation has been rarely assessed at this stage of the life course. Hypothesis: Cardiometabolic burden is related to methylation levels in genes related to CVD risk in adolescents. Methods: A sample of 263 independent adolescents from the population-based Penn State Child Cohort follow-up exam (N=421) was used in this analysis. cMets was calculated as the sum of standardized residuals of five established cardiometabolic risk factors, namely waist circumference, mean arterial pressure, homeostatic model assessment of insulin resistance, triglycerides, and high density lipoprotein cholesterol (HDL) concentration. cMets was log-transformed to improve the distribution. Peripheral leukocyte DNA was extracted and subjected to enhanced, reduced representation bisulfite sequencing. The assay provided single nucleotide resolution of DNA methylation in cytosine-phosphate-guanine (CpG) sites and surrounding regions. Bases with < 10x coverage were excluded, resulting a total of 1,609,424 methylation sites. Linear regression was used to model the association between site-specific methylation level and cMets. All models were adjusted for age, race, and sex. A p < 10x10 -8 was used to determine statistical significance. The significant sites were mapped to the hg19 assembly and subjected to Ingenuity Pathway Analysis (IPA) wherein mapped gene sets were examined for enrichment of downstream function and diseases. Permutations were further performed to confirm the robustness of our findings. Results: On average, the sample was 55% male, 79% white, and aged 16.7 (standard deviation = 2.2) years. cMetS was significantly associated with 52 sites within 43 genes. Among the genes, three were related to glucose tolerance, two to endothelial function, and two more to oxidative stress. IPA indicated that genes associated with these functions were significantly enriched for glucose tolerance (p=0.029), endothelial function (p=0.009), and oxidative stress (p=0.028). Indeed, high cMetS was associated with hypermethylation of PRKCD , which is related to diabetes risk, and PRDX5 , which encodes anti-oxidant peroxiredoxin-5. Higher cMetS also was associated with hypomethylation of ID3 . Conclusion: Despite validation is pending, these preliminary findings suggest that cardiometabolic burden in adolescents is related to DNA methylation in genes related to CVD risk factors in adulthood, including glucose tolerance, endothelial function, and oxidative stress.

Polyphenolic extract attenuates fatty acid-induced steatosis and oxidative stress in hepatic and endothelial cells

2017 ◽  
Vol 57 (5) ◽  
pp. 1793-1805 ◽  
Author(s):  
Laura Vergani ◽  
Giulia Vecchione ◽  
Francesca Baldini ◽  
Elena Grasselli ◽  
Adriana Voci ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Fatty Acid ◽  
Polyphenolic Extract ◽  
And Oxidative Stress

scholarly journals Cardiovascular disease risk factors and oxidative stress among premenopausal women

2018 ◽  
Vol 115 ◽  
pp. 246-251 ◽  
Author(s):  
Chelsea Anderson ◽  
Ginger L. Milne ◽  
Yong-Moon Mark Park ◽  
Dale P. Sandler ◽  
Hazel B. Nichols
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Premenopausal Women ◽  
Cardiovascular Disease Risk Factors ◽  
And Oxidative Stress

scholarly journals Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress

Molecules ◽  
2021 ◽  
Vol 26 (14) ◽  
pp. 4210
Author(s):  
Yan Zhou ◽  
Chunxiu Zhou ◽  
Xutao Zhang ◽  
Chi Teng Vong ◽  
Yitao Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Vascular Function ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Ex Vivo ◽  
Diabetic Mice ◽  
And Oxidative Stress

Coptisine is the major bioactive protoberberine alkaloid found in Rhizoma Coptidis. Coptisine reduces inflammatory responses and improves glucose tolerance; nevertheless, whether coptisine has vasoprotective effect in diabetes is not fully characterized. Conduit arteries including aortas and carotid arteries were obtained from male C57BL/6J mice for ex vivo treatment with risk factors (high glucose or tunicamycin) and coptisine. Some arterial rings were obtained from diabetic mice, which were induced by high-fat diet (45% kcal% fat) feeding for 6 weeks combined with a low-dose intraperitoneal injection of streptozotocin (120 mg/kg). Functional studies showed that coptisine protected endothelium-dependent relaxation in aortas against risk factors and from diabetic mice. Coptisine increased phosphorylations of AMPK and eNOS and downregulated the endoplasmic reticulum (ER) stress markers as determined by Western blotting. Coptisine elevates NO bioavailability and decreases reactive oxygen species level. The results indicate that coptisine improves vascular function in diabetes through suppression of ER stress and oxidative stress, implying the therapeutic potential of coptisine to treat diabetic vasculopathy.

scholarly journals The Role of Antioxidants Supplementation in Clinical Practice: Focus on Cardiovascular Risk Factors

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 146
Author(s):  
Vittoria Cammisotto ◽  
Cristina Nocella ◽  
Simona Bartimoccia ◽  
Valerio Sanguigni ◽  
Davide Francomano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Antioxidant Supplementation ◽  
Oxidative Stress Biomarkers ◽  
Increased Risk ◽  
Human Disorders ◽  
Stress Burden

Oxidative stress may be defined as an imbalance between reactive oxygen species (ROS) and the antioxidant system to counteract or detoxify these potentially damaging molecules. This phenomenon is a common feature of many human disorders, such as cardiovascular disease. Many of the risk factors, including smoking, hypertension, hypercholesterolemia, diabetes, and obesity, are associated with an increased risk of developing cardiovascular disease, involving an elevated oxidative stress burden (either due to enhanced ROS production or decreased antioxidant protection). There are many therapeutic options to treat oxidative stress-associated cardiovascular diseases. Numerous studies have focused on the utility of antioxidant supplementation. However, whether antioxidant supplementation has any preventive and/or therapeutic value in cardiovascular pathology is still a matter of debate. In this review, we provide a detailed description of oxidative stress biomarkers in several cardiovascular risk factors. We also discuss the clinical implications of the supplementation with several classes of antioxidants, and their potential role for protecting against cardiovascular risk factors.

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