Age, Homocysteine, and Oxidative Stress: Relation to Hypertension and Type 2 Diabetes Mellitus

Domínguez, Ligia J.; Galioto, Antonio; Pineo, Antonella; Ferlisi, Anna; Ciaccio, Marcello; Putignano, Elena; Belvedere, Mario; Costanza, Giuseppe; Barbagallo, Mario

doi:10.1080/07315724.2010.10719810

Cited by 45 publications

(37 citation statements)

References 33 publications

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“…For the purpose of laboratory interpretation, it should be noted that total homocysteine levels increase with age and are lower in the pregnant population. 65,66 Genetic counseling should take into account the clinical reason for which the test was performed. Many studies have revealed discrepant findings between Caucasians and Asians.…”

Section: Acmg Practice Guidelinesmentioning

confidence: 99%

ACMG Practice Guideline: lack of evidence for MTHFR polymorphism testing

Hickey

Curry

Toriello

2013

Genetics in Medicine

134

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Section: Acmg Practice Guidelinesmentioning

confidence: 99%

ACMG Practice Guideline: lack of evidence for MTHFR polymorphism testing

Hickey

Curry

Toriello

2013

Genetics in Medicine

134

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“…[8][9][10][11][12] Since both diseases are the primary clinical outcomes of metabolic syndrome, understanding of the cause of hyperhomocysteinemia may shed light on the etiology of metabolic syndrome. Plasma homocysteine levels are determined by three main factors: (1) the remethylation rate of homocysteine to methionine; (2) the conversion rate of homocysteine to cystathionine; and most importantly, (3) the amount of methylation of substrates.…”

Section: Methyl Consumers and Hyperhomocysteinemiamentioning

confidence: 99%

“…8,12 This phenomenon may reflect a difference in the compensatory capacity in the conversion of homocysteine to methionine or cystathionine, since plasma homocysteine levels are also found to go up with age. 9,38,39 Moreover, because the production of homocysteine is mainly determined by diet, 33 metabolic syndrome patients, even those with CVD, may have normal plasma homocysteine if they have shifted to a low methyl consumer diet and/ or have a higher capability to convert homocysteine to methionine (for example, due to folate supplementation) or to cystathionine. From this point of view, it seems that plasma homocysteine may not be a reliable indicator of the imbalance between methyl supply and consumption, especially in the early stage of metabolic syndrome.…”

Section: Pi+ Ppimentioning

confidence: 99%

“…5 To date, although the exact cause of metabolic syndrome remains unknown, it is known that diet may have a major role in the pathogenesis and prevalence of metabolic syndrome. 6 Increasing evidence indicates that the pathogenic mechanism underlying metabolic syndrome and its clinical outcomes may involve oxidative stress, characterized by an increased production of reactive oxygen species (ROS), 1 and aberrant methylation status, characterized by changes in the levels of plasma methyl donors 7 and homocysteine [8][9][10][11][12] and altered DNA methylation (an epigenetic mechanism that alters gene expression). 2 Recently, emerging evidence suggests that DNA methylation may be involved in the regulation of insulin gene expression in T2D and the pathogenesis of insulin resistance.…”

Section: Introductionmentioning

confidence: 99%

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Dietary methyl-consuming compounds and metabolic syndrome

Zhou

et al. 2011

Hypertens Res

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The metabolic syndrome, a major risk factor for type 2 diabetes and cardiovascular disease, is a cluster of metabolic abnormalities including obesity, insulin resistance, hypertension and dyslipidemia. Although systemic oxidative stress and aberrant methylation status are known to have important roles in the development of metabolic syndrome, how they occur remains unclear. The metabolism of methyl-consuming compounds generates reactive oxygen species and consumes labile methyl groups; therefore, a chronic increase in the levels of methyl-consuming compounds in the body can induce not only oxidative stress and subsequent tissue injury, but also methyl-group pool depletion and subsequent aberrant methylation status. In the past few decades, the intake amount of methyl-consuming compounds has substantially increased primarily due to pollution, food additives, niacin fortification and high meat consumption. Thus, increased methyl consumers might have a causal role in the development and prevalence of metabolic syndrome and its related diseases. Moreover, factors that decrease the elimination/ metabolism of methyl-consuming compounds and other xenobiotics (for example, sweat gland inactivity and decreased liver function) or increase the generation of endogenous methyl-consuming compounds (for example, mental stress-induced increase in catecholamine release) may accelerate the progression of metabolic syndrome. Based on current nutrition knowledge and the available evidence from epidemiological, ecological, clinical and laboratory studies on metabolic syndrome and its related diseases, this review outlines the relationship between methyl supply-consumption imbalance and metabolic syndrome, and proposes a novel mechanism for the pathogenesis and prevalence of metabolic syndrome and its related diseases.

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“…Hcy levels can be reduced by folate administration while the production and effects of free radicals can be controlled by antioxidants. 11,12 In this study evaluation of oxidative stress level, antioxidant, homocysteine, and vitamin levels were measured in patients of diabetes mellitus type 2 at different time intervals.…”

mentioning

confidence: 99%

Type 2 Diabetes Mellitus; Homocysteine, Total Anti-Oxidant Levels and Vitamins in Patients of Different Duration

Khawaja¹,

Sarwar²,

Bloach

et al. 2016

TPMJ

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Out of 120 selected subjects, 30 were assigned as control, (group 1) and 90 of DMT2. Based on duration, patients of DMT2 were divided into; group 2 (DMT2 <5 years), 3 (DMT2 = 5-10 years) and group 4 (DMT2 >10 years). Smokers, renal failure, coronary artery disease, thyroid disease and patients on antioxidant treatment were excluded from the study. DMT2 was diagnosed according to American Diabetes Association standards. The fasting plasma glucose levels were measured by glucose oxidase method; HbA1c by automated kit, TAC by calorimetric TAC Assay Kit (BioVision), Vitamin C and E by ELISA Kit (HUMAN) while homocysteine measured by AXSYM HCY assay kit (ABBOTT). Cut off values for HbA1c was taken as ≤6%; FBS ≤110 mg/dl; TAC ≥1.16 mmol/L; Vitamin C ≥2 mg/dl; Vitamin E ≥ 9.5nmol/ml and homocysteine was < 6.3 μmol/L. Results: As the duration of DMT2 increases, levels of vitamin C and TAC fall significantly (p <0.05) in all groups except between groups 1 & 2; however, vitamin E, decreased significantly in all the groups with increased DMT2 duration. A significantly increased level of HbA1c was noticed in groups 2, 3 and 4 compared to group 1 with increased DMT2 duration. The fasting blood sugar increased significantly in all the groups except between group 3 and 4. ANOVA showed significant differences (p <0.05) between each group and within the groups when Hb1Ac, vitamin E, vitamin C, & TAC were compared. A positive significant correlation was observed when HbA1c was correlated with FBS; TAC correlated with vitamin C and E and between vitamin C and vitamin E. Conclusions: The levels of TAC, vitamin C and E gradually decrease with increased DMT2 duration; so should be supplemented in diabetics. TAC status can be taken as early marker to detect complications while homocysteine levels to prevent diabetic complications. Key words:Homocysteine, Total Anti-Oxidant, Vitamins, Diabetes Mellitus Diabetes Mellitus type-2, Homocystein, Anti-oxidants Article Citation: Khawaja R, Sarwar M, Bloach MH, Ahmad I, Munir TA. Type 2 diabetes mellitus; homocysteine, total anti-oxidant levels and vitamins in patients of different duration. Professional Med J 2016;23(9)

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Age, Homocysteine, and Oxidative Stress: Relation to Hypertension and Type 2 Diabetes Mellitus

Abstract: Aging is accompanied by elevated homocysteine and oxidative stress levels similar to those observed in younger subjects with hypertension or diabetes mellitus, independent of age. Hence, these conditions appear to accelerate the age-dependent increase in homocysteine and oxidative stress.

Cited by 45 publications

References 33 publications

ACMG Practice Guideline: lack of evidence for MTHFR polymorphism testing

ACMG Practice Guideline: lack of evidence for MTHFR polymorphism testing

Dietary methyl-consuming compounds and metabolic syndrome

Type 2 Diabetes Mellitus; Homocysteine, Total Anti-Oxidant Levels and Vitamins in Patients of Different Duration

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