15 research outputs found
Type II diabetes mellitus and cardiovascular markers in humans: a prospective study in hellenic homogeneous population
No full textApproximately 200 million people, worldwide, are currently having Type 2 diabetes mellitus (T2DM), a prevalence that has been predicted to increase to 366 million by 2030. Atherosclerotic coronary heart disease (CHD) and other forms of
cardiovascular disease (CYD) are the major cause of mortality in T2DM as well as a major contributor to morbidity and lifetime costs.
A number of unfavorable conditions predisposing to CVD coexist with diabetic status including hyperglycaemia, dyslipidaemia, inflammation and coagulation, many of which may be closely associated with insulin resistance. In addition, mutations and polymorphisms in a number of genes have also been linked with monogenic and polygenic forms of T2DM. In this respect, the possible relationship between these disorders and a number of biochemical factors in a selection of different age groups of diabetic patients was studied.
The purpose of the present work was the identification of biochemical parameters in plasma, which may serve as predisposition factors to CVD in T2DM patients of different age. The variability of hyperglycaemia, dyslipidaemia, and inflammation with age progression were studied.
Four different diabetic groups allocated based on the subjects age (Group A:15-25 years old; Group 13:26-40 years old; Group C:40-60 years old; Group D:60-80 years old) and consisting of ten patients each, in parallel with ten matched for age, sex and ethnic origin healthy controls, were screened for glucose, insulin, lipid profile (total cholesterol, triglycerides, LDL and HDL) and inflammatory mediators (Homocysteine, CRP, IL-6, TNF-a).
Significant differences were observed between the expression of biochemical markers among different age groups. Hyperglycaemia showed no variability with age whereas dyslipidaemia correlated positively with age progression, as well as obesity, low physical activity and family history of heart disease or diabetes. Marked inflammation was prominent only in Groups C and D.
The present study indicates that different biochemical parameters may be used for assessment of CVD risk in T2DM patients of variable age
Inflammatory process in type 2 diabetes - The role of cytokines
No full textPopulation-based studies have shown strong relationship between inflammatory markers and metabolic disturbances, obesity, and atherosclerosis, whereas inflammation has been considered as a “common soil” between these clinical entities and type 2 diabetes (T2D). The accumulation of macrophages in adipose tissue (AT), the common origin of macrophages and adipocytes, the prevalent presence of peripheral mononuclear cells, and apoptotic beta cells by themselves seem to be the sources of inflammation present in T2D, since they generate the mediators of the inflammatory processes, namely cytokines. The main cvtokines involved in the pathogenesis of T2D are interleukin-1 beta (IL-1 beta), with an action similar to the one present in type 1 diabetes, tumor necrosis factor-alpha (TNF-alpha), and IL-6, considered as the main regulators of inflammation, leptin, more recently introduced, and several others, such as monocyte chemoattractant protein-1, resistin, adiponectin, with either deleterious or beneficial effects in diabetic pathogenesis. The characterization of these molecules targeted diabetes treatment beyond the classical interventions with lifestyle changes and pharmaceutical agents, and toward the determination of specific molecular pathways that lead to low grade chronic inflammatory state mainly due to an immune system’s unbalance
Differences in Expression of Cardiovascular Risk Factors among Type 2 Diabetes Mellitus Patients of Different Age
No full textDifferences in expression of cardiovascular risk factors among type 2 diabetes mellitus patients of different age
No full textAtherosclerotic coronary heart disease and other forms of cardiovascular disease (CVD) are the major cause of mortality in type 11 diabetes (T2DM) as well as a major contributor to morbidity and lifetime costs. The purpose of this article is the identification of the biochemical parameters in plasma, which may serve as predisposition factors to CVD in T2DM patients of different ages. The variability of hyperglycemia, dyslipidemia, and inflammation with age progression was also studied for comparison. Four different diabetic groups allocated on the basis of the subjects’ age (Group A: 15-25 years old; Group 13: 26-40 years old; Group C: 40-60 years old; Group D: 60-80 years old) and consisting of 10 patients each, in parallel with 10 healthy controls matched for age, sex, and ethnic origin were screened for glucose, insulin, lipid profile (total cholesterol, triglycerides, LDL, and HDL), and inflammatory mediators (CRP, IL-6, and TNF-alpha). Significant differences were observed among the expressions of biochemical markers among different age groups. Hyperglycemia showed no variability with age whereas dyslipidemia correlated positively with age progression, as well as obesity, low physical activity, and family history of heart disease or diabetes. Marked inflammation was prominent only in Groups C and D. This article indicates that different biochemical parameters may be used for the assessment of CVD risk in T2DM patients of variable age
258 Post-ischemic cardiac remodeling is accelerated in diabetic rats: similarities to clinical and tissue hypothyroidism
No full textWe investigated whether postischemic cardiac remodeling (REM) is accelerated in diabetic rats with possible involvement of thyroid hormone (TH) signaling in this response. Changes in TH signaling occur during REM after acute myocardial infarction (MI) and contribute to cardiac dysfunction.Diabetes was induced in Wistar rats by streptozotocin injection (35mg/Kg i.p.). After 30 days diabetic rats (DM-AMI, n=9) were subjected to MI, while control rats were either sham-operated (SHAM, n=10) or subjected to MI (AMI(1), n=10). After 2 weeks, TRα1 and TRα1 expression and TH levels were measured. Hypothyroid rats by propyl-thiouracil administration (0.05%) in water for 3 weeks were subjected to MI (HYPO-AMI, n=6) while untreated MI rats served as controls (AMI(2), n=6). LV dimensions (LVEDD and LVEDS) and ejection fraction (EF%) were used to assess contractility and REM 2 weeks after MI using echocardiography. Cardiac function was markedly decreased in DM –AMI.Scar (mm2)LVEDD (mm)LVEDS (mm)EF%SHAM-----6.5 (0.1)3.8 (0.2)76 (2.6)AMI(1)79 (4.0)7.7 (0.2)*5.7 (0.2)*52 (1.5)*DM-AMI83 (4.9)8.5 (0.2)**7.0 (0.3)**39 (2.1)***p<0.05 vs SHAM,**p<0.05 vs SHAM and AMI(1)In AMI(1), TRα1 and TRβ1 protein expression were not changed significantly as compared to SHAM while in DM-AMI, both TRα1 and TRβ1 were decreased 1.7 and 1.9 fold respectively as compared to SHAM, p<0.05. T3 and T4 levels were not different between groups. HYPO-AMI hearts, with scar areas comparable to AMI(2) hearts [97(4.7) vs 105 (10.3), p>0.05], showed a similar unfavorable functional response : EF% was found to be markedly reduced [24 (0.9) in HYPO-AMI vs 36.2 (1.0) in AMI(2), p<0.05], while LVEDS was 8.3 (0.2) for HYPO-AMI and 7.5(0.1) for AMI(2), p<0.05. LVEDD equally increased in the 2 groups. Postischemic cardiac remodeling is accelerated both in hypothyroid and diabetic hearts. Tissue hypothyroidism which occurs in DM after myocardial infarction, may at least in part, account for this response
Correlation of liver dysfunction biological markers to the mood status of alcohol-dependent individuals
No full textObjective: Alcohol intake is a major cause of liver cirrhosis as well as chronic liver disease, and commonly coexists with mood disorders such as depression and anxiety. The aim of the present study was to investigate the possible correlation between liver dysfunction related to alcohol intake with anxiety and depressive-like symptomatology prior to and after the detoxification period. Methods: One hundred alcohol abusing/dependent subjects (81 males and 19 females) were treated on an inpatient basis according to a standard detoxification protocol and measurements of serum levels of hepatic enzymes (ASAT, ALAT, gGT), and measures of anxiety (HARS), depression (HDRS) and global functioning (GAS) were also obtained at baseline and at weekly intervals over a period of 4 weeks. Results: Increased levels of hepatic enzymes were observed upon admission that were significantly reduced (P < 0.001) following completion of the detoxification treatment. In addition, the psychopathological profile was improved at the end of the detoxification period and a significant correlation was obtained between the levels of hepatic enzymes and the global functioning of alcohol-dependent individuals. Conclusion: This observation further supports a relationship between the depressogenic action of alcohol and the disordered liver function observed in alcohol-dependent individuals, with possible implications in the diagnosis and treatment of mood disorders associated to alcohol abuse
084 Diabetes prevents compensatory hypertrophy after myocardial infarction and impairs cardiac function; possible implication of stretch induced kinase growth signaling
No full textAimThe present study investigated possible mechanisms underlying postischemic remodeling in diabetic hearts. Diabetes (DM) accelerates postischaemic cardiac remodeling and increases mortality after myocardial infarction.MethodsAcute myocardial infarction (AMI) was induced in rats with type I diabetes (DM) and non diabetic rats (NDM-AMI) while sham operated animals served as controls (SHAM). All groups were subjected to echocardiographic analysis 2 weeks after infarction.ResultsAMI resulted in increased expression of β-MHC and distinct changes in cardiac function and geometry. EF% was decreased in DM-AMI as compared to NDM-AMI. Systolic and diastolic chamber dimensions were increased without concomitant increase in wall thickness and thus, WTI (the ratio of LVIDd/2*Posterior Wall thickness), an index of wall stress, was significantly increased in DM-AMI hearts. The absence of wall thickening in DM-AMI hearts was associated with different pattern of activation of stretch induced kinase hypertrophic signaling p38 MAPK and ERK; Phosphorylated ERK and p38 MAPK levels were increased in NDM-AMI hearts, while were not changed in DM-AMI as compared to non infarcted diabetic hearts (DM-SHAM). TH administration after AMI resulted in decreased β-MHC expression, increased wall thickening and normalized wall stress, while stretch induced p38 MAPK activation was restored.ConclusionsDiabetes reduces the ability of the myocardium to adapt after myocardial infarction by preventing the development of compensatory hypertrophy. This is, at least in part due to inactivation of stress induced kinase signalling
Thyroid hormone can favorably remodel the diabetic myocardium after acute myocardial infarction
No full textGenetic variations of the endothelial nitric oxide synthase gene are related to increased levels of C-reactive protein and macrophage-colony stimulating-factor in patients with coronary artery disease
No full textIt was the objective of this study to investigate the relation between nitric oxide synthase (NOS3) gene polymorphisms, vascular inflammation, endothelial function,and atherosclerosis. We examined the effects of a variable nucleotide tandem repeats (VNTR) in intron 4, G894T in exon 7 and T-786C at the promoter region of NOS3 on i) C-reactive protein (CRP) and macrophage-colony stimulating-factor (MCSF), and ii) augmentation index (AI) measured by pulse-wave analysis, flow-mediated dilation (FMD) of the brachial artery, intima-media thickness (IMT) of the carotid and femoral artery using ultrasonography and ankle-brachial index (ABI) in 122 patients with chronic coronary artery disease (CAD) who underwent coronary angiography. MCSF and CRP were increased in patients with T-786C (77/122) or VNTR (40/122) allele compared to those without (F = 10.8, p = 0.002 and F = 3.8, p = 0.04 for T-786C and F = 3.65, p = 0.04 and F = 3.2 p = 0.049 for VNTR), even after adjustment for traditional risk factors and medication. Patients with combination of VNTR and T-786C (31/122) had higher MCSF or CRP than patients with one or none of these alleles (p < 0.05). Among patients with T-786C, those with MCSF > 262 pg/ml or CRP > 3.2 mg/l (n = 33/77) had a higher femoral and carotid IMT and number of plaques in the peripheral arteries than those with lower values of these inflammatory indices (p < 0.05). Patients with MCSF > 262 pg/ml had also lower FMD and higher Gensini score than those with lower MCSF (p < 0.05). The intron 4-VNTR and T-786C mutation of NOS3 gene enhance the inflammatory process in patients with chronic CAD
