86,562 research outputs found

    The influence of PON1 192 polymorphism on endothelial function in diabetic subjects with or without hypertension.

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    Hypertension and type 2 diabetes mellitus (T2DM) cause endothelial dysfunction probably through increased oxidant stress. Paraoxonase (PON1) is an high-density lipoprotein (HDL)-linked anti-oxidant enzyme whose capacity is influenced by a genetic polymorphism at codon 192. In the present study we have investigated the role of PON1 polymorphism on endothelial function in subjects with T2DM with or without hypertension. Three groups of male subjects were enrolled: 65 healthy control subjects without T2DM or hypertension (CON), 51 with only T2DM (DM), and 67 with both hypertension and T2DM (HYP+DM). The PON1 Gln192Arg polymorphism was determined by polymerase chain reaction (PCR) amplification and restriction analysis. Endothelial function was evaluated as flow-mediated vasodilatation (FMD) of the brachial artery after forearm ischemia. Data were analyzed according to the presence or absence of the Arg allele. Subjects with T2DM had markedly impaired FMD, compared with those of the CON group. In the CON and HYP+DM groups no difference was observed in FMD between subjects homozygous for the Gln allele and those carrying the Arg allele. In the DM group FMD was lower among those carrying the Arg allele compared with Gln/Gln homozygotes (2.1+/-2.4% vs. 6.2+/-5.2%, p=0.002). In conclusion, the present findings demonstrated that FMD was less impaired in normotensive diabetic subjects homozygous for the Gln allele, consistent with the notion that this isoform has a more effective antioxidant action that serves to protect circulating low-density lipoprotein (LDL). Hypertension seems to abolish the protective effect of the Gln isoform. These findings, however, warrant further investigation to clarify their clinical import

    Body mass index, metabolic syndrome and carotid atherosclerosis.

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    OBJECTIVE: Body fatness and fat distribution are widely accepted as coronary heart disease risk factors. In this study, we have evaluated the contribution of generalized adiposity, assessed by body mass index (BMI), to carotid atherosclerosis, in participants with or without metabolic syndrome (MetS). METHODS: We have analysed 840 female and 1002 male participants in a regional Cardiovascular Disease Prevention Campaign. Blood glucose and lipids were analysed by standard methods. According to BMI, calculated as weight (in kilograms)/height (in square metres), participants were divided into normal weight (BMI <25 kg/m2), overweight (BMI between 25 and 29.9 kg/m2) and obese (BMI>29.9 kg/m2). Carotid atherosclerosis was evaluated by echo Doppler. RESULTS: Blood pressure, waist circumference, triglycerides and glucose were significantly higher, and high-density lipoprotein was lower, in overweight and obese participants, compared with normal weight. MetS was more frequent among obese and overweight than normal-weight participants (51.7 vs. 21.5 vs. 9.8%, respectively). The prevalence of carotid atherosclerosis was 45.29% in participants with MetS, significantly higher than in participants without MetS (33.04%, P<0.0001), but it was similar across the three weight categories. Furthermore, in multiple regression analyses BMI was not significantly associated with carotid atherosclerosis. CONCLUSION: The present findings suggest that increasing body weight favours the clustering of coronary heart disease risk factors. Overweight and obesity, however, do not independently associate with carotid atherosclerosis
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