Are you Manuel Delgado?

Claim your profile

Publications (3)4.58 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: A polymorphism (1359 G/A) of the CNR1 gene was reported as a common polymorphism in Caucasian populations and was related to cardiovascular risk factors. The present study aimed to investigate the allelic distribution of polymorphism (G1359A) of the CB1 receptor gene in a geographical area of Spain (Community of Castilla y Leon) and to evaluate the influence of this polymorphism on obesity anthropometric parameters and cardiovascular risk factors in the fasted state in obese patients. A population of 341 obese subjects was analysed. Tetrapolar electrical bioimpedance measurement, blood pressure measurement, a serial assessment of nutritional intake with 3 days of written food records and a biochemical analysis were all performed. One hundred and seventy-seven patients (51.9%) had the genotype G1359G (wild-type group) and 164 (48.1%) patients were A carriers: G1359A (136 patients; 39.9%) or A1359A (28 patients; 8.2%) (mutant type group). The Health Area of Palencia had a lower frequency of wild-type genotype and G allelic frequency than all the other Health Areas. Segovia and Burgos Areas had a higher frequency of wild-type genotype and G allelic frequency than the other Health Areas. High-density lipoprotein (HDL) cholesterol was higher in the mutant type group and blood tryglicerides were lower in the same group. In conclusion, the novel finding of the present study is the association of the mutant type group G1359A and A1359A with a better lipid profile (triglycerides and HDL cholesterol) than the wild-type group. The frequencies of this polymorphism are different among Health Areas of Castilla y Leon (Spain). © 2015 The British Dietetic Association Ltd.
    Journal of Human Nutrition and Dietetics 02/2015; DOI:10.1111/jhn.12297 · 2.07 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background and objectiveObesity and insulin resistance are associated with cardiovascular risk factors. The aim of the present study was to explore the relation of visfatin with insulin resistance, cardiovascular risk factors and anthropometry in obese patients without comorbidities.
    Medicina Clínica 07/2011; 137(5):199-203. DOI:10.1016/j.medcli.2010.09.033 · 1.25 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Obesity and insulin resistance are associated with cardiovascular risk factors. The aim of the present study was to explore the relation of visfatin with insulin resistance, cardiovascular risk factors and anthropometry in obese patients without comorbidities. A population of 270 obese patients was analyzed in a prospective way. In all patients we performed a biochemical analysis (lipid profile, insulin, HOMA and visfatina), and a nutritional evaluation (dietary intake, conventional anthropometry and bioimpedance). Patients were divided in two groups by median visfatin value (8,32 ng/ml), group I (patients with the low values, average value 7,11 (0,7) ng/ml) and group II (patients with the high values, average value 13,5 (10,1) ng/ml). Patients in the group I had higher weight, body mass index, waist circumference, and waist to hip ratio than patients in group II. Patients in group I had lower LDL-cholesterol and C reactive protein than patients in group II. Correlation analysis showed a positive correlation between visfatin levels and LDL cholesterol (r=0.194; p<0.05) and C reactive protein (r=0.266; p<0.05) and a negative corelation with weight (r=-0.162; p<0.05). In the logistic analysis with age-, sex- and dietary intake- adjusted basal visfatin concentration as a dependent variable, the next variables remained in the model; weight with an odds ratio (OR) 0,97 (IC95% 0,95-0,99), LDL cholesterol 1,012(1,010-1.023) and C reactive protein 1,15 (1.03-1.3). LDL cholesterol and c reactive protein levels are positively correlated with visfatin levels. Weight is negatively correlated with visfatin levels, in an independent way and adjusted by age, sex and dietary intake.
    Medicina Clínica 02/2011; 137(5):199-203. · 1.25 Impact Factor