Francisco Gómez-Pérez

Publications of Francisco Gómez-Pérez

• Association of the calpain-10 gene with type 2 diabetes mellitus in a Mexican population.

  Authors: Laura Del Bosque-Plata, Carlos A Aguilar-Salinas, María Teresa Tusié-Luna, Salvador Ramírez-Jiménez, Maribel Rodríguez-Torres, Moisés Aurón-Gómez, Erika Ramírez, María Luisa Velasco-Pérez, Alfredo Ramírez-Silva, Francisco Gómez-Pérez, Craig L Hanis, Takafumi Tsuchiya, Issei Yoshiuchi, Nancy J Cox, Graeme I Bell

  Molecular genetics and metabolism. 03/2004; 81(2):122-6.

  Variation in the calpain-10 gene (CAPN10) has been associated with risk of type 2 diabetes in the Mexican American population of Starr County, Texas. We typed five polymorphisms in the calpain-10Variation in the calpain-10 gene (CAPN10) has been associated with risk of type 2 diabetes in the Mexican American population of Starr County, Texas. We typed five polymorphisms in the calpain-10 gene (SNP-43, -43, -63, and -110 and Indel-19) to test for association with type 2 diabetes in 248 individuals representative of the mestizo population of Mexico City and Orizaba, Mexico including 134 patients with type 2 diabetes and 114 subjects with normal fasting blood glucose levels. We found a significant difference in SNP-44 allele and genotype frequencies between type 2 diabetic and non-diabetic subjects. The rare allele at SNP-44 was associated with increased risk of type 2 diabetes (odds ratio (OR)=2.72, 95% confidence interval (CI)=1.16-6.35, P=0.017). SNP-110, which is in perfect linkage disequilibrium with SNP-44, was also associated with type 2 diabetes. The SNP-43, Indel-19, and SNP-63 haplogenotype 112/121 associated with significantly increased risk (OR=2.16, 95% CI=1.31-3.57) of type 2 diabetes in Mexican Americans was not associated with significantly increased in risk in Mexicans (OR=1.15, 95% CI=0.57-2.34). The results suggest that variation in CAPN10 affects risk of type 2 diabetes in the mestizo population of central Mexico (Mexico City and Orizaba) and in Mexican Americans (Starr County, Texas).

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• Locus on chromosome 6p linked to elevated HDL cholesterol serum levels and to protection against premature atherosclerosis in a kindred with familial hypercholesterolemia.

  Authors: Samuel Canizales-Quinteros, Carlos A Aguilar-Salinas, Eduardo Reyes-Rodríguez, Laura Riba, Maribel Rodríguez-Torres, Salvador Ramírez-Jiménez, Adriana Huertas-Vázquez, Verónica Fragoso-Ontiveros, Alejandro Zentella-Dehesa, José L Ventura-Gallegos, Gerardo Vega-Hernández, Angelina López-Estrada, Moisés Aurón-Gómez, Francisco Gómez-Pérez, Juan Rull, Nancy J Cox, Graeme I Bell, Maria Teresa Tusié-Luna

  Circulation research. 04/2003; 92(5):569-76.

  Heterozygous familial hypercholesterolemia (FH) is a highly atherogenic genetic disorder leading to premature coronary heart disease (CHD), usually before 60 years of age. We studied an extendedHeterozygous familial hypercholesterolemia (FH) is a highly atherogenic genetic disorder leading to premature coronary heart disease (CHD), usually before 60 years of age. We studied an extended multigenerational kindred with FH linked to chromosome 1p32 in which atherosclerotic complications were either delayed or prevented in individuals with elevated HDL cholesterol (HDL-C) levels or hyperalphalipoproteinemia (HA). Premature CHD was observed in FH individuals without HA. The study of this family established that the HA trait in the family also followed an autosomal dominant mode of inheritance with a pattern of segregation independent from FH. We identified a locus on chromosome 6 linked to elevated HDL-C levels (HA) in this family. Haplotype analysis refined the localization to a 7.32-cM interval (73 to 80 cM from pter) flanked by markers D6S1280 and D6S1275. Parametric 2-point and multipoint analyses yielded maximum LOD scores of 3.05 and 3.17, respectively. This finding was confirmed with a nonparametric multipoint score of 3.78 (P=0.0009). We propose that this locus, linked to elevated HDL-C levels, confers protection against premature CHD within an FH context.

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• Association of the calpain-10 gene with type 2 diabetes mellitus in a Mexican population

  Authors: Laura del Bosque-Plata, Carlos A Aguilar-Salinas, Marı́a Teresa Tusié-Luna, Salvador Ramı́rez-Jiménez, Maribel Rodrı́guez-Torres, Moisés Aurón-Gómez, Erika Ramı́rez, Marı́a Luisa Velasco-Pérez, Alfredo Ramı́rez-Silva, Francisco Gómez-Pérez, Craig L Hanis, Takafumi Tsuchiya, Issei Yoshiuchi, Nancy J Cox, Graeme I Bell

  Molecular Genetics and Metabolism.

  Variation in the calpain-10 gene (CAPN10) has been associated with risk of type 2 diabetes in the Mexican American population of Starr County, Texas. We typed five polymorphisms in the calpain-10Variation in the calpain-10 gene (CAPN10) has been associated with risk of type 2 diabetes in the Mexican American population of Starr County, Texas. We typed five polymorphisms in the calpain-10 gene (SNP-43, -43, -63, and -110 and Indel-19) to test for association with type 2 diabetes in 248 individuals representative of the mestizo population of Mexico City and Orizaba, Mexico including 134 patients with type 2 diabetes and 114 subjects with normal fasting blood glucose levels. We found a significant difference in SNP-44 allele and genotype frequencies between type 2 diabetic and non-diabetic subjects. The rare allele at SNP-44 was associated with increased risk of type 2 diabetes (odds ratio (OR)=2.72, 95% confidence interval (CI)=1.16–6.35, P=0.017). SNP-110, which is in perfect linkage disequilibrium with SNP-44, was also associated with type 2 diabetes. The SNP-43, Indel-19, and SNP-63 haplogenotype 112/121 associated with significantly increased risk (OR=2.16, 95% CI=1.31–3.57) of type 2 diabetes in Mexican Americans was not associated with significantly increased in risk in Mexicans (OR=1.15, 95% CI=0.57–2.34). The results suggest that variation in CAPN10 affects risk of type 2 diabetes in the mestizo population of central Mexico (Mexico City and Orizaba) and in Mexican Americans (Starr County, Texas).

• Detection of myocardial viability could be improved by rest GIK (glucose-insulin-potassium solution)-Tc 99m sestamibi compared with TL-201 reinjection, in post myocardial infarction patients.

  Authors: Arturo Orea, Lilia Castillo, Víctor Ochoa, Juan Antonio Rull, Francisco Gómez-Pérez, Verónica Rebollar, Jesus Sepulveda, Joel Dorantes, Enrique Asensio, Jorge Oseguera, Ofelia González

  Revista de investigación clínica; organo del Hospital de Enfermedades de la Nutrición. 56(3):321-6.

  GIK solutions improve detection of myocardium viability after acute infarction because they could change the metabolic conditions, improving myocardial perfusion defects. METHODS AND RESULTS: SeventyGIK solutions improve detection of myocardium viability after acute infarction because they could change the metabolic conditions, improving myocardial perfusion defects. METHODS AND RESULTS: Seventy four patients (52 men, 22 women, mean age 53.3.08 +/- 12.14 years) with previous myocardial infarction (evolution time, 4.2 +/- 3.1 months) underwent pharmacological stress (dipyridamole), rest redistribution and reinjection Tl-201 image as well rest/stress Tc-99m Sestamibi, after the intravenous administration of GIK (200 g glucose +/- 30 UI regular insuline +/- 40 mEq potassiumchloride/500 mL in continuous infusion during 3 hours), Group A (N = 22) or oral administration of 70 g of glucose+/- 40 mEq of potassium chloride taking in advantage the endogenous insulin secretion, to non-diabetic patients (group B = GB, N = 26) and group C (GC, diabetic patients N = 26). All of the 74 patients received 10 mg of sublingual Isorbide previous to 25 mCi of Tc99m Sestamibi administration in a different 2 days protocol. A total of 1,480 myocardial segments were assessed and numbered, and the severity of perfusion defects in the segments involved, were compared between Thallium 201 rest reinjection and GIK-MIBI as the main objective of the study. Involved territories number: 4.02 +/- 2.50 vs. 6.88 +/- 2.12, p = 0.005 for AD; 5.2 +/- 1.44 vs. 6.35 +/- 1.11, p = 0.05 for RC and 1.58 +/- 1.01 vs. 2.05 +/- 1.05, p = 0.05 Cx. For GIK-MIBI vs. Tl-201 reinjection respectively, and defect severity: 8.2 +/- 6.04 vs. 13.22 +/- 5.38, p = 0.01 for LAD; 11.72 +/- 5.08 vs. 15.13 +/- 4.42, p = 0.005 for RC and 2.66 +/- 2.09 vs. 4.69 +/- 3.58, p = 0.003 Cx . For GIK-MIBI vs. Tl-201 reinjection respectively, were found. CONCLUSION: Our data suggest that GIK-MIBI protocol is a safe and easy procedure which improves the detection of perfusion reversible defects compared with Tl-201 reinjection, obtaining better information regarding myocardial viability, with lower acquisition time and less cost.

• [Familial hypertriglyceridemia and diabetes mellitus type 2]

  Authors: Carlos Alberto Aguilar-Salinas, Erika Ramírez-Moguel, José Gallegos-Martínez, Octavio Leyva, Jorge Oseguera, Horacio Lozano, Francisco Gómez-Pérez

  Gaceta médica de México. 141(3):201-5.

  Hypertriglyceridemia is a cardiovascular risk factor in type-2 diabetes. However, this abnormality may be caused by several mechanisms. In familial hypertriglyceridemia, a hyperlipidemia associatedHypertriglyceridemia is a cardiovascular risk factor in type-2 diabetes. However, this abnormality may be caused by several mechanisms. In familial hypertriglyceridemia, a hyperlipidemia associated with type-2 diabetes, plasma accumulation of non atherogenic particles explains the presence of hypertriglyceridemia. Our objective was to compare the prevalence of coronary insufficiency and carotid artery stenosis in patients with type-2 diabetes with or without familial hypertriglyceridemia. Controls were paired against cases based on age, gender, diabetes duration, treatment and other cardiovascular risk factors. Controls had either a normal lipid profile (n=48) or hyperlipidemia (n=15). The intima-media thickness of the carotid arteries was significantly lower in cases compared to controls (0.55 +/- 0.12 vs 0.63 +/- 0.22 in normolipidemic controls and 0.66 +/- 0.18 mm in hyperlipidemic subjects (p=0.02)). Exercise treadmill testing was abnormal in a similar proportion of cases and controls (4.8 vs 6.2%). Incidence of cardiovascular complications was not different between groups. We therefore conclude that severe hypertriglyceridemia due to familial hypertriglyceridemia is not associated with an increased prevalence of symptomatic atherosclerosis in patients with type-2 diabetes.

• Correlations between surrogate measures of insulin resistance and cardiovascular risk factors in obese and overweight patients.

  Authors: Israel Lerman, Antonio R Villa, Juan Manuel Ríos-Torres, Laura Elena Tamez, Francisco Gómez-Pérez, Sonia Luna del Villar Velasco, Juan Antonio Rull Rodrigo

  Journal of diabetes and its complications. 17(2):66-72.

  There are different equations to estimate insulin sensitivity by using OGTT with a reasonable approximation to whole body sensitivity obtained with the glucose clamp. Further work is needed toThere are different equations to estimate insulin sensitivity by using OGTT with a reasonable approximation to whole body sensitivity obtained with the glucose clamp. Further work is needed to address their role in clinical practice as markers of the metabolic syndrome and predictors for cardiovascular disease. In the present study, we determined plasma glucose and insulin values during an OGTT test in 144 overweight and obese individuals. We assessed insulin resistance by the use of different equations and established their relationship with cardiovascular risk factors associated to the insulin resistance syndrome. Distributed the patients by quintiles of body mass index (BMI), the different surrogate measures clearly demonstrated that the more obese individuals were the most insulin resistant, a similar but not significant trend was observed related to the other cardiovascular risk factors. Efforts to use both fasting and post-load glucose and insulin concentrations to create indexes for routine use in clinical practice do not seem to be particularly useful in overweight or obese patients, as most of these patients will be insulin-resistant and insulin resistance is closely linked but not equal to the metabolic syndrome.