Biomedical subjects

Jean W MacCluer

Publications and source records attributed to Jean W MacCluer.

38 records · Page 3Linked to original sources

PubMedDate not supplied

Common set of genes regulates low-density lipoprotein size and obesity-related factors in Alaskan Eskimos: results from the GOCADAN study.

Increasing incidence of cardiovascular disease in traditionally low-risk Alaskan Eskimos is a cause for concern. The purpose of this study was to examine the genetic and environmental correlations of low-density lipoprotein (LDL) subfractions with obesity-related factors in Alaskan Eskimos, using data from the first 954 participants of the Genetics of Coronary Artery Disease in Alaska Natives Study. Estimates of genetic and environmental influence were calculated using a maximum likelihood variance component method implemented in SOLAR. Mean values of weight, body mass index (BMI), and waist were 73.4 +/- 0.5 kg, 27.6 +/- 0.2 kg/m2, and 88.0 +/- 0.4 cm, respectively. LDL, and its small (LDL1), medium (LDL2), and large (LDL3) subfractions, had mean values of 115.8 +/- 1.2 mg/dl, 8.3 +/- 0.4 mg/dl, 19.6 +/- 0.8 mg/dl, and 71.5 +/- 1.5 mg/dl, respectively. Bivariate analysis displayed significant genetic correlations between LDL subfractions and obesity-related factors: LDL1 with BMI (rhoG = 0.67, P < 0.05), waist (rhoG = 0.80, P < 0.001), and subscapular and tricep skinfolds (rhoG = 0.93, P < 0.005, and rhoG = 0.78, P < 0.05, respectively); LDL2 with BMI (rhoG = 0.52, P < 0.05), waist (rhoG = 0.46, P < 0.05), and tricep skinfold (rhoG = 0.60, P < 0.05); and mean LDL size with BMI (rhoG = -0.36), waist (rhoG = -0.42,), and subscapular and tricep skinfolds (rhoG = -0.44 and -0.43, respectively) (P < 0.005). These results show that a common set of genes is influencing LDL size and obesity-related factors in Alaskan Eskimos.

Adolescent↗

PubMedDate not supplied

Evidence for distinct genetic effects on obesity and lipid-related CVD risk factors in diabetic compared to nondiabetic American Indians: the Strong Heart Family Study.

BACKGROUND: The relationship between diabetes and increased cardiovascular disease (CVD) risk is well established. Previous data from the Strong Heart Family Study (SHFS) have demonstrated significant heritabilities for CVD risk factors and implicated diabetes as an important predictor of several of the phenotypes in three large groups of American Indians in Arizona (AZ), Oklahoma (OK), and the Dakotas (DK). However, the genetic architecture of this relationship is not well understood. The purpose of the present paper is to determine whether the genetic effects on CVD risk factors in the SHFS are different in diabetic and nondiabetic individuals. METHODS: Approximately 950 men and women, 18 years or older, in 32 extended families, were examined between 1997 and 1999. Interaction between genotype and diabetes status was estimated for nine CVD risk factors [body fat mass (FAT), body mass index (BMI), high-density lipoprotein cholesterol (HDL-C), log-transformed fibrinogen, log-transformed triglycerides, log-transformed urinary albumin : creatinine ratio (LACR), plasminogen activator inhibitor 1 (PAI-1), systolic blood pressure (SBP), and waist-to-hip ratio (WHR)], using a maximum likelihood variance decomposition technique. RESULTS: We found evidence that genetic factors influencing BMI, FAT, log-transformed triglycerides, HDL-C, and WHR are differentially expressed in individuals with diabetes compared to those without diabetes. CONCLUSION: Thus, in the environmental and genetic milieu of diabetes, there may be distinct genetic determinants of various CVD risk factors.

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