Apolipoproteins A-I, B, and C-III and Obesity in Young Adult Cherokee

Hindawi Journal of Lipids Volume 2017, Article ID 8236325, 7 pages https://doi.org/10.1155/2017/8236325 Research Article Apolipoproteins A-I, B, and C-III and Obesity in Young Adult Cherokee Wenyu Wang,1 Piers Blackett,2 Sohail Khan,3 and Elisa Lee1 1 Center for American Indian Health Research, College of Public Health, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73190, USA 2 Section of Diabetes and Endocrinology, Department of Pediatrics, Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA 3 The Cherokee Nation, P.O. Box 948, Tahlequah, OK 74465, USA Correspondence should be addressed to Piers Blackett; Received 8 February 2017; Accepted 20 March 2017; Published 3 April 2017 Academic Editor: Gerd Schmitz Copyright © 2017 Wenyu Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Since young adult Cherokee are at increased risk for both diabetes and cardiovascular disease, we assessed association of apolipoproteins (A-I, B, and C-III in non-HDL and HDL) with obesity and related risk factors. Obese participants (BMI ≥ 30) aged 20–40 years (𝑛 = 476) were studied. Metabolically healthy obese (MHO) individuals were defined as not having any of four components of the ATP-III metabolic syndrome after exclusion of waist circumference, and obese participants not being MHO were defined as metabolically abnormal obese (MAO). Associations were evaluated by correlation and regression modeling. Obesity measures, blood pressure, insulin resistance, lipids, and apolipoproteins were significantly different between groups except for total cholesterol, LDL-C, and HDL-apoC-III. Apolipoproteins were not correlated with obesity measures with the exception of apoA-I with waist and the waist : height ratio. In a logistic regression model apoA-I and the apoB : apoA-I ratio were significantly selected for identifying those being MHO, and the result (𝐶-statistic = 0.902) indicated that apoA-I and the apoB : apoA-I ratio can be used to identify a subgroup of obese individuals with a significantly less atherogenic lipid and apolipoprotein profile, particularly in obese Cherokee men in whom MHO is more likely. 1. Introduction Since obesity predicts atherosclerotic cardiovascular disease (ACVD), it has significant worldwide health and economic implications [1]. This is particularly true in the Cherokee and other American Indian populations [2] in whom obesity is associated with the metabolic syndrome, which often precedes type 2 diabetes (T2D) [3]. Consequently it has become important to study association of obesity with apolipoproteins, since obesity-associated changes in lipid transport precede and predict subsequent insulin resistance and ultimately the development of ACVD and T2D [4, 5]. Therefore, we selected apolipoproteins known to predict atherosclerosis for study. We also proposed that the obese participants could be classified as two distinct groups based on the presence of metabolic complications including dyslipidemia [6] and that apolipoprotein levels might serve to identify differences between the metabolically healthy obese (MHO) and metabolically abnormal obese (MAO) groups. Apolipoprotein B (apoB) represents the total number of apoB-containing lipoproteins [7] and is considered to be superior to LDL-C and non-HDL-C in predicting cardiovascular disease [8], whereas apolipoprotein A-I (apoA-I) has a known inverse association and low levels are associated with increased body mass index (BMI) [9]. Furthermore, the ratio of apoB to apoA-I (B : A-I ratio), representing the combination of two atherogenic processes, is an even stronger predictor [10]. Apolipoprotein C-III (apoC-III) is secreted with VLDL and becomes distributed among circulating lipoproteins [11] conferring harmful properties resulting in ACVD [3, 12]. LDL particles containing apoC-III are more 2 atherogenic than particles without apoC-III [13] and apoC-III on non-HDL lipoprotein particles independently predicted recurrent coronary events [14] and progression of carotid intima-media thickness during treatment [15]. Following hepatic secretion of apoC-III as VLDL, its subsequent distribution on HDL particles may also be harmful, since HDLapoC-III predicted angiographic progression of atherosclerosis in bypass grafts [16] and more recently HDL-apoC-III has been identified as a proatherogenic HDL subtype with loss of its anti-inflammatory properties [16]. Genetic deficiency [17] and targeted gene disruption [18] of apoC-III have been shown to be associated with protection from atherosclerosis [17]. However, the relative role of apoCIII’s distribution on lipoproteins remains uncertain [19], and preliminary evidence suggests that obesity may play a central role in determining apoC-III levels, lipoprotein distribution, and clinical outcomes [20]. Consequently this study and analysis were done to examine association of obesity with apoB, apoA-I, and apoC-III content of both non-HDL and HDL. 2. Methods With collaboration of the Cherokee Nation of Oklahoma, adults aged 20–40 years in the Cherokee Diabetes Study cohort residing in a 5-county area in northeastern Oklahoma participated in the study (𝑛 = 1051). Of this group 477 (45%) were obese, defined as having a BMI greater than or equal to 30. Nondiabetic participants were excluded according to American Diabetes Association criteria for fasting plasma glucose (FPG) defined as being greater than or equal to 126 mg/dl or being on medications for diabetes. Informed consent was obtained from each subject or his/her legal guardian, following approval of the Institutional Review Boards of the University of Oklahoma Health Sciences Center and the Cherokee Nation. After obtaining clinical measurements, fasting blood specimens were collected for determining FPG, insulin, lipids, and apolipoproteins. 2.1. Lipids and Apolipoproteins. An Abbott VP-Super System automatic analyzer and commercial reagents were used to determine levels of glucose, cholesterol (Boehringer, Mannheim, Germany), and triglyceride (Miles Inc., Tarrytown, NJ) by enzymatic methodology. HDL-C was measured using the heparin-manganese precipitation procedure of the Lipid Research Clinics program and LDL-C was calculated by the Friedewald formula. ApoA-I, apoB, and apoC-III were determined by previously validated electroimmunoassays [21–23]. The apoC-III concentrations in whole plasma and heparin-manganese supernatant were determined by separate assays. ApoC-III in the precipitate was calculated by subtracting the supernatant value from the total plasma apoC-III. 2.2. Glucose and Insulin. Fasting insulin levels were determined in a National Institutes of Health core laboratory at the Endocrinology Department at the University of Chicago. Journal of Lipids Insulin was meas (...truncated)