Genetic polymorphisms in carnitine palmitoyltransferase 1A gene are associated with variation in body composition and fasting lipid traits in Yup'ik Eskimos

Variants of carnitine palmitoyltransferase 1A (CPT1A), a key hepatic lipid oxidation enzyme, may influence how fatty acid oxidation contributes to obesity and metabolic outcomes. CPT1A is regulated by diet, suggesting interactions between gene variants and diet may influence outcomes. The objective of this study was to test the association of CPT1A variants with body composition and lipids, mediated by consumption of polyunsaturated fatty acids (PUFA). Obesity phenotypes and fasting lipids were measured in a cross-sectional sample of Yup'ik Eskimo individuals (n = 1141) from the Center of Alaska Native Health Research (CANHR) study. Twenty-eight tagging CPT1A SNPs were evaluated with outcomes of interest in regression models accounting for family structure. Several CPT1A polymorphisms were associated with HDL-cholesterol and obesity phenotypes. The P479L (rs80356779) variant was associated with all obesity-related traits and fasting HDL-cholesterol. Interestingly, the association of P479L with HDL-cholesterol was still significant after correcting for body mass index (BMI), percentage body fat (PBF), or waist circumference (WC). Our findings are consistent with the hypothesis that the L479 allele of the CPT1A P479L variant confers a selective advantage that is both cardioprotective (through increased HDL-cholesterol) and associated with reduced adiposity. Variants of carnitine palmitoyltransferase 1A (CPT1A), a key hepatic lipid oxidation enzyme, may influence how fatty acid oxidation contributes to obesity and metabolic outcomes. CPT1A is regulated by diet, suggesting interactions between gene variants and diet may influence outcomes. The objective of this study was to test the association of CPT1A variants with body composition and lipids, mediated by consumption of polyunsaturated fatty acids (PUFA). Obesity phenotypes and fasting lipids were measured in a cross-sectional sample of Yup'ik Eskimo individuals (n = 1141) from the Center of Alaska Native Health Research (CANHR) study. Twenty-eight tagging CPT1A SNPs were evaluated with outcomes of interest in regression models accounting for family structure. Several CPT1A polymorphisms were associated with HDL-cholesterol and obesity phenotypes. The P479L (rs80356779) variant was associated with all obesity-related traits and fasting HDL-cholesterol. Interestingly, the association of P479L with HDL-cholesterol was still significant after correcting for body mass index (BMI), percentage body fat (PBF), or waist circumference (WC). Our findings are consistent with the hypothesis that the L479 allele of the CPT1A P479L variant confers a selective advantage that is both cardioprotective (through increased HDL-cholesterol) and associated with reduced adiposity. Obesity is associated with a series of metabolic conditions clinically referred to as metabolic syndrome, which includes hypertension, dyslipidemia, hyperglycemia, and the development of type 2 diabetes (T2D). Approximately sixty percent of obese individuals have metabolic complications (1.Park Y-W. Zhu S. Palaniappan L. Heshka S. Carnethon M.R. Heymsfielow S.B. The metabolic syndrome: prevalence and associated risk factor findings in the US population from the Third National Health and Nutrition Examination Survey, 1988–1994.Arch. Intern. Med. 2003; 163: 427-436Crossref PubMed Scopus (1742) Google Scholar); however, “healthy obese” individuals have been identified with excessive accumulation of body fat that does not translate to dyslipidemia and insulin resistance (2.Blüher M. The distinction of metabolically “healthy” from “unhealthy” obese individuals.Curr. Opin. Lipidol. 2010; 21: 38-43Crossref PubMed Scopus (464) Google Scholar, 3.Wildman R.P. Healthy obesity.Curr. Opin. Clin. Nutr. Metab. Care. 2009; 12: 438-443Crossref PubMed Scopus (76) Google Scholar). For example, some Eskimo/Inuit people indigenous to Alaska are obese, but they have historically demonstrated low prevalence of insulin resistance, metabolic syndrome, and T2D (4.Ebbesson S.O.E. Schraer C.D. Risica P.M. Adler A.I. Ebbesson L. Mayer A.M. Shubnikof E.V. Yeh J. Go O.T. Robbins D.C. Diabetes and impaired glucose tolerance in three Alaskan Eskimo populations. The Alaska-Siberia Project.Diabetes Care. 1998; 21: 563-569Crossref PubMed Scopus (73) Google Scholar, 5.Schraer C.D. Risica P.M. Ebbesson S.O.E. Go O.T. Howard B.V. Mayer A.M. Low fasting insulin levels in Eskimos compared to American Indians: are Eskimos less insulin resistant?.Int. J. Circumpolar Health. 1999; 58: 272-280PubMed Google Scholar, 6.Schraer C.D. Ebbesson S.O.E. Adler A.I. Cohen J.S. Boyko E.J. Nobmann E.D. Glucose tolerance and insulin-resistance syndrome among St. Lawrence Island Eskimos.Int. J. 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The Center for Alaska Native Health Research Study: a community-based participatory research study of obesity and chronic disease-related protective and risk factors.Int. J. Circumpolar Health. 2007; 66: 8-18Crossref PubMed Scopus (81) Google Scholar) is significantly less than that observed in the general US population (10.Cowie C.C. Rust K.F. Ford E.S. Eberhardt M.S. Byrd-Holt D.D. Li C. Williams D.E. Gregg E.W. Bainbridge K.E. Saydah S.H. et al.Full accounting of diabetes and pre-diabetes in the US population in 1988–1994 and 2005–2006.Diabetes Care. 2009; 32: 287-294Crossref PubMed Scopus (941) Google Scholar, 11.Ford E.S. Prevalence of the metabolic syndrome in US populations.Endocrinol. Metab. Clin. North Am. 2004; 33: 333-350Abstract Full Text Full Text PDF PubMed Scopus (107) Google Scholar). Although the mechanisms that allow Yup'ik Eskimo people to carry excess body fat without developing features of metabolic syndrome and T2D are unknown, and are to R. Luick B. Bersamin A. 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