This study examines intercorrelations among waist circumference (WC), intraperitoneal fat (IPF), and subcutaneous abdominal fat (SAF) in ethnically diverse Dallas Heart Study consisting of 1538 women and 1212 men (50% Black). Correlations between fat depots and triglyceride or HOMA2-IR, biomarkers of metabolic syndrome, are also reported. Total abdominal fat (TAF), ASF, and IPF masses were measured by magnetic resonance imaging. The highest correlations with WC according to ethnicity and gender were noted for TAF with progressively lower correlations with ASF (0.65–0.82) and IPF (0.29–0.85). The percentage of IPF relative to TAF was not significantly correlated with WC. For all WC categories, higher IPF/ASF ratios were associated with higher triglyceride levels. In contrast, differences in ratios had little or no association with HOMA2-IR. However, when all data were pooled, IPF was positively correlated with both triglyceride ( (men) and 0.363 (women)) and HOMA2-IR ( (men) and 0.517 (women)); after adjustment for ASF, IPF was still correlated with triglyceride ( (men) and 0.348 (women)) and HOMA2-IR ( (men) and 0.221 (women)). WC measures TAF reliably, but its association with IPF depends on IPF/ASF ratios that vary by gender and ethnicity. 1. Introduction Abdominal obesity is one component of the metabolic syndrome [1]. Clinically, abdominal obesity is identified by an increase in waist circumference (WC). Increased WC has repeatedly been linked to metabolic risk. It is unclear, however, whether this measure is a correlate of increased risk through its correlation with total abdominal fat (TAF) or a specific, metabolically unhealthy depot of adipose tissue. Many investigators postulate that the key component of body fat underlying the metabolic syndrome is intraperitoneal fat (IPF) or visceral fat [2–7]. Others nonetheless contend that abdominal subcutaneous fat (ASF) is a more important pathogenic factor [8–14]. Since previous studies have shown that IPF and ASF are intercorrelated [15], the more important adipose-tissue compartment underlying the metabolic syndrome is difficult to identify. The primary aim of this study was to determine the strength of the correlations between WC and TAF, and ASF and IPF measured by magnetic resonance imaging (MRI). These analyses were made for gender in whites, blacks, and Hispanics of the Dallas Heart Study [16]. We additionally correlated SAF and IPF with plasma triglyceride (TG) and homeostatic model assessment of insulin resistance (HOMA2-IR) [17], both accompanying the metabolic syndrome. 2. Methods Details of
References
[1]
K. G. M. M. Alberti, R. H. Eckel, S. M. Grundy et al., “Harmonizing the metabolic syndrome: a joint interim statement of the international diabetes federation task force on epidemiology and prevention; National heart, lung, and blood institute; American heart association; World heart federation; International atherosclerosis society; And international association for the study of obesity,” Circulation, vol. 120, no. 16, pp. 1640–1645, 2009.
[2]
D. B. Carr, K. M. Utzschneider, R. L. Hull et al., “Intra-abdominal fat is a major determinant of the National Cholesterol Education Program Adult Treatment Panel III criteria for the metabolic syndrome,” Diabetes, vol. 53, no. 8, pp. 2087–2094, 2004.
[3]
F. E. von Eyben, E. Mouritsen, J. Holm et al., “Intra-abdominal obesity and metabolic risk factors: a study of young adults,” International Journal of Obesity, vol. 27, no. 8, pp. 941–949, 2003.
[4]
Y. M. Nakao, T. Miyawaki, S. Yasuno et al., “Intra-abdominal fat area is a predictor for new onset of individual components of metabolic syndrome: metabolic syndrome and abdominal obesity (MERLOT study),” Proceedings of the Japan Academy Series B, vol. 88, no. 8, pp. 454–461, 2012.
[5]
J. D. Smith, A.-L. Borel, J.-A. Nazare et al., “Visceral adipose tissue indicates the severity of cardiometabolic risk in Patients with and without type 2 diabetes: results from the INSPIRE me IAA Study,” Journal of Clinical Endocrinology and Metabolism, vol. 97, no. 5, pp. 1517–1525, 2012.
[6]
I. J. Neeland, A. T. Turer, C. R. Ayers et al., “Dysfunctional adiposity and the risk of prediabetes and type 2 diabetes in obese adults,” Journal of the American Medical Association, vol. 308, no. 11, pp. 1150–1159, 2012.
[7]
A. E. Sumner, L. K. Micklesfield, M. Ricks et al., “Waist circumference, BMI, and visceral adipose tissue in white women and women of African descent,” Obesity, vol. 19, no. 3, pp. 671–674, 2011.
[8]
N. Abate, A. Garg, R. M. Peshock, J. Stray-Gundersen, and S. M. Grundy, “Relationships of generalized and regional adiposity to insulin sensitivity in men,” Journal of Clinical Investigation, vol. 96, no. 1, pp. 88–98, 1995.
[9]
A. Garg, “Regional adiposity and insulin resistance,” Journal of Clinical Endocrinology and Metabolism, vol. 89, no. 9, pp. 4206–4210, 2004.
[10]
M. Chandalla, P. Lin, T. Seenivasan et al., “Insulin resistance and body fat distribution in South Asian men compared to Caucasian men,” PLoS ONE, vol. 2, no. 8, article e812, 2007.
[11]
J. H. Goedecke, N. S. Levitt, E. V. Lambert et al., “Differential effects of abdominal adipose tissue distribution on insulin sensitivity in black and white South African women,” Obesity, vol. 17, no. 8, pp. 1506–1512, 2009.
[12]
D. E. Kelley, F. L. Thaete, F. Troost, T. Huwe, and B. H. Goodpaster, “Subdivisions of subcutaneous abdominal adipose tissue and insulin resistance,” American Journal of Physiology, vol. 278, no. 5, pp. E941–E948, 2000.
[13]
M. K. Tulloch-Reid, R. L. Hanson, N. G. Sebring et al., “Both subcutaneous and visceral adipose tissue correlate highly with insulin resistance in african americans,” Obesity Research, vol. 12, no. 8, pp. 1352–1359, 2004.
[14]
L. Frederiksen, T. L. Nielsen, K. Wraae et al., “Subcutaneous rather than visceral adipose tissue is associated with adiponectin levels and insulin resistance in young men,” Journal of Clinical Endocrinology and Metabolism, vol. 94, no. 10, pp. 4010–4015, 2009.
[15]
G. L. Vega, B. Adams-Huet, R. Peshock, D. Willett, B. Shah, and S. M. Grundy, “Influence of body fat content and distribution on variation in metabolic risk,” Journal of Clinical Endocrinology and Metabolism, vol. 91, no. 11, pp. 4459–4466, 2006.
[16]
R. G. Victor, R. W. Haley, D. L. Willett et al., “The Dallas heart study: a population-based probability sample for the multidisciplinary study of ethnic differences in cardiovascular health,” American Journal of Cardiology, vol. 93, no. 12, pp. 1473–1480, 2004.
[17]
D. R. Matthews, J. P. Hosker, A. S. Rudenski, B. A. Naylor, D. F. Treacher, and R. C. Turner, “Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man,” Diabetologia, vol. 28, no. 7, pp. 412–419, 1985.
[18]
S. Zhu, S. B. Heymsfield, H. Toyoshima, Z. Wang, A. Pietrobelli, and S. Heshka, “Race-ethnicity-specific waist circumference cutoffs for identifying cardiovascular disease risk factors,” American Journal of Clinical Nutrition, vol. 81, no. 2, pp. 409–415, 2005.
[19]
N. Abate, A. Garg, R. Coleman, S. M. Grundy, and R. M. Peshock, “Prediction of total subcutaneous abdominal, intraperitoneal, and retroperitoneal adipose tissue masses in men by a single axial magnetic resonance imaging slice,” American Journal of Clinical Nutrition, vol. 65, no. 2, pp. 403–408, 1997.
[20]
R. Mateo-Gallego, A. M. Bea, E. Jarauta, M. R. Perez-Ruiz, and F. Civeira, “Age and sex influence the relationship between waist circumference and abdominal fat distribution measured by bioelectrical impedance,” Nutrition Research, vol. 32, no. 6, pp. 466–469, 2012.
[21]
X. Li, M. Katashima, T. Yasumasu, and K. J. Li, “Visceral fat area, waist circumference and metabolic risk factors in abdominally obese Chinese adults,” Biomedical and Environmental Sciences, vol. 25, no. 2, pp. 141–148, 2012.
[22]
A. Onat, G. ？. Avci, M. M. Barlan, H. Uyarel, B. Uzunlar, and V. Sansoy, “Measures of abdominal obesity assessed for visceral adiposity and relation to coronary risk,” International Journal of Obesity, vol. 28, no. 8, pp. 1018–1025, 2004.
[23]
B. J. Arsenault, I. Lemieux, J. P. Després et al., “The hypertriglyceridemic-waist phenotype and the risk of coronary artery disease: results from the EPIC-Norfolk Prospective Population Study,” Canadian Medical Association Journal, vol. 182, no. 13, pp. 1427–1432, 2010.
[24]
S. R. Preis, J. M. Massaro, S. J. Robins et al., “Abdominal subcutaneous and visceral adipose tissue and insulin resistance in the framingham heart study,” Obesity, vol. 18, no. 11, pp. 2191–2198, 2010.
[25]
C. S. Fox, J. M. Massaro, U. Hoffmann et al., “Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the framingham heart study,” Circulation, vol. 116, no. 1, pp. 39–48, 2007.
[26]
B. H. Goodpaster, S. Krishnaswami, H. Resnick et al., “Association between regional adipose tissue distribution and both type 2 diabetes and impaired glucose tolerance in elderly men and women,” Diabetes Care, vol. 26, no. 2, pp. 372–379, 2003.
[27]
E. J. Boyko, W. Y. Fujimoto, D. L. Leonetti, and L. Newell-Morris, “Visceral adiposity and risk of type 2 diabetes: a prospective study among Japanese Americans,” Diabetes Care, vol. 23, no. 4, pp. 465–471, 2000.
[28]
S. Nielsen, Z. Guo, C. M. Johnson, D. D. Hensrud, and M. D. Jensen, “Splanchnic lipolysis in human obesity,” Journal of Clinical Investigation, vol. 113, no. 11, pp. 1582–1588, 2004.
[29]
J. M. Miles and M. D. Jensen, “Counterpoint: visceral adiposity is not causally related to insulin resistance,” Diabetes Care, vol. 28, no. 9, pp. 2326–2328, 2005.
[30]
M. D. Jensen, “Is visceral fat involved in the pathogenesis of the metabolic syndrome? Human model,” Obesity, vol. 14, supplement 1, pp. 20S–24S, 2006.
[31]
F. R. Jornayvaz and G. I. Shulman, “Diacylglycerol activation of protein kinase Cε and hepatic insulin resistance,” Cell Metabolism, vol. 15, no. 5, pp. 574–584, 2012.
[32]
Z. Sun and M. A. Lazar, “Dissociating fatty liver and diabetes,” Trends in Endocrinology and Metabolism, vol. 24, no. 1, pp. 4–12, 2013.
[33]
R. P. Hoffman, “Indices of insulin action calculated from fasting glucose and insulin reflect hepatic, not peripheral, insulin sensitivity in African-American and Caucasian adolescents,” Pediatric Diabetes, vol. 9, no. 3, pp. 57–61, 2008.
