Body Fat Distribution Is a Determinant of the High-Density Lipoprotein Response to Dietary Fat and Cholesterol in Women

1995 ◽  
Vol 15 (8) ◽  
pp. 1070-1078 ◽  
Author(s):  
Peter M. Clifton ◽  
Mavis Abbey ◽  
Mannie Noakes ◽  
Sandra Beltrame ◽  
Nicole Rumbelow ◽  
...  
1994 ◽  
Vol 109 (1-2) ◽  
pp. 148 ◽  
Author(s):  
P.M. Clifton ◽  
M. Abbey ◽  
M. Noakes ◽  
P.J. Nestel

2007 ◽  
Vol 92 (7) ◽  
pp. 2665-2671 ◽  
Author(s):  
Anthony J. G. Hanley ◽  
Donald Bowden ◽  
Lynne E. Wagenknecht ◽  
Aarthi Balasubramanyam ◽  
Carl Langfeld ◽  
...  

Abstract Context: Hypoadiponectinemia has emerged as an independent risk factor for type 2 diabetes and cardiovascular disease. Although associations of adiponectin with central obesity and insulin resistance have been reported, very little data are available from studies using detailed measures of insulin sensitivity (SI) and/or body fat distribution in ethnic groups at high risk for metabolic disease. Objective: The aim of the study was to identify the correlates of adiponectin in 1636 nondiabetic Hispanics and African-Americans. Design: A cross-sectional analysis of participants in the Insulin Resistance Atherosclerosis Family Study was conducted. SI was determined from frequently sampled iv glucose tolerance tests with minimal model analysis. Subcutaneous and visceral adipose tissues (SAT, VAT, respectively) were determined with computed tomography. Triglyceride, high-density lipoprotein, C-reactive protein, and adiponectin were measured in fasting samples. Generalized estimating equation (GEE) models were used to identify factors associated with adiponectin concentration. Setting: A multicenter study using a family-based design was conducted. Participants: A total of 1636 nondiabetic Hispanic and African-American subjects participated. Main Outcome Measures: Circulating adiponectin concentration was measured. Results: Age, female gender, high-density lipoprotein, SAT, and SI were positive independent correlates of adiponectin, whereas glucose, CRP, and VAT were negative independent correlates (all P < 0.05). Ethnicity was not an independent correlate of adiponectin in this model (P = 0.27); however, an ethnicity by VAT interaction term was retained, indicating a stronger negative association of VAT with adiponectin in African-Americans compared with Hispanics. Conclusion: Directly measured SI, VAT, and SAT were independently correlated with adiponectin in Hispanic and African-American subjects. The inverse association of VAT with adiponectin was stronger in African-Americans compared with Hispanics, a finding that suggests possible ethnic differences in the effects of visceral obesity.


2009 ◽  
Vol 4 (2) ◽  
pp. 143-149 ◽  
Author(s):  
Marijana Radonjic ◽  
Marjan J. van Erk ◽  
Wilrike J. Pasman ◽  
Heleen M. Wortelboer ◽  
Henk F. J. Hendriks ◽  
...  

2001 ◽  
Vol 86 (9) ◽  
pp. 4330-4338 ◽  
Author(s):  
Anthony P. Goldstone ◽  
E. Louise Thomas ◽  
Audrey E. Brynes ◽  
Jimmy D. Bell ◽  
Gary Frost ◽  
...  

Visceral obesity is detrimental to health, but the mechanisms controlling body fat distribution are not fully understood. In premenopausal adult females (30 nonobese, 14 obese [body mass index> 30kg/m2]), variance in fasting insulin, glucose, insulin/glucose ratio, C-peptide/insulin ratio, triglycerides, and high-density lipoprotein/low-density lipoprotein-cholesterol ratio, were independently influenced by visceral but not total sc or abdominal sc adipose tissue, as measured by whole-body magnetic resonance imaging. Adult females with Prader-Willi syndrome (n = 13) had significantly reduced visceral adiposity, compared with obese controls (visceral/total sc adipose tissue ratio: 0.067 ± 0.017 vs. 0.108 ± 0.021), independent of their total adiposity (P < 0.001), or use of exogenous sex steroids. This is in contrast to that expected by their physical inactivity, hypogonadism, adult GH deficiency, and psychiatric problems. Females with Prader-Willi syndrome not receiving sex steroids (n = 8) had significantly reduced fasting insulin, insulin/glucose ratio, and triglycerides and increased C-peptide/insulin ratio, compared with obese controls, adjusting for total (P < 0.05) but not visceral adiposity (P = 0.3–0.6), supporting their association. The cause of the reduced visceral adiposity in Prader-Willi syndrome may reflect novel hormonal, hypothalamic, and/or genetic influences on body fat distribution.


2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Albert Arjaan Graaf ◽  
Wilrike Pasman ◽  
Daan Schalkwijk ◽  
Andreas Freidig ◽  
Henk Hendriks ◽  
...  

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