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|Objective:||To investigate whether baseline and changes in VAT and subcutaneous adipose tissue (SAT) are associated with future development of atherogenic dyslipidaemia independent of baseline lipid levels|
|Study design:||Community-based prospective cohort study. The duration of follow-up was 5 years.|
|Study population:||452 Japanese Americans (240 men, 212 women), aged 34-75 years (mean 52.6 years) with mean ± standard deviation (SD) body mass index 24.2 ± 3.2 kg/m2. Atherogenic dyslipidaemia (defined below) was present in 269 subjects at baseline.|
|Primary outcome:||Development of atherogenic dyslipidaemia, defined as one or more abnormalities in high-density lipoprotein (HDL) cholesterol (<40 mg/dL or 1.03 mmol/L in men and <50 mg/dL or 1.29 mmol/L in women), triglycerides (≥ 150 mg/dL or 1.69 mmol/L), or non-HDL cholesterol levels (≥ 160 mg/dL or 4.14 mmol/L).|
|Secondary outcome:||Body mass index (BMI), waist circumference, and SAT|
Abdominal fat areas were measured by computed tomography.
Data for triglycerides and HDL cholesterol were log transformed. Multivariate logistic regression analysis was used to investigate whether the incremental change in VAT over 5 years was associated with the development of atherogenic dyslipidaemia in subjects without this dyslipidaemic profile at baseline. Analysis was adjusted for age, sex, diastolic blood pressure, homeostasis model assessment insulin resistance, BMI, change in BMI, SAT, and baseline atherogenic lipid levels.
|Authors’ conclusion:||Baseline and the change in VAT were independent predictors for future development of atherogenic dyslipidaemia. However, BMI, waist circumference, and SAT were not associated with future development of atherogenic dyslipidaemia.|
Previous cross-sectional studies (1,2) have shown an association between accumulation of abdominal fat (i.e. VAT) and atherogenic dyslipidaemia, characterised by elevated triglycerides with or without low HDL cholesterol plasma concentration. However, there has been debate as to whether VAT is independently predictive of future development of atherogenic dyslipidaemia. This prospective, longitudinal study provides clear evidence that this association is independent of lipid levels at baseline, as well as other measures of adiposity including BMI, waist circumference, and SAT. Moreover, and in contrast to other studies (3,4), the lack of association between baseline and the change in SAT and atherogenic dyslipidaemia, implies that the impact of SAT on future metabolic risk is less pronounced than that for VAT. While the authors acknowledge that there may be limitations to the generalisability of these findings due to the ethnicity of the patient population (Japanese American), nevertheless the results do highlight the importance of VAT to dyslipidaemia. In addition, studies by the same group have shown a link between the change in VAT and risk for subsequent development of type 2 diabetes (5).
Undoubtedly central obesity is an important determinant of risk for type 2 diabetes and cardiovascular disease (6). This study adds new evidence showing that VAT is an important predictor of development of atherogenic dyslipidaemia, a key driver of atherogenic risk in individuals with insulin-resistant conditions. The negative metabolic changes associated with VAT may be associated specifically with intrahepatic triglyceride content (7). Consequently, these findings highlight the importance of targeting central obesity to reduce the risk of cardiometabolic abnormalities, notably atherogenic dyslipidaemia. Renewed focus on lifestyle intervention is key to addressing this important driver of atherogenicity.
1. Fox CS, Massaro JM, Hoffmann U et al. Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the Framingham Heart Study. Circulation. 2007;116:39–48.
2. Oka R, Miura K, Sakurai M et al. Impacts of visceral adipose tissue and subcutaneous adipose
tissue on metabolic risk factors in middle-aged Japanese. Obesity (Silver Spring). 2010;18:153–160.
3. Abate N, Garg A, Peshock RM et al. Relationships of generalized and regional adiposity to insulin sensitivity
in men. J Clin Invest. 1995;96:88–98.
4. Goodpaster BH, Thaete FL, Simoneau JA et al. Subcutaneous abdominal fat and thigh muscle composition predict insulin sensitivity independently of visceral fat. Diabetes. 1997;46:1579–1585.
5. Carey VJ, Walters EE, Colditz GA et al. Body fat distribution and risk of non-insulin-dependent diabetes mellitus in women. The Nurses’ Health Study. Am J Epidemiol 1997;145:614–9.
6. Wander PL, Boyko EJ, Leonetti DL et al. Change in visceral adiposity independently predicts a greater risk of developing type 2 diabetes over 10 years in Japanese Americans. Diabetes Care 2013;36: 289–9.3
7. Sattar N, McConnachie A, Ford I et al. Serial metabolic measurements and conversion to type 2 diabetes in the west of Scotland coronary prevention study: specific elevations in alanine aminotransferase and triglycerides suggest hepatic fat accumulation as a potential contributing factor. Diabetes 2007;56:984-91.
|Key words||atherogenic dyslipidaemia; triglycerides; visceral adipose tissue; central obesity|