Menopause Live - IMS Updates

Date of release: 06 June, 2011

Visceral fat accumulation and cardiovascular disease risk profile

In a recent elegant study, 62 postmenopausal women with normal glucose tolerance (normal) were compared with 33 postmenopausal women with impaired glucose tolerance (IGT) and 18 women with type 2 diabetes (T2D) [1]. Women were further divided according to the status of the visceral abdominal fat. The contribution of glucose tolerance status and intra-abdominal fat to cardiovascular disease (CVD) risk was investigated, with subcutaneous and intra-abdominal adipose tissue measured by CT scan and insulin sensitivity measured by the euglycemic hyperinsulinemic clamp method. Compared with normal women having low amounts of visceral adipose tissue (lowest risk group), women with T2D, women with IGT plus high amounts of visceral adipose tissue and normal women with high amounts of visceral adipose tissue demonstrated a worse risk profile: they had lower insulin sensitivity, higher triglyceride levels, higher levels of high-sensitivity C-reactive protein (hsCRP) and lower levels of HDL2 cholesterol. Women with IGT and high levels of visceral adipose tissue had similar lipid–lipoprotein profiles and inflammatory marker levels when compared with normal women having a similar amount of visceral adipose tissue. These findings suggest that greater levels of visceral adipose tissue contribute independently to dyslipidemia and low-grade inflammation. Furthermore, normal women having higher amounts of visceral fat had similar levels of hsCRP and IL-6 to those in women with T2D, again indicative of visceral fat contributing to chronic low-grade inflammation independently of glucose tolerance status. The overall study findings suggest that, in women without T2D, the accumulation of intra-abdominal fat makes a substantial contribution to the deterioration of their CVD risk profile.


It is well known that accumulation of abdominal fat is associated with an increase in risk for the development of insulin resistance, hyperlipidemia and hypertension [2,3]. Also well documented is the fact that women with T2D are at increased risk of CVD. However, the extent to which increased intra-abdominal adipose tissue contributes to CVD risk in postmenopausal women with IGT or T2D is unclear. Better understanding of these risk parameters is important in view of CVD being the leading cause of death and the number of disability-adjusted life years globally in women [4]. The risk of acute coronary events for women increases exponentially with age and following the menopause. The importance of inflammatory mechanisms being involved in acute CVD events has emerged [5]. Of the serum markers of inflammation, CRP may provide the strongest risk prediction for CVD [6]. The cytokine IL-6 is a potent inducer of the hepatic acute-phase response, and hence a regulator of CRP [7]. When IL-6 has been studied in conjunction with CRP, higher levels of either marker were associated with a greater risk of death; an increase in both markers was associated with a greater than two-fold increased likelihood of death by cardiovascular and non-cardiovascular causes [8]. The current study provides further evidence that, in postmenopausal women, visceral fat accumulation increases the levels of the markers of chronic inflammation (IL-6 and hsCRP) and hence CVD risk. With respect to body composition, the menopause is accompanied by a transition from a gynoid to an android central-type pattern of body fat distribution and an increase in total body fat [9]. It has previously been reported that women may develop a more adverse inflammatory profile during the menopausal transition in association with increased central (visceral) adiposity [10]. The present study further demonstrates that these effects of intra-abdominal fat are independent of impaired glucose tolerance. 
Clearly, these data show that the prevention of intra-abdominal fat accumulation, particularly at midlife, is important for the prevention of CVD as well as T2D. In rodents, ovariectomy increases food intake and fat mass and these effects are reversed by estrogen therapy [11,12]. There is some evidence that postmenopausal estrogen use also opposes visceral fat accumulation [13]. However, with postmenopausal hormone therapy falling out of favor, research in this area has dwindled markedly. Studies to evaluate the impact of peri- and early postmenopausal estrogen therapy on visceral fat accumulation and CVD risk markers, as a precedent to impaired glucose tolerance and increased CVD, are still warranted. In the meantime, the key clinical message from the above study is that the weight loss that is associated with reduced intra-abdominal fat is likely substantially to reduce an individual’s CVD risk and needs to be prioritized in health care.


Susan Davis
Director, the Womens Health Research Program, School of Public Health and Preventive Medicine, Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia


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