Relation of Overall & Abdominal Adiposity to Vascular Health
Relation of Overall & Abdominal Adiposity to Vascular Health
In the present study, abdominal obesity defined by WC was associated with significantly higher AI and PWV in diabetic patients; whereas overall obesity defined by BMI did not predict adverse vascular changes in this study population. Abdominal obesity was associated with an adverse effect on blood vessels, independently of age, sex, blood pressure, fasting glucose and BMI. Combination of diabetes mellitus and abdominal obesity, but not overall obesity, was associated with significant deterioration in terms of arterial stiffness parameters.
Findings of the present study concur with recently published data demonstrated stronger association of abdominal obesity than BMI with total mortality among elderly subjects at high risk of cardiovascular disease, particularly among diabetic participants. Additionally, it was shown that the measures of abdominal obesity correlates better than BMI with arterial stiffness evaluated by PWV, and with subclinical atherosclerosis evaluated by C-IMT, in healthy, diabetics and hypertensive subjects.
Previous clinical and experimental data show that abdominal adipose tissue can play an important role in the development of diabetes mellitus and it can also increase the risk of cardiovascular and all-cause mortality. Body fat distribution is one of the major determinants of metabolic health, and visceral adiposity has a stronger correlation with metabolic abnormalities and cardiovascular disease than subcutaneous adipose tissue. Visceral fat is metabolically active and is an important site for adipokines such as adiponectin and leptin, which plays an important role in insulin sensitivity, inflammation, lipid metabolism and atherogenesis. It was shown that low plasma adiponectin levels are significantly correlated with endothelial dysfunction, increased intima media thickness and progression of coronary artery calcification independently of other cardiovascular risk factors. Leptin as well is involved in insulin sensitivity, angiogenesis, vascular and endothelial function. Moreover, novel and traditional cardiovascular risk factors such as asymmetric dimethyl-arginine ADMA levels and LDL-cholesterol are strongly associated with increased arterial stiffness among pre-diabetic subjects.
It has been demonstrated that excess body fat, abdominal visceral fat, and larger waist circumference have been associated with accelerated arterial stiffening independently of blood pressure levels, ethnicity and age in older adults. Moreover, both WC and sagittal abdominal diameter (SAD) are associated with subclinical organ damage such as PWV and carotid intima-media thickness and provided information on inflammation, atherosclerosis and arterial stiffness in type 2 diabetic patients. However, it has also been reported that SAD was more independent in predicting arterial stiffness over time, compared with WC, in middle-aged men and women with type 2 diabetes, Recently , it has been demonstrated that neck circumference is associated with an increased PWV in hypertensive adults, independent of other metabolic risk factors.
The pathophysiology that links abdominal adiposity to arterial stiffening is not precisely known. One suggested mechanism is through insulin resistance, which commonly accompanies obesity. A reciprocal relationship exists between insulin resistance and endothelial dysfunction, considered to be a key initiating step in the atherosclerotic cascade. Reduced insulin action in peripheral tissue impairs endothelium-dependent vasodilatation and increases the local activity of a variety of growth factors in vascular tissue, promoting collagen production and the development of vascular smooth muscle cell (VSMC) hypertrophy. It has been shown that obese young adults who both lower their insulin levels and lose weight showed the greatest improvement in vascular stiffness. In addition, the pro-inflammatory state typical of obesity stimulates reactive oxygen species production, inhibits nitric oxide production by reducing levels of NO synthase in vascular smooth muscle cells and endothelial cells and promotes endothelial apoptosis.
In concurrence with previous studies, the present study did not detect the gender-related differences in the association between abdominal obesity measures and arterial stiffness in diabetic men and women. However, it has also been reported, that increasing BMI, WC, visceral fat area and fat mass were independently associated with higher PWV in women, but not in men, after adjustment for age, hypertension and type 2 diabetes.
The individuals with normal weight and increased levels of abdominal obesity could be genetically predisposed to the development of diabetes mellitus as well as CV disease. Since vascular changes inflicted by multiple environmental and genetic factors, develop years before an event, detection of vascular damage can serve as a predictor of future cardiovascular complications. In the present study, WC was a significant independent predictor of early vascular adverse changes detected by using PWV and AI. Therefore, abdominal obesity defined by WC, might be a better predictor of arterial stiffness as well as future cardiovascular events in diabetic patients.
In conclusion, the present study demonstrated that abdominal obesity, defined by WC is associated with an adverse effect on blood vessels, independently of age, sex, and blood pressure, parameters of glucose homeostasis and BMI in type 2 diabetic patients. Combination of diabetes mellitus and increased WC, but not increased BMI, was associated with significant deterioration in terms of arterial stiffness parameters in this study population. The precise mechanisms for these vascular changes, as well as overall clinical impact of WC reduction on cardiovascular outcomes deserve further investigation.
Discussion
In the present study, abdominal obesity defined by WC was associated with significantly higher AI and PWV in diabetic patients; whereas overall obesity defined by BMI did not predict adverse vascular changes in this study population. Abdominal obesity was associated with an adverse effect on blood vessels, independently of age, sex, blood pressure, fasting glucose and BMI. Combination of diabetes mellitus and abdominal obesity, but not overall obesity, was associated with significant deterioration in terms of arterial stiffness parameters.
Findings of the present study concur with recently published data demonstrated stronger association of abdominal obesity than BMI with total mortality among elderly subjects at high risk of cardiovascular disease, particularly among diabetic participants. Additionally, it was shown that the measures of abdominal obesity correlates better than BMI with arterial stiffness evaluated by PWV, and with subclinical atherosclerosis evaluated by C-IMT, in healthy, diabetics and hypertensive subjects.
Previous clinical and experimental data show that abdominal adipose tissue can play an important role in the development of diabetes mellitus and it can also increase the risk of cardiovascular and all-cause mortality. Body fat distribution is one of the major determinants of metabolic health, and visceral adiposity has a stronger correlation with metabolic abnormalities and cardiovascular disease than subcutaneous adipose tissue. Visceral fat is metabolically active and is an important site for adipokines such as adiponectin and leptin, which plays an important role in insulin sensitivity, inflammation, lipid metabolism and atherogenesis. It was shown that low plasma adiponectin levels are significantly correlated with endothelial dysfunction, increased intima media thickness and progression of coronary artery calcification independently of other cardiovascular risk factors. Leptin as well is involved in insulin sensitivity, angiogenesis, vascular and endothelial function. Moreover, novel and traditional cardiovascular risk factors such as asymmetric dimethyl-arginine ADMA levels and LDL-cholesterol are strongly associated with increased arterial stiffness among pre-diabetic subjects.
It has been demonstrated that excess body fat, abdominal visceral fat, and larger waist circumference have been associated with accelerated arterial stiffening independently of blood pressure levels, ethnicity and age in older adults. Moreover, both WC and sagittal abdominal diameter (SAD) are associated with subclinical organ damage such as PWV and carotid intima-media thickness and provided information on inflammation, atherosclerosis and arterial stiffness in type 2 diabetic patients. However, it has also been reported that SAD was more independent in predicting arterial stiffness over time, compared with WC, in middle-aged men and women with type 2 diabetes, Recently , it has been demonstrated that neck circumference is associated with an increased PWV in hypertensive adults, independent of other metabolic risk factors.
The pathophysiology that links abdominal adiposity to arterial stiffening is not precisely known. One suggested mechanism is through insulin resistance, which commonly accompanies obesity. A reciprocal relationship exists between insulin resistance and endothelial dysfunction, considered to be a key initiating step in the atherosclerotic cascade. Reduced insulin action in peripheral tissue impairs endothelium-dependent vasodilatation and increases the local activity of a variety of growth factors in vascular tissue, promoting collagen production and the development of vascular smooth muscle cell (VSMC) hypertrophy. It has been shown that obese young adults who both lower their insulin levels and lose weight showed the greatest improvement in vascular stiffness. In addition, the pro-inflammatory state typical of obesity stimulates reactive oxygen species production, inhibits nitric oxide production by reducing levels of NO synthase in vascular smooth muscle cells and endothelial cells and promotes endothelial apoptosis.
In concurrence with previous studies, the present study did not detect the gender-related differences in the association between abdominal obesity measures and arterial stiffness in diabetic men and women. However, it has also been reported, that increasing BMI, WC, visceral fat area and fat mass were independently associated with higher PWV in women, but not in men, after adjustment for age, hypertension and type 2 diabetes.
The individuals with normal weight and increased levels of abdominal obesity could be genetically predisposed to the development of diabetes mellitus as well as CV disease. Since vascular changes inflicted by multiple environmental and genetic factors, develop years before an event, detection of vascular damage can serve as a predictor of future cardiovascular complications. In the present study, WC was a significant independent predictor of early vascular adverse changes detected by using PWV and AI. Therefore, abdominal obesity defined by WC, might be a better predictor of arterial stiffness as well as future cardiovascular events in diabetic patients.
In conclusion, the present study demonstrated that abdominal obesity, defined by WC is associated with an adverse effect on blood vessels, independently of age, sex, and blood pressure, parameters of glucose homeostasis and BMI in type 2 diabetic patients. Combination of diabetes mellitus and increased WC, but not increased BMI, was associated with significant deterioration in terms of arterial stiffness parameters in this study population. The precise mechanisms for these vascular changes, as well as overall clinical impact of WC reduction on cardiovascular outcomes deserve further investigation.
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