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Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microalbuminuria has been shown to be an independent predictor of cardiovascular disease in different populations. However, the underlying pathophysiological mechanism behind this observation is not known. The purpose of the present cross-sectional study was to examine the relation of microalbuminuria to intima-media thickness (IMT) of the common carotid artery in a group of 368 clinically healthy 58-year old men. Urinary albumin excretion (UAE) and IMT of the common carotid artery were measured. Body mass index, WHR, systolic and diastolic blood pressure, heart rate, High-density lipoprotein (HDL) cholesterol and common carotid artery IMT were associated with UAE. A stepwise forward multiple regression showed that systolic blood pressure and WHR could explain 10.4% of the variability in log UAE (systolic blood pressure beta-coefficient 0.0047, SE 0.001, P<0.001; WHR beta-coefficient 0.93, SE 0.30, P=0.002). In conclusion, UAE was significantly associated with IMT of the common carotid artery in clinically healthy men. However, after adjustment for systolic blood pressure and WHR this association was not significant. We suggest that microalbuminuria in healthy subjects is not primarily associated with atherosclerosis but rather to blood pressure and abdominal obesity.
Atherosclerosis 2002 Sep
PMID:Microalbuminuria and intima-media thickness of the carotid artery in clinically healthy men. 1211 5

1. The development of atherosclerosis, including the role of the classical and new risk factors, is briefly reviewed an emphasis on the links between some of these risk factors and atherogenesis. 2. While genetic factors are doubtlessly important, they contribute (from the population point of view) little to the overall burden of atherosclerosis. 3. Our studies on the relationship between abdominal obesity and metabolic risk factors in two ethnic groups, namely individuals of Cantonese and European background, suggest that different ranges for at least some of the risk factors should be established for specific ethnic groups (e.g. waist circumference for individuals of Chinese and European background). 4. Using the example of differences between Cantonese heterozygotes for familial hypercholesterolaemia living in Vancouver, Canada, and Canton, China, we demonstrate how the environment can modify a genetic predisposition for atherosclerosis. 5. Gender differences are illustrated by a study of serum lipoprotein (a) as a risk factor in men and women. 6. The principles of current Canadian recommendations for the assessment and treatment of atherosclerosis are outlined; they are based on knowledge gained from both basic and clinical research of atherosclerosis.
Clin Exp Pharmacol Physiol 2002 Sep
PMID:Old and new risk factors for atherosclerosis and development of treatment recommendations. 1216 52

The association between physical activity, dietary behaviors, and elevated cardiovascular disease risk factor components of the insulin resistance syndrome in adults with mental retardation was identified. Established clinical cutoff points were used to identify 145 participants with mild mental retardation and hyperinsulinemia, borderline high triglycerides, low high-density lipoprotein cholesterol, hypertension, and abdominal obesity. Odds ratios were calculated from logistic regression analysis. Those who participated in more frequent bouts of physical activity or who consumed lower dietary fat intakes were approximately one third as likely to have hyperinsulinemia and abdominal obesity compared to those who participated in less frequent physical activity or who consumed higher fat intakes, suggesting that these behaviors are protective against elevated components of the insulin resistance syndrome.
Am J Ment Retard 2002 Sep
PMID:Physical activity, dietary intake, and the insulin resistance syndrome in nondiabetic adults with mental retardation. 1218 77

New Zealanders of Polynesian origin have a higher prevalence of obesity and type 2 diabetes mellitus than those of European origin. Risk factors for type 2 diabetes mellitus--decreased energy expenditure, increased body fat mass, and central body fat--in 30 normoglycemic Maori, Pacific, and European men were studied. Biochemical measures of risk for type 2 diabetes mellitus included an oral glucose tolerance test, insulin, lipids, and glycosylated hemoglobin. The groups did not differ significantly in BMI, height, body mass or fat mass (DEXA), or adjusted resting metabolic rate (indirect calorimetry), but the European subjects had significantly lower subscapular to triceps skinfolds and fat-free mass than the Maori and Pacific groups. Central obesity by anthropometry and DEXA showed strong associations with the biochemical measures for type 2 diabetes risk. These findings emphasize the association between body composition and central fat distribution with risk of diabetes independent of ethnicity.
Food Nutr Bull 2002 Sep
PMID:Central obesity and risk for type 2 diabetes in Maori, Pacific, and European young men in New Zealand. 1236 20

The aim of the present study was to investigate the association between the serum lipid profile and components of the metabolic syndrome, such as central obesity (anthropometric, computed tomography and fat cell data), insulin, sex-hormone-binding-globulin (SHBG) and different hormones influencing this important syndrome, e.g. sex steroids, leptin and tumor necrosis factor-alpha (TNF-alpha). The sample consisted of 85 obese patients (30 men and 55 women) who had undergone abdominal surgery. Fasting serum lipids were analysed, as well as anthropometric and computed tomography data, perivisceral and subcutaneous fat cell size and serum glucose and hormones. Abdominal fat revealed itself as an important correlator of the adverse changes in plasma lipoprotein levels, the waist-to-hip-ratio and waist-to-thigh-ratio being the best morphological correlators in men and women, respectively. Intra-abdominal fat (VA) correlated significantly and positively to perivisceral fat cell size in women, while no correlation was found between subcutaneous fat accumulation (SA) and adipocyte size in both genders. Perivisceral fat cell size showed the greatest number of correlations with the adverse plasma lipid profile compared to that in the subcutaneous depot. SHBG and sex steroids showed a negative correlation with serum lipids considered a cardiovascular risk. In contrast, TNF-alpha and C-peptide were inversely correlated with potential protector lipids. In conclusion, abdominal obesity, adipocyte hypertrophy from visceral fat, serum TNF-alpha and C-peptide seem to be the best correlators of the lipoprotein disturbance characteristic of the metabolic syndrome, whereas SHBG and sex steroids could play a protective role regarding the lipid profile associated to this syndrome.
J Physiol Biochem 2002 Sep
PMID:Interrelationship between serum lipid profile, serum hormones and other components of the metabolic syndrome. 1260 9

The clustering of several metabolic and cardiovascular disease risk factors has been termed the metabolic syndrome. The metabolic syndrome seems to result from a collision between susceptible "thrifty genes" and a society characterized by an increased prevalence of obesity and a sedentary lifestyle. The typical patient is characterized by abdominal obesity, a varying degree of glucose intolerance, dyslipidemia and often hypertension. The components of the metabolic syndrome are associated with insulin resistance, disturbances of coagulation and fibrinolysis, endothelial dysfunction and elevated markers of sub-clinical inflammation. The current review focuses mainly on the new definitions of the syndrome, the results of recent epidemiological studies and the consequences of the metabolic syndrome as an important risk factor for cardiovascular disease, premature death and diabetes. The metabolic syndrome constitutes a major challenge for public health professionals in the field of preventive medicine since more than 40 million U.S. adults seem to be affected by the syndrome. Lifestyle changes could have a profound influence on the syndrome and its development.
Life Sci 2003 Sep 26
PMID:A major health hazard: the metabolic syndrome. 1295 49

The effects of adrenal corticosteroids on subsequent adrenocorticotropin secretion are complex. Acutely (within hours), glucocorticoids (GCs) directly inhibit further activity in the hypothalamo-pituitary-adrenal axis, but the chronic actions (across days) of these steroids on brain are directly excitatory. Chronically high concentrations of GCs act in three ways that are functionally congruent. (i) GCs increase the expression of corticotropin-releasing factor (CRF) mRNA in the central nucleus of the amygdala, a critical node in the emotional brain. CRF enables recruitment of a chronic stress-response network. (ii) GCs increase the salience of pleasurable or compulsive activities (ingesting sucrose, fat, and drugs, or wheel-running). This motivates ingestion of "comfort food." (iii) GCs act systemically to increase abdominal fat depots. This allows an increased signal of abdominal energy stores to inhibit catecholamines in the brainstem and CRF expression in hypothalamic neurons regulating adrenocorticotropin. Chronic stress, together with high GC concentrations, usually decreases body weight gain in rats; by contrast, in stressed or depressed humans chronic stress induces either increased comfort food intake and body weight gain or decreased intake and body weight loss. Comfort food ingestion that produces abdominal obesity, decreases CRF mRNA in the hypothalamus of rats. Depressed people who overeat have decreased cerebrospinal CRF, catecholamine concentrations, and hypothalamo-pituitary-adrenal activity. We propose that people eat comfort food in an attempt to reduce the activity in the chronic stress-response network with its attendant anxiety. These mechanisms, determined in rats, may explain some of the epidemic of obesity occurring in our society.
Proc Natl Acad Sci U S A 2003 Sep 30
PMID:Chronic stress and obesity: a new view of "comfort food". 1297 24

Considerable data on the pathophysiology, epidemiology, and treatment of dyslipidemia-induced coronary heart disease (CHD) have accumulated in recent years. These data have been assessed and incorporated into the guidelines of the National Cholesterol Education Program Expert Panel on the Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel [ATP] III). A major focus of the new guidelines is the assessment of the near-term (i.e., 10-yr) risk of experiencing a CHD event and matching the intensity of treatment to this risk. Patients with diabetes and those with a greater than 20% 10-year risk of experiencing a CHD event have been elevated to the risk level of CHD equivalent. The ATP III guidelines also modify several lipid and lipoprotein classifications. A low-density lipoprotein cholesterol (LDL) level below 100 mg/dl is now considered optimum for all individuals. In addition, high-density lipoprotein cholesterol (HDL) and triglyceride cutoff points have been modified to reflect more accurately the risk associated with abnormalities in these lipoproteins. As with the previous guidelines, the primary target of therapy remains LDL. Therapeutic lifestyle changes consisting of diet, weight reduction, and increased physical activity should be included in all treatment regimens. Based on their potent LDL-lowering properties and their proven ability to decrease mortality in a variety of patient populations, statins are generally the first choice for pharmacologic therapy. A secondary target of therapy includes non-HDL goals for patients with high triglyceride levels and the metabolic syndrome, which is characterized by abdominal obesity, elevated triglyceride levels, low HDL levels, and insulin resistance. Management of these secondary targets includes weight reduction and increased physical activity, and treatment of the lipid and nonlipid risk factors. Overall, ATP III represents an aggressive approach to treating dyslipidemia, greatly extending the number of individuals who qualify for treatment.
Pharmacotherapy 2003 Sep
PMID:Update on the National Cholesterol Education Program Adult Treatment Panel III guidelines: getting to goal. 1452 36

Visceral obesity represents an important risk factor associated with hypertension, diabetes and cardiovascular diseases. Since this condition is associated with a disruption of the functioning of the HPA axis, stress-induced HPA axis activation has been identified to play an important role in this preferential body fat accumulation. HPA axis activation increases cortisol (corticosterone) production which has been shown to exert hyperphagic and antithermogenic effects. Since abdominal adipose tissue has more cells per mass units, higher blood flow and more glucocorticoid receptors, glucocorticoids affect abdominal fat to a greater extent than subcutaneous adipose tissue. Cushing's syndrome in humans is the best evidence showing a link between hypercortisolemia and accumulation of central fat. The Hervey's hypothesis which suggests that fat cells take up and catabolize glucocorticoids is one of the possible regulatory effect that supports the adaptive role of visceral fat in response to stress. This is also supported by other evidence showing that abdominal obesity is associated with an increased cortisol clearance. Hormonal and enzymatic changes have been implicated in this preferential body fat accumulation in response to stress. Specific genetic background may also accentuate this visceral fat accumulation in some individuals exposed to stress. Alternatively, obesity could also be a source of stress promoting the visceral fat accumulation since visceral fat is able to release cytokines which stimulate the HPA axis. Even if the available literature does not permit to establish clearly which comes first, it suggests that visceral obesity could represent a non optimal physiological adaptation to stress. In this context, visceral obesity treatment should focus on stress management and weight loss strategies in order to stop this vicious circle.
Panminerva Med 2003 Sep
PMID:Is visceral obesity a physiological adaptation to stress? 1461 17

With the increased attention being given to cardiovascular risk factor reduction, the opportunity exists to substantially decrease the largest cause of mortality in diabetic patients. The concept that type 2 diabetes and CVD are linked via a common etiologic pathway (metabolic syndrome) has substantial ramifications for the care of individual patients. Many of the metabolic abnormalities that contribute to both glycemic disorders and CVD are interrelated. For example, hyperinsulinemia and insulin resistance coupled with abdominal obesity further worsens HTN and hyperlipidemia. Likewise, the procoagulant state and endothelial dysfunction increase with worsening glycemic control. Specific interventions include tobacco cessation, a food management and physical activity plan, choice of antidiabetic agent (such as metformin), and use of ACE inhibitors for hypertension and microalbuminuria (Table 5). Programs to enhance cardiovascular risk factor reduction as part of the comprehensive evaluation and management of diabetic patients have been described [95,99]. One community-based program provided free screening to diabetic patients with randomization to either annotated result reports provided to the patient and their physician or results provided by a project nurse (either face-to-face or over the phone). Greater improvements in mean glycohemoglobin, cholesterol, and blood pressure were noted with verbal presentation of results [99]. Recent data from the Centers for Disease Control and Prevention Diabetes Cost-effectiveness Group support the idea that interventions to decrease CVD in diabetics are economically beneficial. Intensive management of hypertension, glycemic control, and hyperlipidemia each improved health outcomes. Hypertension control reduced costs. Although intensive treatment of glucose and hyperlipidemia increased costs, the increase was comparable to that of other frequently used health care interventions [100]. Further directions include further exploration of the implications and management of metabolic syndrome as it relates to CVD prevention. Interventions such as exercise, which can impact on all outcomes, require special attention. Efforts by physicians, health systems, and society are necessary to increase physical activity for individuals of all ages. It makes clinical sense that the recommendations for prevention of CVD in diabetics described in this article may also benefit patients with prediabetes (fasting glucose 110-125 mg/dl), but this remains to be definitively shown.
Prim Care 2003 Sep
PMID:Preventing cardiovascular disease in diabetes and glucose intolerance: evidence and implications for care. 1469 2


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