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

The current concept of metabolic syndrome comprises abdominal obesity and cardiovascular risk factors (HT and metabolic disorders). Compared to a control group, individuals with metabolic syndrome have a fourfold higher risk of cardiovascular disease and an increased risk of diabetes. Apart from cardiovascular morbidity, these patients also appear to have an increased incidence of urolithiasis. Urologists must therefore recognize this syndrome in order to identify this particular subgroup of urolithiasis patients. The objective of this article is to review the metabolic syndrome in order to help urologists to recognize this syndrome so that they can identify patients requiring more specific management and medical follow-up.
Prog Urol 2006 Sep
PMID:[Metabolic syndrome, obesity and urolithiasis]. 1706 32

Spigelian hernias are rare and generally difficult to diagnose because of their location and vague non-specific symptoms. They are situated between the muscular layers of the abdominal wall and can be easily overlooked because of abdominal obesity. The diagnosis has been considerably aided by the introduction of ultrasonography and computed tomography (CT). These hernias require surgical treatment. We report a 31 years old patient from the Sultan Qaboos University Hospital who presented with colicky lower abdominal pain associated with a tender swelling above and lateral to the inguinal canal. A diagnosis of Spigelian hernia was made and confirmed on exploration. The hernia was reduced and the defect repaired. Her recovery was uneventful.
J Pak Med Assoc 2006 Sep
PMID:Spigelian hernia: a rarity. 1709 57

Asian Indians have a unique phenotype characterized by increased abdominal obesity and visceral fat despite low body mass index [BMI]. Though studies have indicated some adipocytokines to be associated with diabetes and obesity in Indians, there are virtually no studies relating adipocytokines and proinsulin with diabetes and obesity in Asian Indians. In this study we looked at adipocytokines--leptin, adiponectin and tumour necrosis factor-a [TNF-alpha] and insulin and proinsulin in subjects with diabetes and obesity. Thirty five diabetic subjects and 50 healthy controls were recruited for the study. Leptin [p=0.002J and adiponectin levels [p=0.011] were lower and proinsulin values higher [p<0.001] in diabetic subjects compared to non-diabetic subjects. In addition, leptin [p<0.001] and proinsulin [p<0.001] were higher and adiponectin [p<0.001] lower, in obese subjects compared to non-obese subjects. TNF-alpha failed to show any significant difference between the study groups. Leptin and proinsulin showed a significant and positive correlation with BMI [p<0.001] and waist circumference [p<0.001]. Adiponectin showed an inverse correlation with BMI [p=0.050] and waist circumference [p=0.002]. Proinsulin showed a significant negative association with adiponectin [p=0.002]. Logistic regression analysis revealed leptin to be negatively associated [Odds ratio [OR]: 0.864, 95% confidence interval [95% CI]: 0.775 -0.963, p=0.008] and proinsulin [OR: 1.567, 95% CI: 1.246-1.971, p<0.001] to be positively associated with diabetes even after adjusting for age, gender and BMI. Leptin [OR: 1.365, 95% CI: 1.170-1.592, p<0.001] and proinsulin [OR: 1.617, 95% CI: 1.218 -2.147, p=0.001] showed a significant positive association with obesity, while adiponectin [OR: 0.927, 95% CI: 0.865 - 0.995, p=0.035] had a significant inverse association. Linear regression analysis revealed that adiponectin is inversely associated with proinsulin even after the addition of age, gender and diabetes status [beta= -0.61, p=0.033] into the model. In conclusion, in urban Asian Indians in western India, proinsulin levels showed a positive association, while leptin and adiponectin showed a negative association with diabetes. With regard to obesity, leptin and proinsulin had a positive association, while adiponectin had a negative association. Proinsulin levels showed an inverse association with adiponectin indicating a possible link between insulin secretion and insulin resistance.
J Assoc Physicians India 2006 Sep
PMID:Association of adipocytokines (leptin, adiponectin TNF-alpha), insulin and proinsulin with diabetes--the Mumbai Obesity Project [MOP]. 1721 14

Glucocorticoids act primarily in a feed-forward fashion on brain to activate CNS pathways that implement wanting appropriate to physiological needs. Thus, depending on the available conditions, elevated glucocorticoids may augment the behavioural want to run, fight or feed. Although glucocorticoids stimulate intake of chow, fat and sucrose, insulin appears to sculpt calorie-associated desires toward foods high in fat, acting through hepatic branch afferents of the vagus nerve. Both conditions of reduced food allowance and chronic stress excite glucocorticoid-augmented central neural networks that may lead toward ultimate abdominal obesity.
J Physiol 2007 Sep 01
PMID:Glucocorticoids and insulin both modulate caloric intake through actions on the brain. 1776 46

Tesaglitazar (GALIDA; AstraZeneca, Wilmington, DE) is a dual peroxisome proliferator-activated receptor alpha/gamma agonist previously in clinical development for the treatment of glucose and lipid abnormalities associated with type 2 diabetes mellitus and insulin resistance. This study compared the efficacy of tesaglitazar with that of pioglitazone as adjunctive therapy to atorvastatin in subjects with abdominal obesity and dyslipidemia. In this open-label, 3-way crossover study, 58 subjects received atorvastatin 10 mg once daily in a 6-week run-in period, followed by tesaglitazar 3 mg, pioglitazone 45 mg, or placebo, as adjunctive therapy to atorvastatin, in a randomized sequence for 6 weeks each. Serum triglycerides and other lipids, apolipoproteins, glucose, and insulin concentrations were compared between treatments. Tesaglitazar adjunctive therapy reduced serum triglycerides significantly more from baseline (-1.07 mmol/L) than pioglitazone (-0.33 mmol/L; P = .007) or placebo (-0.09 mmol/L; P < .0001). Tesaglitazar also resulted in significantly greater improvements in free fatty acids, very low-density lipoprotein cholesterol, low-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio, low-density lipoprotein particle size, apolipoprotein (apo) B, apo C-III, and the apo B/apo A-I ratio compared with pioglitazone or placebo. Tesaglitazar adjunctive therapy also reduced fasting plasma glucose, fasting plasma insulin, and insulin resistance (homeostasis model assessment index) significantly more than pioglitazone or placebo (P < .0001 for all comparisons). Tesaglitazar was generally well tolerated in combination with atorvastatin, but hemoglobin and absolute neutrophil count decreased and serum creatinine increased more with tesaglitazar than with pioglitazone or placebo. These effects, also shown in previous trials, led to the discontinuation of the clinical development of the drug. In conclusion, the addition of tesaglitazar to a background of atorvastatin therapy further improved the dyslipidemia associated with insulin resistance.
Metabolism 2007 Sep
PMID:The dual peroxisome proliferator-activated receptor alpha/gamma agonist tesaglitazar further improves the lipid profile in dyslipidemic subjects treated with atorvastatin. 1769 74

This study aimed to examine the relation between central obesity and other metabolic disorders of metabolic syndrome (MS) and compare the long-term risks of cardiovascular disease (CVD) between patients with MS with or without central obesity in middle-aged Chinese. The study included 30,378 Chinese aged 35 to 64 years at baseline with complete measurements for MS components and follow-up data for new acute CVD events from 1992 to 2003. The 10-year relative and absolute CVD risks in the MS groups with or without central obesity were compared. Results showed that 78% of patients with MS had central obesity and 22% with MS had no central obesity, diagnosed using updated Adult Treatment Panel III criteria with cut-off values appropriate for Asian populations. Central obesity, as well as other metabolic disorders in patients with MS, except for increased triglycerides, increased CVD risk significantly. There were no significant differences in 10-year absolute and relative risks of coronary heart disease events and ischemic CVD events between the 2 MS groups. In conclusion, MS with or without central obesity has a significantly increased 10-year risk of CVD in middle-aged Chinese.
Am J Cardiol 2007 Sep 01
PMID:Ten-year cardiovascular disease risk of metabolic syndrome without central obesity in middle-aged chinese. 1771 29

Overweight and obesity, particularly abdominal adiposity, increase the risk for type 2 diabetes mellitus and cardiovascular disease (CVD). Metabolic syndrome, a constellation of risk factors that includes elevated triglycerides, low high-density lipoprotein cholesterol, elevated blood pressure, elevated fasting glucose, and abdominal obesity, predicts the development of CVD and diabetes to an even greater degree. Excess abdominal adipose tissue is associated with insulin resistance, the precursor to type 2 diabetes, and creates an atherogenic inflammatory milieu, characterized by high levels of C-reactive protein and other inflammatory markers (e.g., fibrinogen, plasminogen activator inhibitor-1, cytokines, and adhesion molecules). High levels of these biomarkers correlate with an increased incidence of diabetes and CVD. Recent evidence suggests that patients with nonalcoholic fatty liver disease have an increased incidence of obesity, metabolic syndrome, and insulin resistance and/or type 2 diabetes. Relatively small reductions in body weight may significantly reduce abdominal adipose tissue, reduce insulin resistance, lower triglycerides and low-density lipoprotein cholesterol, reduce inflammation, and decrease overall cardiometabolic risk.
Am J Med 2007 Sep
PMID:Abdominal adiposity and cardiometabolic risk: do we have all the answers? 1772 Mar 54

Central obesity is associated with type 2 diabetes mellitus, hypertension and dyslipidaemia. This cluster of risk factors is known as the metabolic syndrome, and also occurs in people with primary glucocorticoid excess (Cushing's syndrome). Exogenous glucocorticoid use also increases the risk of cardiovascular disease. Circulating glucocorticoid concentrations are tightly controlled by the hypothalamic-pituitary-adrenal axis, however tissue glucocorticoid levels are also enhanced by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1). Transgenic overexpression of 11beta-HSD1 in either adipose tissue or the liver in mice causes components of the metabolic syndrome, while transgenic deletion of 11beta-HSD1 prevents adverse metabolic complications of obesity. Although plasma glucocorticoid levels are not elevated in obesity, dysregulation of 11beta-HSD1 is observed with decreased activity in the liver and increased activity in adipose tissue. 11beta-HSD1 is highly regulated, and dietary composition may be a powerful determinant of activity. Polymorphisms in the 11beta-HSD1 gene are also associated with components of the metabolic syndrome. Inhibition of this enzyme appears to be an attractive option to treat metabolic disease. Selective 11beta-HSD1 inhibitors in rodents cause weight loss, improve insulin sensitivity and delay progression of cardiovascular disease. Trials in humans though will be the ultimate test to determine if inhibition of 11beta-HSD1 offers a new tool in the treatment of metabolic disease.
Minerva Endocrinol 2007 Sep
PMID:Glucocorticoids and 11beta-hydroxysteroid dehydrogenase type 1 in obesity and the metabolic syndrome. 1791 54

The prevalence of the metabolic syndrome among developed countries is rising, and this is largely driven by increasing obesity rates. Central obesity plays a key role in the pathogenesis of the metabolic syndrome: it promotes inflammation, hypertension and dyslipidaemia, and leads to the development of type 2 diabetes mellitus and atherosclerosis. Clinical management should be focused on multifactorial intervention to address all the associated cardiovascular risk factors. The atherogenic mixed dyslipidaemic profile associated with the metabolic syndrome is an important target for intervention to reduce the risk of type 2 diabetes and premature cardiovascular disease.
Diab Vasc Dis Res 2007 Sep
PMID:Clinical implications of the metabolic syndrome. 1793 57

Although obesity and, in particular, abdominal obesity is clearly a risk factor for developing coronary artery disease, once coronary artery disease has been established, the correlation of obesity with total mortality, cardiovascular mortality, myocardial infarction, and revascularization is unclear and still remains a matter of debate. The relationship between obesity and mortality in patients with coronary artery disease has so far only been investigated by posthoc analysis of cohort studies, which have produced contradictory results. When a higher percentage body fat has been found to be a strong independent predictor of event-free survival, the phenomenon has been described as an 'obesity paradox' or 'reverse epidemiology'. A recent meta-analysis, appearing in the August 19 issue of Lancet on 250,152 patients with documented coronary artery disease, suggests that after grouping 40 cohort studies with adjusted risks, overweight patients were consistently associated with a better survival and lower cardiovascular events than patients with a low body mass index, whereas obesity was associated with a higher total mortality only in patients with history of coronary artery bypass graft, and severe obesity was associated with a significantly higher cardiovascular mortality but not with an increased risk for total mortality. Far from proving that obesity is harmless, these findings suggest that alternative methods might be required to better characterize individuals who truly have excess body fat and that additional studies with different methods are needed. Moreover, still unknown is the unique contribution of higher muscle-to-fat ratio, which may be merely a surrogate of increased physical fitness. Future research is needed to assess the link between high muscle mass, high body fat and clinical outcomes.
Monaldi Arch Chest Dis 2007 Sep
PMID:[Is obesity still a coronary risk factor?]. 1836 Dec 11


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