Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0311277 (abdominal obesity)
2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intra-abdominal obesity is associated with cardiovascular disease and non-insulin-dependent diabetes mellitus, and physical training has been suggested to alleviate these conditions. We compared epinephrine-stimulated lipolysis in vivo in three intra-abdominal adipose tissues (ATs: retroperitoneal, parametrial, and mesenteric) and in subcutaneous AT, and we also studied the effect of physical training. Moreover, we studied the effect of physical training on epinephrine-stimulated lipolysis in muscle in vivo. Female rats were either swim trained (15 wk, n = 8) or sedentary (n = 7). Under anesthesia, a two-stage intravenous epinephrine infusion (60 min of 80 and 200 ng. kg(-1). min(-1), respectively) was carried out, and local interstitial glycerol concentration was measured by the microdialysis technique. Blood flow was measured by microspheres. Training increased blood flow in all ATs [on average: 73 +/- 12 (trained) vs. 14 +/- 4 (sedentary) ml. 100 g(-1). min(-1), P < 0. 05]; nevertheless, epinephrine-stimulated interstitial glycerol concentrations were increased or unchanged. Interstitial glycerol concentration was higher in intra-abdominal than in subcutaneous AT in both trained and sedentary rats. In skeletal muscle, interstitial glycerol concentration and blood flow did not differ between trained and sedentary rats. In conclusion, in vivo lipolysis is higher both in the basal state and during epinephrine-stimulation in intra-abdominal than in subcutaneous AT, and training may be beneficial in alleviating intra-abdominal obesity by enhancing lipolysis in intra-abdominal fat depots.
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PMID:Effect of exercise training on in vivo lipolysis in intra-abdominal adipose tissue in rats. 1095 Aug 26

Untreated growth hormone deficiency (GHD) might explain the increased mortality reported in patients with hypopituitarism. These statistics appear to be largely attributable to cardiovascular disease. Differences in fibrinolytic activity regulators, together with dyslipidaemias, abdominal obesity and raised blood pressure in hypopituitarism might explain this increased risk. There is growing evidence that treatment with growth hormone (GH) can rectify most of the cardiovascular abnormalities associated with GHD. The reported improved psychosocial well-being in response to GH treatment may also be important in lowering risk in this group of patients.
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PMID:Untreated growth hormone deficiency explains premature mortality in patients with hypopituitarism. 1099 96

An increased prevalence and incidence of cardiovascular disease is the most important clinical consequence of abdominal obesity. Although defects in glucose handling in skeletal muscle have been extensively investigated, they have failed to clarify why insulin resistance is linked to vascular disease. Non-classic actions of insulin such as those on haemodynamics, nerve function and haemostasis and on lipoprotein metabolism would appear of greater interest in this respect. It is now clear that obese individuals exhibit resistance to some of the non-classic effects of insulin. These include resistance to insulin action on large vessel compliance, nitric oxide-dependent stimulation of vasodilation in resistance vessels, activation of the sympathetic nervous system by insulin but not other stimuli, platelet anti-aggregation and suppression of hepatic very low density lipoprotein production. The exact cause(s) of resistance to these non-classic insulin actions are unclear but their understanding would seem important to understand the links between obesity and cardiovascular disease.
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PMID:Vascular actions of insulin in obesity. 1099 3

Sex steroid hormones in both males and females have been closely related to the regulation of adiposity, either through direct or indirect physiological mechanisms. Evidence also suggests a direct relationship between sex hormones and risk factors for cardiovascular disease. In the present review article, we will discuss recent studies that have examined the complex interrelationships between sex hormones, SHBG, obesity and risk factors for cardiovascular disease. Male obesity and excess abdominal adipose tissue accumulation is associated with reductions in gonadal androgen and low adrenal C19 steroid concentrations. Reduced C19 steroids are also related to an altered metabolic risk factor profile including glucose intolerance and an atherogenic dyslipidemic state. However, the concomitant visceral obese state appears as a major correlate in these associations. In women, menopause-induced estrogen deficiency and increased androgenicity are associated with increased abdominal obesity and with the concomitant alterations in the metabolic risk profile. The accelerated accretion of adipose tissue in the intra-abdominal region coincident with the onset of menopause may explain part of the increased risk of cardiovascular disease in postmenopausal women. In both men and women, plasma levels of sex hormone-binding globulin are strong correlates of obesity and risk factors for cardiovascular disease, and more importantly, the relationships between low SHBG and altered plasma lipid levels appear to be independent from the concomitant increased levels of visceral adipose tissue. SHBG concentration may, therefore, represent the most important and reliable marker of the sex hormone profile in the examination of the complex interrelation of sex steroid hormones, obesity, and cardiovascular disease risk.
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PMID:Sex steroid hormones, sex hormone-binding globulin, and obesity in men and women. 1124 20

Insulin resistance can be linked to diabetes, hypertension, dyslipidemia, cardiovascular disease and other abnormalities. These abnormalities constitute the insulin resistance syndrome. Because resistance usually develops long before these diseases appear, identifying and treating insulin-resistant patients has potentially great preventive value. Insulin resistance should be suspected in patients with a history of diabetes in first-degree relatives; patients with a personal history of gestational diabetes, polycystic ovary syndrome or impaired glucose tolerance; and obese patients, particularly those with abdominal obesity. Present treatment consists of sensible lifestyle changes, including weight loss to attain healthy body weight, 30 minutes of accumulated moderate-intensity physical activity per day and increased dietary fiber intake. Pharmacotherapy is not currently recommended for patients with isolated insulin resistance.
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PMID:Insulin resistance syndrome. 1127 52

In women as well as in men cardiovascular disease is common, and almost as many women as men suffer from myocardial infarction every year in Sweden. In spite of this, studies on female cardiovascular disease are few in number. Knowledge about differences in risk factors, prevention, treatment and management is not common. Female cardiovascular disease starts approximately ten years later than in men and consequently most women are excluded from studies because of low age limits for inclusion. Primary preventive effects of e.g. acetylsalicylic acid, lipid-lowering drugs, vitamins and exercise have only been studied in healthy men, but the conclusions have been applied on women as well. The effects of reducing triglyceride levels or abdominal obesity in women--important risk factors for cardiovascular disease--have not been studied in controlled randomized studies. In women, angina is a non-specific symptom, and false positive ECG's are much more frequent than in men. The fact that a woman has to present as a man in order to be treated professionally (the Yentl syndrome) is still at hand. There is a great need for spreading current knowledge regarding gender differences among colleagues and medical students.
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PMID:[Management of cardiovascular diseases is characterized by male perspective. Women are subjected to incorrect management, diagnosis and treatment]. 1152 32

It is well recognized that aberrant fat localization such as visceral obesity rather than total body fat mass is a major risk factor for cardiovascular disease and type 2 diabetes mellitus. During recent decades, several studies have described a range of metabolic disturbances associated with abdominal obesity, including glucose intolerance, hyperinsulinaemia, insulin resistance, hypertension and dyslipoproteinaemia, now widely known as the metabolic syndrome. Several abnormalities in the hypothalamic-pituitary axis have been described associated with visceral obesity, suggesting a central neuroendocrine dysregulation including increased cortisol concentration and impaired gonadotropin and growth hormone (GH) secretion. Some steps in the chain of events in this theory still remain unclear, however, although these findings have introduced new therapeutic possibilities. These include therapy with sex steroids in both viscerally obese men and women, and several attempts to use GH to treat the endocrine abnormalities present in visceral obesity. The results of these studies are promising, but the therapies are still not recommended for general use.
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PMID:Visceral obesity and the role of the somatotropic axis in the development of metabolic complications. 1152 97

Cardiovascular complications are a major cause of morbidity and mortality in Type 2 diabetes. Diabetes patients have a higher risk of developing cardiovascular disease and a poorer outcome from cardiovascular events than do patients without diabetes. Although part of this increased risk may be related to glycaemic control, other factors are also involved. Several of the known cardiovascular risk factors are increased in patients with Type 2 diabetes, including hyperinsulinaemia, hypertension, dyslipidaemia (decreased high density lipoprotein cholesterol levels and increased plasma triglycerides and a preponderance of small, dense low density lipoprotein particles) and abdominal obesity. All these changes appear to be related to insulin resistance, which is a key feature of Type 2 diabetes. Addressing cardiovascular risk factors, particularly insulin resistance, therefore, should be an equally important part of the management of Type 2 diabetes as glycaemic control.
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PMID:Epidemiology of cardiovascular disease in type 2 diabetes. 1159 45

Cardiovascular risk is increased in GH deficiency (GHD). GHD adults are frequently abdominally obese and display features of the metabolic syndrome. Otherwise healthy abdominally obese subjects have low GH levels and show features of the metabolic syndrome as well. We investigated in healthy nonobese males the effect of the GH receptor antagonist pegvisomant in different metabolic conditions. This is a model for acute GHD without the alterations in body composition associated with GHD. We compared the effect of pegvisomant with that of placebo before and after 3 d of fasting. In addition, we investigated the effect of pegvisomant under normal, i.e. fed, conditions. Three days of fasting as well as pegvisomant alone decreased serum free IGF-I levels (1.0 +/- 0.15 vs. 0.31 +/- 0.05 ng/ml and 0.86 +/- 0.23 vs. 0.46 +/- 0.23 ng/ml, respectively). Fasting in combination with pegvisomant also decreased serum free IGF-I levels (1.0 +/- 0.15 vs. 0.31 +/- 0.07 ng/ml). Treatment with pegvisomant had no additional influence on the decline of free IGF-I induced by fasting. Pegvisomant alone had no influence on insulin sensitivity. The increase in insulin sensitivity induced by fasting was comparable to the increase in insulin sensitivity induced by fasting combined with pegvisomant. Among serum lipid concentrations, only serum triglycerides increased significantly as a result of pegvisomant alone (1.0 +/- 0.2 vs. 1.6 +/- 0.4 mmol/liter). The changes in lipid concentrations induced by fasting alone or pegvisomant were not different from those induced by pegvisomant alone. von Willebrand factor antigen levels declined significantly under the influence of pegvisomant alone (1.1 +/- 0.07 vs. 0.8 +/- 0.06 U/ml). In conclusion, in different metabolic conditions the GH receptor antagonist pegvisomant induces no significant acute changes in the major risk markers for cardiovascular disease. These data suggest that the secondary metabolic changes, e.g. abdominal obesity or inflammatory factors, that develop as a result of long-standing GHD are of primary importance in the pathogenesis of atherosclerosis in patients with GHD.
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PMID:Acute effect of pegvisomant on cardiovascular risk markers in healthy men: implications for the pathogenesis of atherosclerosis in GH deficiency. 1170 72

Arterial stiffness has recently been recognized as an important cardiovascular risk marker. Physiological concentrations of insulin diminish wave reflection in the aorta in vivo. This decreases central blood pressure augmentation and augmentation divided by pulse pressure [the augmentation index (AgI)], a measure of arterial stiffness. In the present study, we examined whether a defect in this action of insulin is a feature of insulin resistance and how it relates to other acute actions of insulin, including stimulation of glucose uptake, peripheral blood flow, and autonomic control of heart rate variation. These actions of insulin were quantitated in 50 healthy men (age, 34 +/- 2 yr; body mass index, 27 +/- 1 kg/m2) during 2 sequential insulin infusions, each lasting 120 min (1 and 2 mU/kg x min). Insulin decreased AgI significantly within 30 min, whereas significant increases in peripheral blood flow and normalized low frequency power of heart rate variation, a measure of sympathetic control of heart rate variation, were observed at 150 and 210 min. A blunted decrease in the AgI was significantly associated with a low rate of insulin-stimulated glucose uptake, but not with the other actions of insulin. Insulin action of the AgI was correlated with body mass index and the waist to hip ratio independently of basal AgI, age, and low density lipoprotein cholesterol. We conclude that physiological concentrations of insulin diminish large artery stiffness within 30 min in nondiabetic men. This action precedes insulin action on peripheral vasodilation, heart rate, and autonomic control of heart rate variation. It is correlated with insulin stimulation of glucose uptake and is blunted by known causes of insulin resistance, including overall and abdominal obesity. Resistance of large arteries to insulin-induced decrease in their stiffness is therefore another facet of insulin resistance that could contribute to the association between insulin resistance and cardiovascular disease.
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PMID:Resistance to acute insulin induced decreases in large artery stiffness accompanies the insulin resistance syndrome. 1170 89


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