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Query: UMLS:C0311277 (abdominal obesity)
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The structure of a large neural system that responds to and regulates energy balance and that encompasses that PVN and activity of the HPA axis has begun to emerge from these experiments (Fig. 6). Several large loops have been delineated within this context of the maintenance of energy balance. Corticosteroids stimulate both feeding and insulin secretion. The actions of corticosteroids in the periphery are catabolic, causing mobilization of energy stores; their actions in the central nervous system are stimulatory to energy acquisition (food intake). By contrast, the action of insulin in the periphery is anabolic, causing energy storage; its action in the central nervous system is inhibitory to energy acquisition (food intake). At the level of the CNS, insulin inhibits and corticosteroids stimulate expression of NPY mRNA in the arcuate nuclei, and these actions may explain, in part, the reciprocal actions of the hormones on energy acquisition. Thus over the long term, stimulation of insulin secretion by corticosteroids tends to supply an automatic brake on the effects of corticosteroids on feeding. The neural system that controls energy balance and responds to the reciprocal signals of corticosterone and insulin also regulates responsivity to restraint stress in the HPA axis. The low-amplitude ACTH responses to restraint, corticosteroid feedback, and prior stress-induced facilitation that are observed under conditions of relative fasting in the PM can be produced in the AM by a 14-h, overnight fast. By contrast, NPY injected ivt stimulates identical ACTH responses in the AM in fed rats and in rats fasted overnight, suggesting that NPY acts to stimulate CRF secretion at a site closer to the PVN than the stress of restraint, which is filtered through the neural energy balance system. In the periphery, corticosteroids and insulin also have reciprocal effects on energy storage; effects that are opposite those exerted in the CNS on energy acquisition. Thus, together, the two hormones may be construed as a bihormonal system that regulates overall energy balance. Although under normal conditions this system is well designed to accomplish energy balance, and provides a mechanism by which total energy stores may be increased appropriately (e.g., prior to hibernation or migration), it seems probable that under conditions of chronic stress, this regulatory system may be maladaptive. Chronic stress and glucocorticoid treatment cause increases in mean daily concentrations of both corticosteroids and insulin. Increases in the absolute levels of both hormones, with the normal ratio between them maintained, results in remodeling of body energy stores-away from muscle stores and toward fat stores, particularly abdominal fat stores. It seems quite likely that some conditions of abdominal obesity in man may be explained, at least in part, by increased activity in the HPA axis. Because abdominal obesity is associated with cardiovascular diseases, these responses, when they persist, are clearly maladaptive. Exploration of the role and control of the HPA axis in and by the larger neural network that regulates energy balance has to date been instructive. Clearly this work has just begun and is primarily still at the level of phenomenology. However, once the phenomenology is understood, mechanistic work can be performed that will flesh out our understanding of this very large and physiologically essential system.
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PMID:The neural network that regulates energy balance is responsive to glucocorticoids and insulin and also regulates HPA axis responsivity at a site proximal to CRF neurons. 859 46

Although resistance to insulin-mediated glucose disposal has emerged as a link between abdominal obesity and hypertension, abnormalities of nonesterified fatty acid metabolism may play a greater role. Analyses were performed on existing data from 17 abdominally obese subjects (11 hypertensive, 6 normotensive) to determine whether fatty acid concentration and turnover were related to blood pressure independently of hyperinsulinemia and resistance to insulin-mediated glucose disposal. Glucose utilization, fatty acid concentration, and fatty acid turnover were obtained fasting and during euglycemic hyperinsulinemia at 10 and 40 mU/m/min. Analyses were also performed on another group of 30 subjects with a wide range of risk factors who had blood pressure data as well as glucose and fatty acid measurements during an insulin tolerance test. Fatty acid concentration and turnover were markedly more resistant to suppression by insulin in obese hypertensive than in lean or obese normotensive individuals. In the 17 obese subjects, blood pressure measured at screening, in the laboratory, and over a period of 24 hours correlated significantly with fatty acid concentration and turnover but not with glucose disposal measured during the hyperinsulinemic clamp. These correlations remained significant after fasting insulin, the insulin area under the curve during an oral glucose tolerance test, and glucose disposal during the clamp were controlled for. In the second group of subjects, plasma fatty acids 15 minutes after intravenous insulin also correlated with blood pressure. These correlations remained significant after insulin and an index of sensitivity to insulin-mediated glucose disposal were statistically controlled for. The data indicate that blood pressure is related to the effects of insulin on fatty acid metabolism. The findings raise the possibility that resistance of hormone-sensitive lipase to insulin participates in elevating the blood pressure of abdominally obese hypertensive subjects by increasing fatty acid concentration and turnover.
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PMID:Obesity hypertension is related more to insulin's fatty acid than glucose action. 861 31

The effect of chronic stress on tissue-type plasminogen activator (TPA) and plasminogen activator inhibitor-1 (PAI-1) antigens was studied in 69 healthy middle-aged men. Chronic stress, defined as feelings of fatigue, lack of energy, increased irritability, and demoralization, was positively associated with plasma concentrations of PAI-1 antigen but was unrelated to TPA. The association remained unaltered after controlling for age, smoking, alcohol consumption, and physical activity but became nonsignificant after further controlling for abdominal obesity, BMI, and serum insulin and triglyceride levels. This attenuated association implies that the relationship between vital exhaustion and PAI-1 may be secondary to the effects of the metabolic variables. Thus, the present study shows that long-term stress affects the fibrinolytic system and suggests that obesity and insulin and triglyceride concentrations, which are closely correlated with the fibrinolytic parameters, may mediate the association. These findings are consistent with the hypothesis that chronic stress causes increased synthesis of PAI-1, thus promoting the risk for atherothrombotic disease by decreasing the likelihood of spontaneous fibrinolysis and increasing the likelihood of fibrin deposition.
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PMID:Association of chronic stress with plasminogen activator inhibitor-1 in healthy middle-aged men. 863 Jun 60

Resistance to the capacity of insulin to suppress lipolysis may be an important link in the association between abdominal obesity and hypertension. Furthermore, a more active renin-angiotensin system in adipose tissue may contribute to insulin-resistant lipolysis in abdominally obese hypertensive subjects. We determined nonesterified fatty acid concentrations and turnover as well as lipid oxidation under basal conditions and during steady-state euglycemia with two levels of insulinemia (72 and 287 pmol/L) in lean normotensive, abdominally obese normotensive, and abdominally obese hypertensive subjects. To assess the role of the renin-angiotensin system in determining non-esterified fatty acid turnover, we repeated studies in the abdominally obese hypertensive subjects after double-blind random assignment to placebo or enalapril for 1 month each. The main findings were the following: (1) Nonesterified fatty acid flux was significantly higher in abdominally obese hypertensive subjects at both levels of insulinemia than in either abdominally obese normotensive or lean normotensive subjects and correlated significantly with both mean blood pressure and total systemic resistance during the higher level of insulinemia. (2) Enalapril significantly improved insulin-resistant lipolysis in the abdominally obese hypertensive subjects. The improvement in insulin suppressibility of nonesterified fatty acid flux at the high hormonal concentrations correlated positively with the magnitude of reduction in blood pressure. (3) Basal lipid oxidation and suppression in response to insulin were similarly impaired in both obese groups. Resistance to the antilipolytic actions of insulin is thus a characteristic feature in abdominally obese hypertensive subjects and may be linked to the elevated blood pressure in these individuals. A more active renin-angiotensin system may partly explain the insulin-resistant lipolysis in this form of hypertension.
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PMID:Insulin-resistant lipolysis in abdominally obese hypertensive individuals. Role of the renin-angiotensin system. 867 51

The high incidence of breast cancer in Western women has been linked to nutritional factors such as high-fat/low-fibre diet, obesity and timing of weight gain. A mechanism is postulated through which the Western diet could act in conjunction with inadequate exercise and excessive weight gain at the time of a major change in hormonal balance. All these factors favour the manifestation of insulin resistance, and the concomitants of hyperinsulinaemia might then synergise with oestrogen in promoting the development of breast cancer. The mechanism is compatible with the 'breast tissue age' model of mammary carcinogenesis. The concomitants of hyperinsulinaemia could also influence the growth of established disease subsequent to its promotion, and it is suggested that the hypothesis be tested by an adjuvant randomised trial of a high-fibre/low-fat diet in patients following primary surgery for early breast cancer. It has been suggested that the development of insulin resistance may link the Western lifestyle not only to an increased risk of hypertension and arteriosclerosis, but also to increased breast cancer risk. Large abdominal fat deposits in women are frequently a marker of the presence of insulin resistance and are generally associated with an increased level of bio-available oestrogen. There is evidence that predominantly abdominal distribution of fat in women may be a marker of increased breast cancer risk from puberty onwards. Abdominal obesity may however be hidden, and it is more reliably demonstrated by imaging techniques such as CAT or MRI scans, than by anthropometric measurements such as increased waist-to-hip ratio.
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PMID:Obesity and breast cancer. 869 16

The effects of testosterone treatment of abdominally obese men have been assessed by evaluating the following parameters: The metabolic activity of different adipose tissue regions in vivo (using lipid label as a tracer) and in vitro (measuring lipoprotein lipase (LPL) activity), the total and visceral adipose tissue mass, insulin sensitivity, fasting blood glucose, blood lipids, and blood pressure as well as prostate volume. Middle-aged men with abdominal obesity were treated with transdermal administration of testosterone (T), dihydrotestosterone (DHT) or placebo (P) during 9 months. The study was double-blind. Treatment with T was followed by an inhibited uptake of lipid label in adipose tissue triglycerides, a decreased LPL-activity and an increased turn-over rate of lipid label in the abdominal adipose tissue region in comparisons with the DHT and P groups. These effects on adipose tissue metabolism were not detected in the femoral adipose tissue region in any of the groups. T treatment was also followed by a specific decrease of visceral fat mass (measured by CT-scan), by increased insulin sensitivity (measured with the euglycemic glucose clamp), by a decrease in fasting blood glucose, plasma cholesterol and triglycerides as well as a decrease in diastolic blood pressure. In the DHT group an increased visceral mass was detected. No other changes in these variables were found in the DHT and P groups. There were no detectable changes in prostate volume (measured by ultra-sound), prostate specific antigen concentration, genito-urinary history or urinary flow measurements in any of the groups. It is suggested that T substitution to a selected group of men results in general metabolic and circulatory improvements. The prostate area needs further careful attention.
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PMID:Testosterone and regional fat distribution. 869 64

It is postulated that the metabolic/endocrine concomitants of insulin resistance resulting from high animal fat intake and weight gain after the age of 30 could be contributing to the increasing incidence of postmenopausal breast cancer and recent changes in its biologic characteristics. Case/control studies have shown that hyperinsulinaemia and abdominal obesity, which are recognized as markers of insulin resistance, are risk markers for postmenopausal breast cancer also. Excess weight gain linked to high dietary intake of saturated fat is thought to be a major cause of insulin resistance. The hypothesis is compatible with the "breast tissue age" model for breast cancer risk. Biological evidence suggests that the concomitants of insulin resistance may stimulate growth activity in existing breast cancer also. The hypothesis that nutritional factors which favour hyperinsulinaemia may also favour breast cancer growth can be tested. Restriction of dietary fat and high intake of fibre and complex carbohydrate have been shown to normalise insulin levels in a proportion of subjects with hyperinsulinaemia. Restriction of dietary fat intake has also been shown to reduce bioavailable oestrogen levels in healthy postmenopausal women. A randomised trial of a low fat, high fibre, high complex carbohydrate regimen is proposed as adjuvant treatment following primary surgery in postmenopausal women with early breast cancer. A cancer preventive or delaying ability can be assessed by comparing the incidence of contralateral second breast cancer and the metastasis rate in the diet and control groups. Insulin levels, abdominal obesity, and body mass should be monitored although normalisation of insulin levels need not necessarily involve decrease in body mass.
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PMID:Nutrition and breast cancer risk: can an effect via insulin resistance be demonstrated? 873 75

The prevalence of diabetes mellitus and impaired glucose tolerance (IGT) and their relationship to age and obesity was estimated in the rural town of Shikarpur in Sindh Province, Pakistan by a population-based survey in 1994. Oral glucose tolerance tests were performed in a stratified random sample of 967 adults (387 men, 580 women) aged 25 years and above. The diagnoses of diabetes and IGT were made on the basis of WHO criteria. The response rate was 71% for men and 80% for women. The prevalence of diabetes was 16.2% (9.0% known, 7.2% newly diagnosed) in men, and 11.7% (6.3% known, 5.3% newly diagnosed) in women. The prevalence rose with age to a peak of 30% and 21% in 65-74 year-old men and women respectively. IGT was detected in 8.2% of men and 14.3% of women. Thus, total glucose intolerance (diabetes and IGT combined) was present in 25% of subjects examined. These results indicate that glucose intolerance in South Asians can no longer be regarded as a problem confined to migrant communities. Of the 72 subjects previously known to have diabetes, none was using insulin treatment, but 57 (79%) took oral hypoglycaemic agents. Central obesity and positive family history were strongly associated with diabetes, as was prevalence of hypertension. The association with central obesity was greater for women than for men, and suggests important, modifiable risk factor(s) related to lifestyle.
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PMID:Pakistan national diabetes survey: prevalence of glucose intolerance and associated factors in Shikarpur, Sindh Province. 875 Feb 23

Excessive deposition of visceral adipose tissue is known to predispose to cardiovascular diseases. Considerable epidemiological and experimental evidence suggests that many physiological factors are involved in the aetiology of premature atherosclerosis associated with visceral obesity. Insulin resistance is frequently associated with abdominal obesity, and probably plays an important role in the pathophysiology of hypertriglyceridaemia, low levels of plasma high-density lipoprotein (HDL)-cholesterol, hypertension and reduced fibrinolytic activity. Exercise training may counteract the aberrant metabolic profile associated with abdominal obesity both directly and as a consequence of body fat loss. Exercise may increase insulin sensitivity, favourably alter the plasma lipoprotein profile and improve fibrinolytic activity. Changes in the activity of insulin-sensitive glucose transporters and of skeletal muscle lipoprotein lipase are some of the possible explanations for the increased insulin sensitivity and improved blood lipid profile associated with regular exercise. This review presents physical training as a relevant nonpharmacological tool in the treatment of abdominal obesity and associated metabolic disorders. The impact of regular exercise on the different aspects of the insulin resistance syndrome is discussed. The roles of gender, age and the state of insulin resistance on the metabolic effect of physical training are also considered.
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PMID:Effects of exercise training on abdominal obesity and related metabolic complications. 877 9

Conicity index (C index), an index of abdominal obesity that was developed based on a model of geometric reasoning, proved to be a sensitive and better than the waist to hip ratio indicator of risk for hyperlipidemia in Western populations. To evaluate comparatively the C index and the Waist-to-Hip Ratio (WHR) as predictors of blood pressure levels, insulin and triglyceride concentrations, we performed a cross-sectional study on 280 healthy women, 18-24 year-old. C index was found to be within the expected range (0.95 to 1.73) and significantly correlated with WHR (r = 0.562, p = 0.0001) and body weight (r = 0.312, p = 0.0001). Additionally, C index correlated with fasting insulin levels (r = 0.13, p = 0.03), and systolic blood pressure (r = 0.14, p = 0.02). WHR correlated with fasting insulin levels (r = 0.12, p = 0.05), systolic blood pressure (r = 0.12, p = 0.13) and triglycerides (r = 0.22, p = 0.0006). C index and WHR are equally good, albeit weak, predictors of fasting insulin and blood pressure levels, while WHR proved to be a better than C index predictor of triglyceride concentrations in this population of healthy premenopausal Greek women. Further epidemiologic studies to comparatively evaluate the two indexes as predictors of risk for the development of metabolic disorders and cardiovascular disease in various populations are needed.
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PMID:Conicity index as a predictor of blood pressure levels, insulin and triglyceride concentrations of healthy premenopausal women. 882 Sep 92


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