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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 28-year-old woman had hypothalamic disorders (amenorrhea, obesity, psychiatric abnormalities, polydipsia and fever) and chronic glomerulonephritis. She also suffered from general edema associated with cyclical oliguria and polyuria. Her body weight and plasma osmolality increased during the oliguria phase lasting 2 to 8 days and decreased after paroxysmal polyuria accompanied by the natriuresis. These episodes occurred repeatedly, regardless of the treatment with or without diuretics. The release of arginine vasopressin in response to increased plasma osmolality was exaggerated, but changes in plasma volume did not affect arginine vasopressin release. Plasma atrial natriuretic hormone increased in response to a rise in plasma arginine vasopressin and plasma volume during the oliguria phase, thereby resulting in the diuresis and natriuresis. The renin-angiotensin-aldosterone system was secondarily activated by body fluid depletion and diuretics, and this might play an additive role in general swelling. Plasma gonadal hormones did not change to explain the edema. The mechanism of this cyclical edema remains unknown, but it is likely that hypothalamic dysfunction related to psychiatric abnormalities may exaggerate arginine vasopressin release, and enhanced renal sympathetic activity may cause retention of Na and water, and the increase in atrial natriuretic hormone release responding to the plasma volume expansion may bring about the diuresis and natriuresis.
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PMID:Cyclical edema in a patient with hypothalamic disorders and chronic glomerulonephritis: arginine vasopressin-dependent atrial natriuretic hormone release. 183 31

A 55-year-old woman with bilateral multiple adenomas showed hypertension, muscle weakness, hypokalemia, moon-like face and truncal obesity. Increased serum and urinary levels of aldosterone were observed. Serum cortisol level did not show a normal circadian rhythm. Microscopic examination of the resected tumors showed two types of adenoma cells; one (golden yellow tumor) was a large clear cell with foamy cytoplasm which possibly secreted aldosterone and the other (dark brown tumor) was an acidophilic cell with lipofuscin which might have produced cortisol. This is a very rare case of primary aldosteronism with Cushing's syndrome due to multiple bilateral adrenal adenomas.
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PMID:Primary aldosteronism with cortisol overproduction from bilateral multiple adrenal adenomas. 186 73

Neuropeptide Y (NPY), acting through various medial hypothalamic nuclei, is found to have potent effects on a variety of endocrine, physiological and behavioral systems that modulate energy balance. This peptide affects the release of various hormones, such as corticosterone, insulin, aldosterone and vasopressin, which modulate energy metabolism, as well as food intake. It also has direct impact on energy metabolism through an effect on substrate utilization and lipogenesis. Finally, NPY has a remarkably potent stimulatory effect on feeding behavior, which is characterized by a selective increase in carbohydrate ingestion that is strongest at the beginning of the active feeding cycle and is dependent upon circulating levels of corticosterone. This evidence has led to the proposal that NPY exerts anabolic effects to restore energy balance at specific times of energy depletion. Increased NPY activity may occur at the beginning of the active cycle or after a period of food deprivation. Further evidence, that chronic NPY stimulation produces profound hyperphagia and obesity and that endogenous NPY concentration is increased in genetically obese animals, strongly suggests that hypothalamic NPY may contribute to the development of eating disorders and obesity.
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PMID:Brain neuropeptide Y: an integrator of endocrine, metabolic and behavioral processes. 195 27

Epidemiological evidence suggests that there is a close association between obesity, non-insulin-dependent diabetes (NIDDM) and hypertension. Obesity and NIDDM are the classical insulin-resistant states. Even in the absence of these conditions, essential hypertension is associated with insulin resistance. In view of the acute effects of insulin on renal sodium reabsorption, the sympathetic nervous system, the renin-angiotensin-aldosterone system, the transmembranous cation transport, the cardiovascular reactivity, the atrial natriuretic peptide and the kallikrein-kinin system, hyperinsulinaemia may contribute to the development of hypertension in these diseases. Preliminary evidence suggests that sensitivity to these possible blood-pressure-elevating action(s) of insulin is still present despite the resistance to the glucose-lowering action of the hormone. However, extrapolation of the epidemiological data and results of acute experiments indicate that the impact on blood pressure is rather small. The pathophysiological mechanisms of hypertension in the above-mentioned conditions are also not always consistent with insulin action(s). Moreover, some data suggest that insulin resistance, and not hyperinsulinaemia per se, underlies the blood pressure elevation, while the possibility cannot be excluded that both hypertension and insulin resistance are co-inherited, but unrelated, abnormalities.
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PMID:Insulin and blood pressure regulation. 204 23

The association between arterial hypertension and obesity has been known for many years and demonstrated by epidemiological studies. The physiopathological mechanisms involved consist of increased extracellular volumes, hyperactivity of the sympathetic nervous system and the renin-angiotensin-aldosterone system, and abnormal ion exchanges between extra- and intracellular compartments. Recent studies have demonstrated an association between arterial hypertension and insulin resistance. Insulin resistance may well be the most important aetiological factor in this type of arterial hypertension as it stimulates both renal sodium reabsorption and sympathetic nervous system activity and reduces vascular Na-K-ATPase activity.
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PMID:[Arterial hypertension in patients with obesity. Role of hyperinsulinism and insulin resistance]. 209 34

The aims of this study were to determine whether chronic hyperinsulinemia, comparable to that found in obese hypertensives, elevates mean arterial pressure (MAP) or potentiates the hypertensive effects of angiotensin II (ANG II). Studies were conducted in conscious dogs with kidney mass reduced by 70% in order to increase their susceptibility to hypertensive stimuli. Insulin infusion (0.5 or 1.0 mU.kg-1.min-1 iv) for 7 days with plasma glucose held constant raised plasma insulin more than fivefold but did not increase MAP in four dogs on 138 meq/day Na intake. In seven dogs maintained on a high Na intake (319 meq/day), insulin infusion (1.0 mU.kg-1.min-1) for 28 days raised fasting insulin from 9.8 +/- 1.5 to 56-78 microU/ml but did not increase MAP, which averaged 106 +/- 2 mmHg during control and 102 +/- 2 mmHg during 28 days of insulin infusion. Insulin caused transient sodium and potassium retention followed by renal "escape" that was associated with increased glomerular filtration rate (12-27%). Plasma renin activity and plasma aldosterone were not altered by insulin. In five dogs infused with ANG II (2.0 ng.kg-1.min-1) to cause mild hypertension, insulin infusion (1.0 mU.kg-1.min-1) for 6-28 days did not increase MAP further. Thus chronic hyperinsulinemia did not elevate MAP, even when kidney mass was reduced, and did not potentiate the hypertensive effects of ANG II. These findings suggest that additional factors besides hyperinsulinemia per se are responsible for obesity-associated hypertension.
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PMID:Chronic hyperinsulinemia and blood pressure regulation. 218 Mar 21

25 patients with various degree of obesity treated with a very low-caloric diet (Dresden diet) were followed up dynamically. By an average clinical stay of 22 days a satisfactory reduction of the body mass with mean 6.6 kg was achieved at mean reduction of the body mass index from 34 to 31. The blood sugar level, immunoreactive insulin in the course of the oral glucose tolerance test, the 24 h rhythm of the plasma cortisol and the aldosterone level at rest and in orthostatic position at the beginning and the end of the dietetic treatment were followed up. The results achieved are discussed in relation to the reduction of the body mass.
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PMID:[Treatment of obesity with a very low-energy dietetic regimen--the endocrine parallels]. 220 8

The relation between intra-abdominal visceral fat accumulation and blood pressure was investigated in 67 obese women (mean body mass index, 33.6 +/- 3.1; average age, 50 +/- 11 years). As an index of intra-abdominal fat accumulation, the ratio of the intra-abdominal visceral fat area to subcutaneous fat area was determined using a computed tomographic section at the level of the umbilicus. When the obese subjects were divided into a hypertensive group and a normotensive group, the ratio of the intra-abdominal visceral fat area to subcutaneous fat area in the hypertensive group was significantly higher (0.53 +/- 0.33 versus 0.29 +/- 0.12, p less than 0.01). Significant correlations between the ratio of intra-abdominal visceral fat area to subcutaneous fat area and systolic blood pressure (r = 0.62, p less than 0.001) and diastolic blood pressure (r = 0.53, p less than 0.001) also were found. However, no significant difference existed in either the body mass index or the waist-to-hip circumference ratio between the hypertensive and normotensive groups. Plasma renin activity, aldosterone, epinephrine, and norepinephrine levels were not significantly different between the two groups. Moreover, the correlation between the ratio of the intra-abdominal visceral fat area to subcutaneous fat area ratio and blood pressure was found independent of age and body mass index by multiple regression analyses. We conclude that intra-abdominal fat accumulation itself may play an important role in the pathogenesis of hypertension in obesity.
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PMID:Close correlation of intra-abdominal fat accumulation to hypertension in obese women. 222 47

In the United States, obesity and hypertension are more common in blacks than in whites, but that general statement hides some important sex differences. Thus, in black women the prevalences of both obesity and hypertension are greater than in white women, whereas in men, although there is no racial difference in obesity, in blacks hypertension is more common and more severe than in whites. For white people, there is a well-documented causal relationship between obesity and hypertension, however, results from the second National Health and Nutrition Examination (NHANES II) suggest that this relationship is not so strong for blacks. Obesity is also an important risk factor for diabetes, which in itself is associated with hypertension. The mechanism of obesity-associated hypertension appears to be an inadequate vasodilation in the face of the increased blood volume and cardiac output, which are the natural consequences of an increased body mass. This defect in control of vascular resistance has been attributed to increased activity of the sympathetic nervous system, abnormal renin-angiotensin-aldosterone relationships, and insulin resistance. However, none of these attributes has been found to be the exclusive characteristic of obese hypertensive as compared with normotensive obese subjects.
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PMID:Obesity and hypertension in blacks. 227 1

Hypertension in the obese may be related to hyperinsulinaemia. To investigate this relationship further, we infused somatostatin (250 micrograms/h in 100 ml saline) or saline, single-blind and in a random order, for 10 h in seven obese hyperinsulinaemic hypertensive patients and in seven normo-insulinaemic hypertensive controls. Every 2 h, blood pressure, plasma insulin, glucose, sodium, potassium, renin, cortisol and aldosterone concentrations and the urinary sodium:creatinine ratio were determined. Two hours after the somatostatin infusion was started, mean arterial blood pressure was significantly reduced in the obese hyperinsulinaemic patients (from 128 +/- 11 to 114 +/- 11 mmHg, P less than 0.05) but not in the controls and this reduction persisted throughout the study. The somatostatin infusion reduced plasma insulin and increased plasma glucose similarly in both groups. Plasma sodium, potassium, renin, cortisol and aldosterone concentrations and the urinary sodium:creatinine ratio were unchanged after the somatostatin infusion. These results suggest that hyperinsulinaemia could help sustain the blood pressure rise in obesity.
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PMID:Reduction of blood pressure in obese hyperinsulinaemic hypertensive patients during somatostatin infusion. 257 63


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