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

Diabetes may be associated with systolic hypertension secondary to atherosclerosis, renal hypertension secondary to diabetic nephropathy, and essential hypertension. The latter is by far the most prevalent, and a wealth of epidemiologic data suggests that such an association is independent of age and obesity. Considerable evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive subjects, whether obese or of normal body weight, are compared to age- and weight-matched normotensive controls, a heightened plasma insulin response to a glucose challenge is found consistently. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. With the use of the glucose clamp technique coupled with tracer glucose infusion and indirect calorimetry, it can be shown that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal, and is directly correlated with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms--sodium retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and altered muscle fiber composition. Physiologic maneuvers such as caloric restriction in the overweight individual and regular physical exercise can improve tissue sensitivity to insulin; good preliminary evidence shows that these measures can also lower blood pressure in both normotensive and hypertensive individuals. A strong case can therefore be made for the use of physiologic intervention in the treatment of essential hypertension.
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PMID:The association of essential hypertension and diabetes. 268 84

A total of 100 patients, aged 16-25 years, suffering from metabolic-alimentary obesity were investigated under clinical conditions. An analysis was made of deviations from the normal parameters of arterial pressure, blood serum lipids, and other risk factors of the development of atherosclerosis, coronary heart disease, essential hypertension and other metabolic diseases. The shifts detected could be directly dependent of the disorders in nutrition. Alimentary correction of the disorders noted, reduction of body mass resulted in the improvement of the subjective conditions of patients, and in normalization of the above parameters. However, in some patients significant improvement in the metabolic status of the patients (lipid, in particular) was not achieved. The necessity of dispensary follow-up of young patients with obesity has been considered.
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PMID:[Excess body weight at a young age as a risk factor for developing metabolic diseases]. 271 10

In order to evaluate the role of beta-endorphin in the pathogenesis of obesity and essential hypertension 44 subjects were investigated: 12 nonobese hypertensives, 11 obese hypertensives, 11 obese normotensives and 10 normal subjects. Plasma concentrations of beta-endorphin and cortisol were measured by radioimmunological and ACTH by immunoradiometric methods. The plasma concentrations and the circadian rhythms of ACTH and cortisol secretion were normal in all groups investigated. A circadian rhythm of beta-endorphin secretion was demonstrated in nonobese hypertensives and in normal subjects. The plasma concentrations of beta-endorphin were twice higher than those in nonobese subjects. Also, in all obese patients the circadian rhythm of beta-endorphin secretion was blunted. The increased concentrations and the altered circadian rhythm of beta-endorphin in all obese subjects may point to a role of beta-endorphin in the pathogenesis of obesity rather than in that of essential hypertension.
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PMID:The possible role of beta-endorphin in pathogenesis of obesity and essential hypertension. 283 3

The role of alpha 2-adrenoceptor stimulation by clonidine on the secretion of beta-endorphin, ACTH, and cortisol in essential hypertension and obesity was studied in 45 subjects: 15 non-obese hypertensives, 10 obese hypertensives, 11 obese normotensives, and 9 healthy subjects. The circadian rhythm of plasma beta-endorphin, ACTH, and cortisol was determined after placebo and after three days on clonidine 0.45 mg daily. Clonidine lowered the blood pressure and blood ACTH and cortisol levels in all the subjects. A significant decrease in beta-endorphin after clonidine occurred in the healthy subjects. In obese normotensives basal beta-endorphin concentrations were significantly higher than in healthy subjects and did not change after clonidine. In about 50% of non-obese and obese hypertensives a significant increase in beta-endorphin secretion after clonidine was noted (responders). In the subgroup of non-obese hypertensive responders no circadian rhythm of beta-endorphin was observed. The results suggest that adrenergic regulation of beta-endorphin secretion is altered in obesity and in certain patients with essential hypertension.
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PMID:Effect of clonidine on beta-endorphin, ACTH and cortisol secretion in essential hypertension and obesity. 284 28

Progression from normotension between 1964 and 1972 to essential hypertension by age 55 years was documented in 1,031 adult members of the Kaiser Permanente Medical Care Program (Northern California region) from computerized multiphasic health checkup records and medical record review. Each case was matched to a persistently normotensive control on age, sex, race, number, and dates of multiphasics. In 609 pairs with baseline measurements of subscapular and triceps skinfolds, mean interval from baseline to the case's first hypertensive multiphasic was 5.7 years, and mean age at onset of hypertension was 47 years. Baseline measures of body mass index, subscapular skinfold, and triceps skinfold were each predictive of development of hypertension (odds ratios 3.85, 3.75, and 2.29 respectively, comparing highest with lowest quintiles, p less than 0.0001 for each). When both skinfolds were included in the same model, subscapular skinfold was highly predictive and triceps skinfold was no longer related to risk. When the authors controlled for overall obesity (body mass index), subscapular skinfold remained highly predictive (p less than 0.0001). In 330 pairs who also had skinfold measurements at the hypertensive multiphasic, weight gain was a strong predictor of hypertension. Increase in subscapular skinfold conferred a small increase in risk in women only. The authors conclude that centrally deposited body fat increases risk for developing essential hypertension independent of the overall level of obesity, while peripherally deposited fat does not.
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PMID:Precursors of essential hypertension. The role of body fat distribution pattern. 291 71

Hypertension and obesity are two disorders that are closely related; each occurs more frequently with the other than in an otherwise normal population. These two disorders, however, exert disparate effects on cardiovascular structure and function. The hallmark of essential hypertension is an increased total peripheral resistance, and hypertensive patients have a contracted intravascular volume and normal cardiac output but an increased left ventricular stroke work due to a high afterload. In contrast, obese patients have an increased intravascular volume, left ventricular filling pressure, cardiac output and a lower total peripheral and renal vascular resistance. Left ventricular adaptation will consist of eccentric hypertrophy in obesity regardless of the level of arterial pressure and concentric hypertrophy in lean hypertensive patients. Although obesity may mitigate the harmful effect of a chronically elevated total peripheral and renal vascular resistance and lessen target organ damage in essential hypertension, the combination of obesity and hypertension presents a double burden to the left ventricle and is associated with systolic and diastolic dysfunction and a propensity for high grade ventricular dysrhythmias. It is not surprising that congestive heart failure and sudden death are common sequelae of obesity hypertension. Weight reduction reduces arterial pressure by decreasing intravascular volume and cardiac output associated with a fall in sympathetic activity and reversal of cardiac hypertrophy. Therefore, weight loss unloads the heart from the two-fold burden caused by obesity and hypertension and should become a major goal in the prevention and treatment of heart disease.
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PMID:Cardiovascular adaptation to obesity and hypertension. 294 41

To determine the impact of the renin-angiotensin-aldosterone system on left ventricular function and structure, 36 untreated patients with essential hypertension (WHO class I and II) were examined. Posterior wall thickness, relative wall thickness, and left ventricular mass were determined by M-mode echocardiography. Plasma renin activity, aldosterone, angiotensin I, and angiotensin II levels were measured by radioimmunoassay. Plasma renin activity was related to 24-hour urinary sodium excretion. Of all the endocrine parameters, only the angiotensin II level correlated with posterior wall thickness (r = 0.50, p less than 0.05) and relative wall thickness (r = 0.46, p less than 0.05). This relationship was confirmed by stepwise multiple regression analysis taking arterial pressure, obesity, and sodium excretion into account (p less than 0.05). Plasma renin activity but not the angiotensin II level correlated positively with the ejection fraction (r = 0.42, p less than 0.05) and velocity of circumferential fiber shortening (r = 0.57, p less than 0.01). Thus, angiotensin II emerged as a determinant of left ventricular structural adaptation in essential hypertension.
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PMID:Does the renin-angiotensin-aldosterone system modify cardiac structure and function in essential hypertension? 297 63

Insulin resistance occurs in a variety of conditions, including diabetes, obesity and essential hypertension, but its underlying molecular mechanisms are unclear. In type 2 (non-insulin-dependent) diabetes mellitus, it is insulin-resistance in skeletal muscle, the chief site of insulin-mediated glucose disposal in humans, that predominantly accounts for the low rates of glucose clearance from the blood, and hence for impaired glucose tolerance. Human type 2 diabetes is characterized by a decrease in non-oxidative glucose storage (muscle glycogen synthesis), and by the deposition of amyloid in the islets of Langerhans. Amylin is a 37-amino-acid peptide which is a major component of islet amyloid and has structural similarity to human calcitonin gene-related peptide-2 (CGRP-2; ref. 8). CGRP is a neuropeptide which may be involved in motor activity in skeletal muscle. We now report that human pancreatic amylin and rat CGRP-1 are potent inhibitors of both basal and insulin-stimulated rates of glycogen synthesis in stripped rat soleus muscle in vitro. These results may provide a basis for a new understanding of the molecular mechanisms that cause insulin resistance in skeletal muscle.
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PMID:Pancreatic amylin and calcitonin gene-related peptide cause resistance to insulin in skeletal muscle in vitro. 305 May 30

An age-related increase in autonomic nervous system activity, as reflected by increased plasma norepinephrine levels, has been reported by a number of investigators. This increase in plasma norepinephrine levels cannot be solely explained by increased obesity and decreased norepinephrine clearance with ageing. It has also been suggested that enhanced autonomic nervous system (sympathetic) activity may play a role in the pathogenesis of essential hypertension. However, recent studies from several laboratories have demonstrated that plasma norepinephrine levels increase with age in normotensives but not in patients with essential hypertension. A recent study from our laboratory has demonstrated no difference in basal or cardiopulmonary baroreflex-mediated increases in plasma norepinephrine levels in older hypertensives compared with middle-aged hypertensives. These observations suggest that elevated norepinephrine levels, per se, are not sufficient to explain the high prevalence of hypertension in the elderly, who are otherwise normal. In fact, it is likely that high norepinephrine levels in the elderly may be due to factors other than a primary hyperadrenergic state. Although arterial baroreceptor sensitivity decreases with ageing, studies from our laboratory indicate that cardiopulmonary baroreflex control of vascular resistance is relatively well preserved in older subjects with mild-to-moderate established essential hypertension. Thus, the relative influence of altered baroreflex sensitivity with ageing, or of a disturbed sympathetic outflow affecting autonomic nervous system activity and leading to variable blood pressure in the elderly, remains to be determined.
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PMID:Autonomic nervous system function. 306 94

Data from several epidemiologic studies have suggested that the prevalence of hypertension in patients with diabetes mellitus is approximately 1.5-2.0 times greater than in an appropriately matched nondiabetic population. In patients with insulin-dependent diabetes mellitus (IDDM), hypertension is generally not present at the time of diagnosis. As renal insufficiency develops, blood pressure rises and may exacerbate the progression to end-stage renal failure. In non-insulin-dependent diabetes mellitus (NIDDM), many patients are hypertensive at the time of diagnosis. The incidence of hypertension in NIDDM is related to the degree of obesity, advanced age, and extensive atherosclerosis that is typically present, and it probably includes many patients with essential hypertension. Several other pathophysiologic mechanisms also contribute to the genesis and maintenance of hypertension in the patient with diabetes. Hyperglycemia and increases in total-body exchangeable sodium may lead to extracellular fluid accumulation and expansion of the plasma volume. In some patients, alterations in the function of the renin-angiotensin-aldosterone system and vascular sensitivity to vasoactive hormones may also play a role. It has recently been suggested that hyperinsulinemia and insulin resistance may also contribute to the maintenance of an elevated blood pressure because insulin is known to promote sodium retention and enhance sympathetic nervous system activity. The evidence for these hypotheses and their respective contributions to the etiology of hypertension in IDDM and NIDDM are discussed.
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PMID:Etiology and prevalence of hypertension in diabetic patients. 307 72


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