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

Regular exercise is an effective nonpharmacologic therapy for stress, sleep disorders, depression, and anxiety, as well as such chronic conditions of aging as hypertension, obesity, diabetes mellitus, coronary artery disease, hyperlipidemia, and constipation. Pre-exercise office assessment of cardiac risk, possible limitations, and contraindications is advised. A balanced fitness training program includes activities to increase flexibility, strength, and cardiovascular endurance. The most effective exercise prescription begins with a type of aerobic activity the patient enjoys. A prescribed schedule of stepwise increments in frequency, duration, and intensity gradually leads to a maintenance level of fitness.
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PMID:Prescribing physical activity for older patients. 163 24

With the rapidly increasing average age of the population of the Western world, care and treatment of the elderly are becoming increasingly important. Cardiovascular diseases are major causes of death and disability in the elderly; hence, identification of cardiovascular risk factors and effective treatment are essential. Evidence indicates that these risk factors in the elderly are similar to those in the young; namely, high blood pressure, hyperlipidemia, glucose intolerance, hyperfibrinogenemia, obesity, and cigarette smoking. The latter two relate to general patient management, whereas the remainder can be significantly influenced by modern drug therapy such as celiprolol. This drug is a third-generation highly selective beta 1-adrenoceptor antagonist with beta 2-agonist and vasodilatory activity giving a unique and advantageous pharmacologic profile for antihypertensive therapy with particular benefits for the elderly. The impact of therapy with celiprolol on the cardiovascular risk factors in the elderly hypertensive patient is reviewed.
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PMID:Efficacy of celiprolol in the elderly hypertensive patient. 167 27

In a randomized, single-blind, controlled study (400 patients aged 25-63 yr; 374 males, 26 females), 206 subjects were administered a magnesium-rich diet, and 194 subjects their usual diet, for 6 wk. Age, sex, body weight, hypertension, hyperlipidemia, smoking, obesity, diuretic therapy, and diabetes were comparable between the two groups, as were laboratory data at entry to the study. Intervention-group A received a significantly higher amount of dietary magnesium and potassium compared to group B, which received its usual diet. After 6 wk, there was a significant fall in total serum cholesterol (228.5 +/- 46.2 mg/dL), LDL cholesterol 146.5 +/- 75.5 mg/dL), and triglyceride (143.8 +/- 40.5 mg/dL) in group A compared to serum cholesterol (242.5 +/- 58.2 mg/dL), LDL cholesterol (157.0 +/- 78.4 mg/dL), and triglyceride (156.5 +/- 60.0 mg/dL) at entry to study, but no such changes in group-B subjects. HDL cholesterol showed a marginal mean decrease of 0.8 mg/dL in group B and a 2.5 mg/dL increase in group A. The changes in blood lipids were consistent with an increased intake of magnesium and with a rise in serum levels. Although a general blood-lipid-reducing effect of such a diet cannot be excluded, it is possible that dietary magnesium may have contributed to the reduction of total serum cholesterol, LDL cholesterol, and triglyceride, and the marginal rise in HDL cholesterol. More studies with longer follow-up periods are needed to confirm this observation.
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PMID:Does dietary magnesium modulate blood lipids? 171 69

Central and lateral hypothalamic concentrations of 9 regulatory peptides implicated in the control of feeding behaviour were measured in corpulent (cp/cp) JCR:LA-cp rats which develop spontaneous obesity, hyperinsulinaemia and hyperlipidaemia, and in lean (+/?) controls. In female cp/cp rats, central hypothalamic levels of neuropeptide Y (NPY), neurotensin, somatostatin and substance P were significantly lower (p less than 0.02) than in lean female controls. Following food restriction with a 16% reduction in body weight, these differences were apparently reversed and there were also significant rises in the lateral hypothalamic concentrations of neurotensin and of galanin. The other 4 peptides examined (bombesin, calcitonin gene-related peptide, neuromedin B and vasoactive intestinal peptide) did not differ significantly between cp/cp and lean females, either fed freely or food-restricted. Male cp/cp rats showed no significant differences from lean males in central or lateral hypothalamic concentrations of any of the 9 peptides. NPY and galanin are powerful and specific central appetite stimulants, whereas neurotensin, substance P and somatostatin inhibit feeding when injected centrally. Disturbances in these putative appetite-regulating peptides may be involved in the hyperphagia and other hypothalamic abnormalities in this spontaneous obesity syndrome. The apparent absence of differences between the male corpulent and lean groups may relate to sexual dimorphism of the syndrome, which is more marked in the females.
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PMID:Hypothalamic regulatory peptide disturbances in the spontaneously obese JCR: LA-corpulent rat. 172 Mar 64

The Japanese Mazindol study group investigated the action of an anorexiant, mazindol, and found that it reduced food intake by directly suppressing neurons in the lateral hypothalamus, inhibited gastric acid secretion, increased motor activity, decreased glucose absorption, and inhibited insulin secretion. It thus appears that the main effect of mazindol is to decrease food intake through suppressing feeding centers in the hypothalamus. A multicenter open study of mazindol in Japan revealed that loss of body weight and relative body weight in 14 wk were 4.6 kg and 9.2%, respectively, with suppression of appetite in the majority of obese patients. A multicenter double-blind study demonstrated that mazindol was superior to the placebo in the treatment of simple obesity. We also suggest that mazindol is effective in the maintenance of reduced body weight after obesity therapy and in the treatment of obesity-related diseases such as diabetes, hypertension, or hyperlipidemia.
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PMID:Clinical and basic aspects of an anorexiant, mazindol, as an antiobesity agent in Japan. 172 34

Excessive intake of dietary fat contributes to the development and maintenance of both obesity and hyperlipidemia. Inhibition of gastrointestinal lipases could decrease the amount of ingested fat that is absorbed systemically by preventing the hydrolysis of triglycerides. Ro 18-0647, a chemically synthesized derivative of the natural product lipstatin, inhibits the action of gastrointestinal lipases. Initial studies in humans have shown that Ro 18-0647 can reliably increase fecal fat excretion. Ro 18-0647 has also been shown to be well tolerated in the majority of normal volunteers and obese patients studied. Further research must be conducted to determine whether clinical endpoints of weight loss or cholesterol lowering can be produced by using this new pharmacologic principle.
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PMID:Initial studies in humans with the novel gastrointestinal lipase inhibitor Ro 18-0647 (tetrahydrolipstatin). 172 45

Although the pathogenesis of obesity in OZR is unknown, the association among hyperinsulinemia, insulin resistance, and hyperlipidemia suggests that investigations using OZR may help define how a number of vascular disease risk factors interact to cause end-organ damage. Like other rat strains, OZR do not develop atherosclerosis spontaneously. Nevertheless, in an endothelial injury model, atherosclerosis was worse in OZR than in LZR. Perhaps more intriguing is the fact that OZR develop spontaneous glomerular injury. Although the mechanisms important in the development and progression of glomerular injury in OZR remain to be clarified, both lipid abnormalities and glomerular hemodynamic alterations could play a role.
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PMID:The Zucker rat model of obesity, insulin resistance, hyperlipidemia, and renal injury. 173 Apr 47

Exogenous obesity is characterized hemodynamically by expanded intravascular (plasma) volume associated with an increased cardiopulmonary volume and cardiac output. In contrast, essential hypertension is related to an increased total peripheral resistance that is more or less uniformly distributed throughout the component organ circulations associated with a contracted plasma volume in proportion to the height of arterial pressure. Thus, both cardiac output and total peripheral resistance are elevated in obesity hypertension, and both impose a load on the left ventricle, resulting in both a volume and a pressure overload left ventricular hypertrophy. Although renal vascular resistance is not as increased as it is in lean hypertensive patients, these patients are subjected to hyperfiltration and proteinuria. Additionally, these hemodynamic alterations coexist with carbohydrate intolerance, hyperinsulinemia, hyperlipidemia, and hyperuricemia. With weight reduction and associated pressure reduction, the hemodynamic and metabolic changes reverse toward normal. However, should this not be achievable, the angiotensin converting enzyme inhibitors and calcium antagonists provide rational physiological approaches to drug therapy. With these agents pressure reduction is achieved through a fall in vascular resistance without intravascular volume expansion, and this is associated with reduced left ventricular mass and preserved cardiac and renal function, and without exacerbation of preexisting metabolic perturbations. Hence, these two classes of antihypertensive agents may provide a rational and physiological means for reversing the pathophysiological alterations of hypertensive disease in those obese patients in whom weight control is not possible.
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PMID:Obesity hypertension. Converting enzyme inhibitors and calcium antagonists. 173 Apr 48

The value of the vascular examination cannot be over-estimated. Symptoms of vascular disease present in the foot and lower extremity may actually be manifestations of severe life-threatening disease. Symptoms, their location, and the frequency and quality of the patient's pain often provide valuable clues for the clinician's diagnosis. Central nervous system symptoms, ocular disturbances, cardiac symptoms, impotence, or constitutional disturbances may all indicate systemic arterial disease. Risk factors for this disease include smoking, hypertension, hyperlipidemia, genetic predisposition, diabetes, emotional stress, and physical inactivity. Those factors attributable to hypercoagulability and venous disease are birth control pill use, estrogen chemotherapy, obesity, prolonged immobilization, paralysis, previous thrombotic episodes, venous stasis disease, and varicose veins. An accurate bilateral assessment of blood pressure, pulses, and capillary perfusion is of critical importance. Careful inspection of the extremity for trophic changes, skin color, texture, temperature, edema, ulceration, atrophy, or paresis, will provide clues of vasculopathy. A relatively accurate assessment of circulatory status may be obtained without the use of exotic instruments. Simple tests such as the elevation and dependency tests, capillary bed return test, venous filling time test, along with blood pressure, pulse, and possibly oscillometry data are valuable in arterial evaluation. Such venous tests as inspection, percussion, Homan's sign, Trendelenburg, and Perthes' tourniquet are useful in the determination of the presence of venous disease. Fortunately, over the past few years tremendous advances have been made in the technology of the vascular laboratory. If symptoms are discovered during the vascular history and physical examination, the complete noninvasive study will provide impressive data to quantitate and specifically establish the diagnosis.
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PMID:The vascular history and physical examination. 173 54

Mandibuloacral dysplasia (MAD) is a syndrome with onset in midchildhood. The predominant characteristics of MAD include flexion contractures; mandibular hypoplasia; loss of body fat; atrophic, speckled skin; and progressive osteolysis of the clavicles. We studied three males with MAD. Each had lipodystrophy of the extremities, with sparing of the face and neck. All had moderate hyperlipidemia. In response to oral glucose, each had a diabetic response, with peak insulin levels between 2870 and 22,960 pmol/L. Insulin-stimulated glucose disposal was determined in two patients with MAD. At an insulin infusion rate of 120 mU/m2 per minute, glucose disposal was less than 25% of that measured at similar levels of insulinemia in nondiabetic control subjects, indicating marked insulin resistance in patients with MAD. The insulin resistance occurred without obesity, excessive levels of counterregulatory hormones, or anti-insulin-receptor antibodies. We suggest that MAD is a previously undescribed form of lipodystrophic insulin-resistant diabetes mellitus.
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PMID:Severe insulin resistance and diabetes mellitus in mandibuloacral dysplasia. 173 53


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