Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The problem of the association between adult diabetes, obesity and manic-depressive psychosis is examined in the light of new endocrinological and psychopharmacological findings. After a critical review of the vast old and recent literature on the matter, a physiopathological interpretation of the clinical association is put forward on the basis of mental, nervous and endocrine correlations in carbohydrate metabolism, with special reference to manic-depressive psychosis. The insulin-like effect of lithium on carbohydrate metabolism and correlated ions (phosphates, calcium, magnesium, potassium) at cell membrane level is then discussed. Theoretical and practical conclusions are drawn on the basis of these data. The former propose an essentially "structural" or "intersection" hypothesis of the association and suggest depth study of the insulin function especially in the "normal" phase of manic-depressive psychosis. The latter show the possibility of a clinical trial with lithium and other anti-depressant drugs in obese diabetics, with a close cooperation between psychiatrist and diabetologist.
 ...
PMID:[Introduction to new research on correlations between manic-depressive psychosis and adult obesity-linked diabetes]. 123 Jan 36

Coronary heart disease is the most frequent cause of death in Western, industrialized countries. Coronary risk factors are prevalent in such countries and sometimes combine to constitute the so-called syndrome X--hypertension, central obesity, serum lipid and clotting disturbances, and insulin resistance. beta-Blockers, unlike calcium antagonists, have proved highly effective in secondary prevention of myocardial infarction. If present at the time of the myocardial infarction, beta-blockers (unlike calcium antagonists and diuretics) probably decrease mortality 1 month later. Early intervention (within 12 h) of chest pain with intravenous beta-blockers results in a 15% reduction in cardiovascular mortality at 1 week. Later intervention (3-28 days) with oral non-ISA beta-blockers results in a 30% reduction in mortality after 1 year; ISA-containing beta-blockers are probably less effective (less decrease in heart rate). Hydrophilicity/lipophilicity of beta-blockers is unimportant in terms of decreased mortality. Primary prevention of myocardial infarction, unlike stroke, in hypertensive patients has been disappointing, possibly due to treatment-induced biochemical/lipid changes or inappropriate lowering of diastolic blood pressure in high-risk subjects (J-curve effect). beta-Blockers should be first-line therapy for hypertensive patients up to the age of 65 years, particularly men (and nonsmokers) as Q-wave myocardial infarction is significantly decreased by beta-blockers and significantly increased by diuretics. However, in elderly hypertensive subjects, beta-blockers have not significantly decreased myocardial infarction (unlike stroke), whereas diuretics have. The effects of beta-blockers and diuretics on heart size (and thus coronary flow reserve) in the elderly may be important. Thus, beta-blockers should be second-line therapy for the elderly hypertensive individual but first-line if overt ischemia (e.g., angina or recent myocardial infarction) also is present. In patients with angina but normal blood pressure, beta-blockers tend to decrease and calcium antagonists increase cardiovascular events. Thus, beta-blockers are highly effective agents in the secondary prevention of myocardial infarction and are moderately effective in primary prevention of myocardial infarction in hypertensive patients (particularly men) under the age of 65 years.
 ...
PMID:Beta-blockers: primary and secondary prevention. 128 45

Insulin resistance and hyperinsulinemia is now recognized in non-insulin-dependent diabetes, essential hypertension, obesity, atherosclerotic heart disease, dyslipidemia, heart failure, and in heavy smokers. Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Some of the nonpharmacological methods to control hyperinsulinemia are of benefit in the management of hypertension, most notably weight loss, exercise program, and reduced salt intake. High-fiber and reduced-protein diets also reduce hyperinsulinemia. Thiazide diuretics can result in insulin resistance, and insulin secretion may be inhibited, possibly associated with concomitant hypokalemia. beta-Blockers result in some reduction of glucose tolerance and mask some of the features of hypoglycemia. Angiotensin-converting enzyme (ACE) inhibitors and alpha-receptor blockers do not effect insulin resistance; probably the same is true for calcium antagonists. Although the effect on risk factors should not be discounted, it is the effect of treatment on hard end points, cerebrovascular accidents, myocardial infarction, or death that is most important. Evidence in hypertension is at present restricted to diuretics and beta-blocking drugs.
 ...
PMID:Hypertension and insulin resistance. 128 47

Glucose intolerance and noninsulin-dependent diabetes are commonly associated with hypertension. Epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. When hypertensive patients whether obese or of normal weight are compared with matched normotensive control subjects, an increased plasma insulin response to a glucose challenge is consistently observed. Studies using insulin glucose clamp techniques in combination with tracer glucose infusion and indirect calorimetry have demonstrated that the insulin resistance in hypertensive subjects is located in muscles and restricted to glycogen synthesis. The relations between hyperinsulinemia and blood pressure do not prove that the relationship is a causal one. However, at least four mechanisms may link hyperinsulinemia with hypertension: Na+ retention, sympathetic nervous system overactivity, disturbed membrane ion transport and proliferation of vascular smooth muscle cells. Diuretics and beta-blockers may enhance insulin resistance, which is not affected by calcium antagonists, but decreased by the ACE inhibitor captopril. Weight reduction and regular physical exercise can improve insulin sensitivity and decrease blood pressure values. These nonpharmacological interventions should be more strongly recommended to diabetic and nondiabetic hypertensive patients.
 ...
PMID:Hyperinsulinemia, insulin resistance and essential hypertension. 130 12

Obesity is associated with altered bone mass. However, reports on bone status in obesity are inconsistent. Increased or normal bone mass was reported in obese adults but decreased bone mineral content was described in obese children. Therefore we evaluated the obese fa/fa rat as a possible model to assist in studies of bone metabolism in obesity. Obese and lean 14-week-old male rats underwent 24 h balance studies for calcium, magnesium and phosphate. Plasma calcium, magnesium, phosphate, immunoreactive parathyroid hormone, urinary cAMP (cyclic adenosine monophosphate) and femur bone histomorphometry were also analysed. Obese rats were heavier and had higher plasma insulin, cholesterol and triglycerides levels (P less than 0.05). A comparable positive balance for calcium, magnesium and phosphate was found in obese and lean rats. Total plasma calcium was higher in the obese, but albumin corrected calcium and plasma magnesium, phosphate and glucose were similar to the lean. In contrast to human obesity, obese rats were hypercalciuric, hypermagnisuric and hyperphosphaturic (P less than 0.05). iPTH and urinary cAMP were higher in the obese. Femora of fa/fa rats were shorter and lighter. Their bone osteoid surface and bone calcium content were similar to controls. Femora metaphysis in the obese had increased number of trabeculae, decreased trabecular width and higher erosion surface/bone surface ratio. Their diaphysis had increased cortical area/bone area and cortical width/bone width ratios and decreased medullary area. In summary, obese rats have higher iPTH, are hypercalciuric and have decreased bone mass. These last two observations differ from what is described in adult human obesity. Therefore, the obese fa/fa rat is of limited assistance in studies of bone status in adult human obesity. It might be of help in studies of bone metabolism in juvenile obesity.
 ...
PMID:Bone structure and calcium metabolism in obese Zucker rats. 131 32

To evaluate the effectiveness of highly purified glucomannan in childhood obesity a study has been carried out in 23 obese children (12 boys and 11 girls, aged 5.2-15.8 years), with excess weight of 51 +/- 16%, treated with 2-3 caps twice a day of glucomannan fibres (DICOMAN 5:2-3 gr/die), and in 30 obese children (aged 5-18 years) with excess weight of 51 +/- 10%, studied as controls. After a three-days food recall, a balanced diet with adequate caloric intake was provided to all obese children. In all patients before and 2-4 months after the auxological data (weight, height, weight excess) and laboratory data (serum levels of cholesterol, HDL, triglycerides, glucose, fructosamine, glycosylated hemoglobin, RBC, WBC, hemoglobin, iron, calcium, Cu and Zn) have been determined. Excess weight and triglycerides levels were significantly decreased in treated obese patients than in obese controls 4 months after the beginning of the study. A decrease of cholesterol levels was also observed in treated obese patients, but not in controls, whereas serum iron, calcium, copper and zinc persisted unchanged. No important side-effects were observed in treated patients. On the basis of our results highly purified glucomannan fibres may be employed with effectiveness in obese and dyslipidemic children together with diet.
 ...
PMID:[The use of highly purified glucomannan-based fibers in childhood obesity]. 132 83

To investigate the alterations in insulin secretion induced by aging, 2-month-old, 12-month-old, and 12-month old lean rats (submitted to a caloric restriction during the last month that causes a weight loss of approximately 20%) were studied. As expected, glucose intolerance and increased insulin response were observed during IV-GTT in 12-month-old rats. These effects were, however, reversed by weight loss. Insulin secretion was investigated in isolated islets both during static incubation and perifusion. In 12-month-old rats insulin secretion and 45Ca2+ efflux were lower only in the second phase of the hormonal secretion, suggesting an involvement of voltage-sensitive calcium channels in these phenomena. Considering that in vivo and in vitro alterations were reversed after weight loss, it is possible to conclude that obesity is probably a major cause of impaired insulin secretion in 12-month-old albino rats. Since 14C-glucose metabolism was not changed in islets from aged rats, the effect of obesity on insulin secretion is not due to altered glucose metabolism in pancreatic B-cells.
 ...
PMID:Obesity is the major cause of alterations in insulin secretion and calcium fluxes by isolated islets from aged rats. 132 24

The possible relationships between altered brain serotonin and calmodulin contents on the development of obesity were studied. Eight groups of mice separated by differences in phenotype, sex and age were used in this study. The brain contents of tryptophan, serotonin, 5-hydroxyindoleacetic acid (5-HIAA) and calmodulin were assayed. The contents of brain tryptophan showed no significant differences in any of the mice. The amount of brain serotonin in obese mice was 82% higher than that in their lean counterparts at four weeks of age, but only 11% higher at eight weeks of age. Regardless of age and sex, brain serotonin was positively correlated to the brain calmodulin in the lean mice (r = 0.559, p < 0.01), yet this was not found in obese mice. There was a strong positive correlation between serotonin and 5-HIAA in all mice (r = 0.679, p < 0.001). The elevated amount of serotonin in the brain of four-week-old obese mice is suggested to have important effects on thermoregulation in young genetically obese mice. The results also suggest that abnormal brain serotonin synthesis in obese mouse regulated by calmodulin might interact with certain factors, such as calcium ions, to complete the activation of serotonin-synthesized enzymes in the development of obesity.
 ...
PMID:Relationship between brain serotonin and calmodulin in young, genetically obese (ob/ob) mice. 136 Feb 91

The results of the study have shown that the nutrition of rural population is characterized by excessive consumption of bread and baked products, by high content of phosphorus, magnesium and iron, low content of animal proteins, vegetable oils, calcium, vitamins A, ascorbic acid and riboflavin. The incidence of cardiovascular, respiratory and alimentary diseases in this group of population was rather high. The nutrition of students is characterized by excessive consumption of polysaccharides, vegetable oils, thiamine, niacin, ascorbic acid (in winter-spring period), and calcium. Diseases associated with nutrition disorders (obesity, hepatitis, cholecystitis, colitis) are most often recorded in this group of population.
 ...
PMID:[Actual nutrition and health of several groups of rural and urban population of the Republic of Georgia]. 138 91

We have investigated the cellular basis for the clinical and epidemiologic linkage of hypertension, left ventricular hypertrophy (LVH), obesity, and non-insulin-dependent diabetes mellitus (NIDDM) and have studied cytosolic free calcium and free magnesium levels in these syndromes. Specifically, intracellular free calcium is elevated and free magnesium is deficient in hypertension, and both are related (directly and inversely, respectively) to the ambient level of blood pressure, to LV mass index (and thus to the degree of cardiac hypertrophy), and to the hyperinsulinemia and insulin resistance of essential hypertension. Dynamically, the ability of dietary salt loading to elevate blood pressure corresponds to its ability to elevate cytosolic free calcium and reciprocally to suppress free magnesium levels. Conversely, the ability of calcium channel blockade to reverse salt-induced hypertension is related to its ability to prevent these transmembrane ionic effects. Higher steady-state free calcium or lower free magnesium, or both, are also observed in clinical states linked to hypertension, such as obesity and NIDDM. Oral glucose loading in normal subjects itself elevates free calcium and suppresses free magnesium levels, as does hyperglycemia in vitro. These data suggest an ionic hypothesis of cardiovascular and metabolic disease, in which a generalized defect in cell ion handling is present in all tissues, resulting in higher steady-state free calcium and lower free magnesium levels. In pancreatic beta cells, this would produce hyperinsulinemia; in fat and skeletal muscle, cause peripheral insulin resistance; and in renal tissue, increase proximal sodium resorption and increase urinary calcium excretion--all features of essential hypertension. In vascular smooth muscle, high cytosolic free calcium would increase smooth muscle tone and cause vasoconstriction, and in heart muscle, independent of blood pressure, would increase contractility and predispose to LVH. Therefore, what may appear clinically to be the separate syndromes of hypertension, obesity, and NIDDM may pathophysiologically be different manifestations of the same underlying cellular defect, thus explaining their frequent clinical coexistence. Therapeutically, reversal of this excess free calcium accumulation and/or free magnesium deficit with ion-specific agents, such as calcium channel blocking drugs, may thus ameliorate not only the elevated blood pressure of hypertension but also the concurrent excess morbidity and mortality of the concurrent cardiac, vascular, and metabolic aspects of the hypertensive state.
 ...
PMID:Cellular calcium and magnesium metabolism in the pathophysiology and treatment of hypertension and related metabolic disorders. 138 62


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>