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 advent of SAL (suction-assisted lipectomy) has dramatically increased the number of obese patients coming to our consultation offices. Despite several articles suggesting a conservative approach to fat suction, some reports insinuate that SAL might be a useful tool for obesity treatment. This hypothesis is refuted by a vast body of evidence that concludes that the adipose tissue may regenerate in adult humans. Therefore, surgical procedures are not advised as the method of choice to manage the disease. On the other hand, the terms obesity and being overweight may not be interchangeable. Obesity may be a disease whereas being overweight is a sign of the disease. Consequently, proper preoperative selection of candidates for SAL becomes mandatory. The hCG (human chorionic gonadotropin) method for obesity treatment appears to be a complete program for the management of obesity. It contains pharmacologic, dietetic, and behavior modification aspects in a 40-day course of treatment. Some data suggest hCG to be lipolytic, thus explaining former clinical observations regarding body fat redistribution in treated patients. hCG commercial preparations contain beta-endorphin, an opioid peptide linked to mood behavior. This article speculates on the possible actions of the complex hCG beta-endorphin in the neuromodulation of mood and energy metabolism. The method comprises a behavior modification that helps in handling the patient better. There are some correlations between a current behavior modification program and the basic guidelines contained in the hCG protocol. Thus, the hCG method appears to be a reasonable alternative in the management of a long-standing, unsolved problem of human metabolism.
 ...
PMID:Controversies in plastic surgery: suction-assisted lipectomy (SAL) and the hCG (human chorionic gonadotropin) protocol for obesity treatment. 331 9

Relatively few studies of humans have evaluated the effects of opioids on food intake and body weight. Most have focused on the potential role of opioids in the etiology of obesity. Measurements of endogenous opioids in plasma or spinal fluid of humans reveal higher levels, particularly of beta-endorphin, in obese subjects. Opioid agonists such as methadone and butorphanol tartrate stimulate food intake, and all studies with naloxone, an opioid antagonist, demonstrate a reduction of short-term food intake in obese or lean humans. Long-term studies with naltrexone, an antagonist similar to naloxone, show no effect on food intake or body weight. Opioid agonists or antagonists have little effect on nutrient selection in humans. The effects on feeding-related hormones is equivocal. Further studies with more specific opioid receptor activities are needed.
 ...
PMID:Opioid regulation of food intake and body weight in humans. 354 77

There is increasing evidence that peptides in the brain are important in the control of food intake. Administration of opioid and CCK peptides have elicited hunger and satiety, respectively. To evaluate the interaction of these peptides and their role in the central nervous system, concentrations of met-enkephalin were measured in the hypothalamus of rats following peripheral administration of CCK; in addition, effects of feeding and fasting and obesity were studied. In CCK- vs. saline-injected rats met-enkephalin concentrations were decreased in the paraventricular nucleus (PVN), suprachiasmatic nucleus (SC), supraoptic nucleus (SON), dorsomedial hypothalamus (DMH) and ventromedial hypothalamus (VMH). In fed compared with fasted rats met-enkephalin concentrations were higher in the anterior hypothalamus (AH) and lower in the SC; in obese compared with lean rats, concentrations were higher in the AH, PVN, SC, SON, DMH, lateral hypothalamus and VMH. These results show that peripheral injections of CCK can decrease concentrations of met-enkephalin in the brain and suggest a mechanism by which these peptides may interact to influence behavior. In addition, the findings support the hypothesis that the hyperphagia which is typical of obese rats may be due to increased concentrations of met-enkephalin.
 ...
PMID:Changes in brain met-enkephalin concentrations with peripheral CCK injections in Zucker rats. 371 42

A study was made of change in hormone secretion in 243 patients with alimentary-constitutional and hypothalamic obesity. Activation of the somatostatin mechanism, a decrease in somatotropic and thyrotropic function of the hypophysis, an increment of corticotropin, beta-lipotropin and vasopressin levels in the blood, disturbance of circadian fluctuations of hormone secretion, an increase in insulin and C-peptide secretion, a decrease in glucagon secretion and triiodothyronine and cortisol levels in the blood, activation of the renin-aldosterone system and cortisol secretion rate were equally expressed both in alimentary-constitutional and primary hypothalamic obesity. The central mechanisms of the regulation of endocrine functions were incorporated in a pathological process even in alimentary-constitutional obesity. Disorders of the hypothalamic regulation lay in the basis of both types of obesity.
 ...
PMID:[Comparative evaluation of the hormonal changes in alimentaro-constitutional and hypothalamic obesity]. 395 72

The relationship of the endogenous opioid system and the hypothalamic-pituitary-adrenal axis to obesity was studied. Morning levels of plasma cortisol and beta-endorphin immunoreactivity in obese patients before diet treatment were found to be no different from those in matched family members of normal weight. In 32 untreated obese patients, no relationship between weight or body mass index (a measurement of obesity) and plasma levels of beta-endorphin immunoreactivity or cortisol was found. However, plasma cortisol levels were significantly correlated with obese patient ratings on the depression subscale of the General Health Questionnaire. Dexamethasone administration failed to suppress plasma beta-endorphin levels in untreated obese patients, but this finding has been reported in normal subjects in whom a similar assay methodology was used; it suppressed plasma cortisol levels in 29 of 32. The three patients resistant to suppression also suffered from benign essential hypertension. Plasma beta-endorphin immunoreactivity was unchanged, but cortisol levels significantly decreased as weight was lost on a 400-calorie/day modified protein fast. Patients who failed to complete the 6-month diet program had significantly increased plasma beta-endorphin levels compared to those who successfully completed the program.
 ...
PMID:Plasma cortisol and beta-endorphin immunoreactivity in human obesity. 609 83

Following the oral administration of 100 g of glucose, morbidly-obese subjects and non-obese controls demonstrated increased levels of plasma immunoreactive beta-endorphin. There was a slow rise in plasma immunoreactive beta-endorphin in the non-obese controls throughout the 3-h observation period. The obese subjects demonstrated a delayed and significantly greater rise of plasma immunoreactive beta-endorphin, when compared to the controls. These findings may have implications for further research in human obesity.
 ...
PMID:Plasma immunoreactive beta-endorphin response to glucose ingestion in human obesity. 609 96

Due to asymmetry of brain neurotransmitters and differential hemispheric information processing modes, it is suggested that the excessive use of one information processing mode could engender a state of brain reactivity whose neurochemical correlates would be either a rise in melatonin or beta-endorphin in systemic circulation. Since melatonin and beta-endorphin have opposite effects on lung-mediated regulation of prostaglandins, it is further suggested that the pulmonary inactivation of prostaglandin E1 would either be increased or inhibited. Low levels of PGE1 would engender high levels of PGE2 whose effects would explain the findings in schizophrenics of: 'reducing' pattern of visual evoked response, cerebral atrophy, and viral and autoimmune phenomena. The primacy of the disordered cognitive style in leading up to the immunological, biochemical and neuropathological processes is stressed. Implications of this model for understanding depression, anxiety and phobic disorders, autism, attention deficit disorder, obesity, alcoholism, smoking, drug addiction, sexual deviations, and certain psychosomatic and psychophysiological disorders are suggested.
 ...
PMID:How information processing mode could affect prostaglandin E1 metabolism and lung inactivation: relevance of hemispheric specialization, neurotransmitter asymmetry and brain reactivity. 614 17

Obese mice (C57BL/6J ob/ob) and their lean littermates were studied at various ages from immediately post weaning until 62 weeks of age, at which mortality increased markedly. Several age-related changes were noted. 1) Plasma glucose levels were elevated in obese mice 5-20 weeks and 62 weeks of age, but were similar to those in the lean mice at 20-60 weeks of age. Plasma insulin levels were elevated in obese mice, and there were no age-related differences. 2) Brain serotonin was elevated in obese mice at all ages and increased with age in both obese and lean animals. 3) Pituitary contents of ACTH and beta-endorphin were elevated in young obese mice and increased further as these mice approached their life expectancy. 4) The ratios of ACTH to beta-endorphin immunoreactivities were similar in obese and lean mice, except in obese mice over 50 weeks of age where this ratio was increased. We conclude that: 1) the obese mouse is characterized by hyperinsulinemia and hyperadrenocorticism throughout its life; 2) the insulin resistance of the obese mouse improves at 20 weeks of age, yet deteriorates as its life expectancy is approached; 3) the obese mouse has an elevated brain serotonin content similar to previously described elevations of the putative neurotransmitters dopamine and norepinephrine in these mice; and 4) as the obese mouse approaches its life expectancy, abnormalities may occur in the synthesis, processing, or secretion of ACTH and/or beta-endorphine.
 ...
PMID:A longitudinal hormonal profile of the genetically obese mouse. 624 69

The role of beta-endorphin in the development of several obesity syndromes was examined. Adult female hooded rats received ventromedial hypothalamic lesions, dorsolateral tegmental lesions, parasagittal hypothalamic knife cuts, intraventricular 5,7-dihydroxytryptamine, ovariectomy, control surgery, or were deprived to 75% of normal body weight. Dose-dependent suppression of food intake by the opiate antagonist naloxone (0.5, 1.8, 6.8, or 25.0 mg/kg, ip) was measured during once-daily 4-h food access periods. No difference was found among the groups at any dose. Pituitary beta-endorphinlike immunoreactivity (BELI) was substantially decreased in knife-cut rats, but was unaltered by other treatments. Obesity had no effect on BELI. In another experiment, rats made obese by prolonged maintenance on palatable foods had elevated pituitary BELI levels. Feeding mechanisms involving opioid peptides do not appear to be of etiological significance in the syndromes examined.
 ...
PMID:Pituitary beta-endorphin, naloxone, and feeding in several experimental obesities. 626 42

Naltrexone, an opiate antagonist, was administered to young obese (ob/ob) and lean mice for five weeks. Animals had continuous access to food and received 10 mg/kg SC twice daily with equivalent volumes of saline given to controls. The effects on body weight, and pituitary and plasma levels of beta-endorphin-like material were measured. Naltrexone-injected obese animals gained weight more slowly over the first three weeks while the weight gain of lean animals was not affected by naltrexone. Plasma levels of beta-endorphin were shown to be significantly higher in untreated ob/ob mice and this difference increased with age (4-20 weeks). With naltrexone treatment, plasma levels in +/? mice rose and exceeded those in ob/ob. Saline treatment appeared to be a stress, and pituitary beta-endorphins rose 4-6 fold in ob/ob compared with +/?. While naltrexone reduced the levels of ob/ob pituitary towards normal, no effect on beta-endorphin levels in pituitary of lean mice was obtained. In vitro studies of effects of the opiate antagonists, naloxone, on insulin secretion by isolated islets provided additional evidence of resistance of lean mice to naloxone relative to ob/ob. (IRI secretion fell only in naloxone treated ob/ob islets). These observations support the contention that this form of genetic obesity is characterized by elevated endogenous opiate levels and an increased sensitivity to opiate antagonists such as naltrexone or naloxone.
 ...
PMID:Naltrexone reduces weight gain, alters "beta-endorphin", and reduces insulin output from pancreatic islets of genetically obese mice. 627 40


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