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

3 cases of retinal thrombosis in young patients on oral contraception (OC) are presented. Pathology disappeared completely as soon as the patients changed contraceptive method. Retinal thrombosis can be arterial or venous, but the incidence is not clear. The major complication with treatment with OC is cerebrovascular thrombosis, which also could be arterial or, more rarely, venous. The mechanisms causing such effects are not completely clear; it is known that OC increases hypercoagulability in 25-30% of women on OC, and that it diminishes the antithrombin 111 factor. Risk factors, such as familiar antecedents of thrombosis, phlebitis, obesity, arterial hypertension, smoking, age over 40, are all strong contraindications to OC. The authors also report on the abundant literature on this subject.
Bull Mem Soc Fr Ophtalmol 1978
PMID:[Neuro-ophthalmologic accidents caused by hormonal contraception]. 75 8

The insulin resistance of animal models of obesity (the gold thioglucose obese mouse and the o b/o b mouse) is characterized by several abnormalities. At the receptor step, both the binding function (decreased number of sites) and the enzymatic, tyrosine kinase function (decreased insulin activation) are altered. At postreceptor steps, phosphatidylinositol 3-kinase (PI3-K) plays an important role in insulin signalling, particularly for the stimulation of glucose transport in muscle and adipocyte. Insulin activation of PI3-K is markedly diminished in obese mice; starving the obese animals restores normal responses of PI3-K, glucose transport, and glycogen synthesis, to insulin. These observations emphasize the multi-site, and largely reversible, nature of insulin resistance in these animal models of obesity. Similar alterations have been reported in the literature with regard to the sites of insulin resistance in human obesity and non insulin-dependent diabetes.
Bull Mem Acad R Med Belg 1996
PMID:[Insulin resistance: lessons from animal models of obesity]. 922 Oct 53

Non-insulin-dependent (or type 2) diabetes mellitus is a common, underdiagnosed and growing disease in our society. It is responsible for increased morbidity and mortality and represents an important public health problem. This polygenic disease is often expressed late in life and its evolution is accelerated by environmental factors leading to obesity. It combines defects in both insulin secretion and insulin action, and such defects are present in various proportions according to the type of patient and the stage of the disease. Diet and physical activity recommendations are the basis of the treatment. Current pharmacological approaches aim at improving insulin secretion and/or insulin cellular action. After secondary failure to oral drugs, insulin therapy should be initiated, the patient becoming "insulin-requiring". A synergy should be searched in the combination of various therapeutic modalities in order to improve the glycaemic control.
Bull Mem Acad R Med Belg 1996
PMID:[Non-insulin-dependent diabetes: from physiopathology to treatment]. 922 Oct 54

The hypothalamic disorders of obesity include hyperphagia, a low central orthosympathetic tone (with reduced thermogenesis), vagal hyperinsulinism, low serotonin efficacy, a hyperactive hypothalamo-hypophyseal-adrenal axis, a hypoactive GHRH-GH-IGF axis and hypogonadism of central origin. Hyperlipogenesis, glucose intolerance and excessive gluconeogenesis are secondary features. Most frequently the hypothalamic ARC reacts poorly to the leptin hypersecreted by adipose tissue, so that the local synthesis of NPY is unchecked. Fortunately, two prostaglandins derived from dietary arachidonic acid bind fat cell PPAR gamma and hepatic PPAR alpha. Both nuclear proteins are phosphorylated through an insulin pathway, thereby inhibiting the expression of genes favoring obesity and stimulating that of genes accelerating fatty acid oxidation. The array of dietetic and pharmacologic tools considered today is analyzed.
Bull Mem Acad R Med Belg 1997
PMID:[Molecular endocrinology of hereditary obesity]. 949 39

The characterization in 1989 of the gene encoding the beta 3-adrenoceptor helped to interpret the results of pharmacological experiments on atypical effects of catecholamines distinct from the classical activation of beta 1 and beta 2 adrenoceptors. In rodents, the beta 3 adrenoceptor is abundantly expressed in white adipose tissue where energy is stored in the form of triglycerides and in brown adipose tissue that is specialized for thermogenesis. Treatment of rodents with beta 3 adrenoceptor agonists induces a weight loss related to the stimulation of lipolysis in the two types of tissues. These results led to propose the use of these agonists for the treatment of human obesity and NIDDM. However, the poor lipolytic effect of these agonists in human adipose tissue and the recent discovery of functional beta 3 adrenoceptors in the human heart raise new questions on the therapeutic use of beta 3-adrenoceptor agonists in man. In the human ventricle, these agonists induce a negative inotropic effect. In vessels, stimulation of beta 3-adrenoceptors produces a vasodilation. If these effects are conserved in the failing heart, they could shed a new light on the pathogenic role of the hyperadrenergism associated with cardiac failure, as well as on its treatment with beta-adrenoceptor blockers.
Bull Mem Acad R Med Belg 2000
PMID:[Beta 3 adrenergic receptor: physiologic role and potential therapeutic applications]. 1138 23

The risk of becoming obese is higher in some families than in others. The risk (the lambda coefficient) is two to three fold for moderate obesity, but up to five to eight fold for severe obesity. Several genes exhibit mutations that can cause early onset severe obesity. These mutations are rare and account for only a small fraction of the cases of obesity. At this time, more than fifty genes have been shown in various studies to influence the energy balance, nutrient partitioning, or the age of onset of obesity. The results of these studies are generally disappointing and often contradictory. One approach is to scan the genome with a high number of polymorphic markers to identify chromosomal regions harboring genes implicated in the development of obesity. Such studies can be helpful in defining new targets to explore.
Bull Mem Acad R Med Belg 2001
PMID:The genetics of human obesity: recent progress. 1237 Dec 66

Obesity results from an imbalance between energy intake and energy expenditure. Human studies indicate that obese individuals have an increased basal metabolic rate secondary to an increased fat-free mass. A blunted dietary thermogenesis is observed but is not of sufficient magnitude to lead to a major weight gain. Indirect evidence suggests that physical activity may be low in obese individuals. In healthy lean subjects, overfeeding leads to a stimulation of spontaneous physical activity. The ensuing increase in energy expenditure may play a role in the prevention of weight gain. This response, however, shows a high interindividual variability. There is overall little evidence that major alterations of energy expenditure are present in obese individuals. It is likely that an alteration of mechanisms of food intake control plays a prominent role in the pathogenesis of this disease.
Bull Mem Acad R Med Belg 2001
PMID:[Physiopathology of obesity]. 1237 Dec 67

Obesity is now recognized as a chronic disease. Its treatment implies a prolonged negative energy balance, by reducing caloric intake and/or increasing energy expenditure. In practice, three therapeutic approaches can be considered: 1) life-style modifications, combining well-balanced hypocaloric diet and regular physical exercise, the key-issue in obesity management; 2) in case of failure and as adjunct treatment, anti-obesity drugs, especially orlistat, an intestinal lipase inhibitor, and sibutramine, a central appetite regulator; and 3) in patients with extreme refractory obesity, surgical procedures consisting of gastric restriction (gastroplasty) or intestinal bypass. Anti-obesity treatments must be evaluated in the long run, in terms of efficacy/safety ratio, upon criteria of weight loss, reduction in associated risk factors, improvement of quality of life and, if possible, reduction of morbidity and mortality.
Bull Mem Acad R Med Belg 2001
PMID:[Obesity: therapeutic aspects]. 1237 Dec 68

The db/db mouse has defective leptin receptors. The defects lead to impairments of leptin regulation of food intake and body weight, and result in the expression of diabetic symptoms such as hyperinsulinemia, hyperglicemia, and extreme obesity. Recent studies have proposed that leptin may also affect memory and learning processes. To examine this possibility, we compared the ability of leptin-receptor-deficient db/db mice and their normal lean litter mates to form and extinguish a conditioned taste aversion (CTA) for saccharin. We used a short-term (10 s) lick test and a long-term (48 h) two bottle preference test for measurement of consumption of test solutions. On the first day after conditioning to avoid saccharin, the db/db mice showed preference scores for saccharin as low, and aversion thresholds for sucrose lower than that of the lean mice. During the extinction test trials beginning from the second up to the 30th day after conditioning, numbers of licks and preference scores for aversive saccharin and sucrose appeared to be larger, and recovered faster to the control levels in db/db mice. These results indicate that db/db mice with leptin-receptor-deficiency may show equal capacity to form CTAs for saccharin, greater generalization from saccharin to sucrose, and a faster rate of extinction. This suggests that disruption of leptin signalling does not inhibit acquisition of CTA learning, but impairs its extinction. This differential contribution of the leptin system on CTA processes may be due to differential distribution of leptin receptors in the CTA-related brain areas.
Neurobiol Learn Mem 2003 Sep
PMID:Conditioned taste aversion learning in leptin-receptor-deficient db/db mice. 1293 25

We have investigated the neurochemical mechanisms of memory reconsolidation and, in particular, the functional requirement for intracellular mechanisms initiated by beta-adrenergic signaling. We show that propranolol, given in conjunction with a memory reactivation session, can specifically disrupt the conditioned reinforcing properties of a previously appetitively reinforced conditioned stimulus (CS), whether the stimulus had been associated with self-administered cocaine or with sucrose. These data show that memories for both drug and nondrug CS-US associations are dependent on beta-adrenergic receptor-mediated signaling for their reconsolidation, with implications for the potential development of a novel treatment for drug addiction and some forms of obesity.
Learn Mem 2008 Feb
PMID:Reconsolidation of appetitive memories for both natural and drug reinforcement is dependent on {beta}-adrenergic receptors. 1823 9


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