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

161 cases of simple obesity with or without hyperlipemia were treated by pellet pressure on auricular acupoints plus body acupuncture for 3 months in a single-blind experiment. Patients on Capsulae Olei Oenothera Erythrosepalae were taken as positive controls. Body weight, circumference of chest, abdomen, arms and legs, the appetite, sleep, bowel movement, blood TC, TG and HDL-C were recorded for comparison. The results indicated that treatment in the auricular and body acupoint group was superior to treatment in the control group. In the acupoint group body weight dropped by an average of 5.04 kg in 84.55% of the patients, who also showed decreased appetite, blood TC and TG.
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PMID:Simple obesity and obesity hyperlipemia treated with otoacupoint pellet pressure and body acupuncture. 850 54

The existence of mice (ob/ob mice) with a genetic defect causing obesity and type II diabetes has been known since 1950. The mutated ob gene was recently identified and characterized. The gene encodes a 167 amino acid protein that has been given the name leptin, from the greek word leptos, meaning thin. The functionally active hormone, which is synthesised and secreted by adipocytes, is lacking in homozygote ob/ob mice, causing an increase in body fat. Injection of recombinant leptin in ob/ob mice induces loss of fat due to decreased appetite and increased energy expenditure. The ob gene product leptin acts via binding sites in the hypothalamus, where the centre for appetite and satiety is located. Research is now focused on the identification, characterization and cloning of leptin-receptors. Other mice, also with a genetic defect causing obesity and type II diabetes, do not respond to leptin treatment and are therefore suspected to have defective leptin receptors.
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PMID:[The hormone leptin reduces body weight. A mutant gene makes the mouse obese]. 865 79

To study the effects of maternal nutritional status on lactational performance, the diets of laboratory rats were manipulated with food restriction or increases in fat concentration. Compared with rats fed control diets ad libitum, conception rate, milk production and litter growth decreased and milk fat concentration increased in both chronically food restricted and obese animals. Chronically food restricted rats mobilized body fat and reduced their energy expenditure for maintenance and activity. Differences in suckling pattern between control and food-restricted rats affected hormone concentrations important for successful lactation. Obese rats experienced greater difficulty than controls in delivering their pups and more of their pups died in the first days of life. Milk production among obese rats may be constrained by poor appetite and the high heat production that characterizes lactation in litter-bearing species. There are many parallels as well as important differences between results obtained from these models and findings in nursing women. Nevertheless, these models provide useful information about the possible mechanisms by which maternal nutritional status affects lactational performance.
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PMID:Effects of under- and overnutrition on lactation in laboratory rats. 947 33

The regulation of appetite relies on complex hypothalamic neurocircuitry of which the arcuate nucleus, and the hormone leptin play important roles. Arcuate nucleus neurones are essential for the regulation of eating behaviour, but they can be intoxicated by elevated serum levels of the amino acid glutamate (GLU). Neurotoxic effects of GLU are mediated by the N-methyl-D-aspartate receptor (NMDA-R). But the neurotoxic effects of GLU can be prevented. Concurrent administration of dizocilpine maleate (MK-801), a selective and highly potent non-competitive NMDA-R antagonist, antagonises GLU-gated Ca2+ ion channels and completely prevents the adverse effects of GLU. Also the non-competitive NMDA-R antagonist memantine displays neuroprotective properties. In view of a previously published hypothesis that human obesity results from chronic over-consumption of GLU, we performed a therapeutic trial in five obese, but otherwise healthy women. Memantine treatment markedly decreased appetite within few hours and complete suppressed the binge-eating disorder within 24 h. Body weight decreased markedly within a few days. The findings strongly support the hypothesis that elevated levels of nutritional GLU play an important role in the pathomechanism of human obesity. We suggest to treat human obesity by protecting the hypothalamic signalling cascade of leptin action with low to moderate affinity, non-competitive NMDA-R antagonists that selectively block the GLU-gated Ca2+ ion channels.
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PMID:A new anti-obesity drug treatment: first clinical evidence that, antagonising glutamate-gated Ca2+ ion channels with memantine normalises binge-eating disorders. 1588 75

Recently developed therapeutics for obesity, targeted against cannabinoid receptors, result in decreased appetite and sustained weight loss. Prior studies have demonstrated CB1 receptors (CB1Rs) and leptin modulation of cannabinoid synthesis in hypothalamic neurons. Here, we show that depolarization of perifornical lateral hypothalamus (LH) neurons elicits a CB1R-mediated suppression of inhibition in local circuits thought to be involved in appetite and "natural reward." The depolarization-induced decrease in inhibitory tone to LH neurons is blocked by leptin. Leptin inhibits voltage-gated calcium channels in LH neurons via the activation of janus kinase 2 (JAK2) and of mitogen-activated protein kinase (MAPK). Leptin-deficient mice are characterized by both an increase in steady-state voltage-gated calcium currents in LH neurons and a CB1R-mediated depolarization-induced suppression of inhibition that is 6-fold longer than that in littermate controls. Our data provide direct electrophysiological support for the involvement of endocannabinoids and leptin as modulators of hypothalamic circuits underlying motivational aspects of feeding behavior.
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PMID:Integration of endocannabinoid and leptin signaling in an appetite-related neural circuit. 1636 7

Phendimetrazine tartrate is a newer drug that acts as a central stimulant and indirectly acting sympathomimetic with a host of uses similar to the class amphetamines. Its main use is as an anorectic in the short-term treatment of obesity, although stimulants are no longer indicated for this purpose. This drug appeals to the younger American population for immediate weight loss through decreased appetite and early satiety. The European Union markets have already withdrawn this medication as well as other countries, but phendimetrazine is still used within the United States. Rhabdomyolysis is a potentially life-threatening complication reported with higher doses of amphetamines. We present a case of rhabdomyolysis and myoglobinuria developing in a 23-year-old patient after oral administration of phendimetrazine tartrate for 3 days in suggested therapeutic doses. The medication was taken for short-term treatment of obesity, and patient did not have any predisposing factors to precipitate rhabdomyolysis. Rhabdomyolysis resolved within 5 days. To our knowledge, this is the first reported case of rhabdomyolysis from administration of therapeutic amounts of phendimetrazine tartrate. The purpose of this case report is to create an awareness among physicians about the potentially life-threatening complications associated with phendimetrazine use as an anorectic even in suggested therapeutic doses as was the case in our patient. Additional awareness is needed to educate their patients about the side effects associated with these drugs and to strongly discourage their unsupervised use.
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PMID:Rare case of rhabdomyolysis with therapeutic doses of phendimetrazine tartrate. 1664 36

Ghrelin has been implicated in the control of food intake and in the long-term regulation of body weight. We theorize that preventing the ability of ghrelin to interact with its receptors, would eventually lead to decreased appetite and thereby decrease body weight gain. To test our hypothesis, pigs were actively immunized against ghrelin. Ghrelin((1-10)) was conjugated to BSA and emulsified in Freund's incomplete adjuvant and diethylaminoethyl-dextran. Primary immunization was given at 19 weeks of age (WOA), with booster immunizations given 20 and 40 days after primary immunization. Body weight (BW) and plasma samples were collected weekly beginning at 19 WOA, and feed intake was measured daily. Fourteen days after primary immunization, the percentage of bound (125)I-ghrelin in plasma from immunized pigs was increased compared with control animals (P<0.001). Voluntary feed intake was decreased more than 15% in animals that were actively immunized against ghrelin compared with controls. By the end of the experiment, immunized pigs weighed 10% less than control animals (P<0.1). Concentrations of GH were increased (P<0.05) in immunized pigs. Apoptosis was not observed in post-mortem samples obtained from the fundic region of the stomach. Our observations suggest that immunization against ghrelin induces mild anorexia. This procedure could potentially be used as a treatment to control caloric intake and obesity.
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PMID:Active immunization against ghrelin decreases weight gain and alters plasma concentrations of growth hormone in growing pigs. 1679 35

Energy homeostasis and fuel metabolism undergo significant modifications in the course of ageing. During the second half of life many humans increase their body mass and develop glucose intolerance that may lead to obesity and type 2 diabetes. However, many old people suffer from being underweight, and this "anorexia of elderly" may seriously compromise their health under certain circumstances. Experimental studies into the causes of ageing-related impairments of food intake regulation were performed mainly on rat, and to some extent, on non-human primates. It was found that the expression of NPY, the most potent orexigenic peptide, and of NPY receptors, is highly suppressed in the hypothalamus of old rats. Moreover, the increase of NPY mRNA after fasting was severely blunted in old as compared to young rats. Similar reductions, although of lower magnitude, were reported for other hypothalamic orexigenic compounds such as, AgRP and orexins. Interestingly, ageing does not significantly alter hypothalamic mRNA levels of important anorexigens such as CART and aMSH. The presented findings suggest that, at least in rodents, ageing is associated with the general down-regulation of hypothalamic peptides that stimulate food intake and unchanged expression of anorexigenic peptides. This situation may be responsible for the decreased appetite drive in senescent animals and loss of weight at the end-of-life period. If similar changes of the central control of food intake underly "anorexia of ageing" observed in some elderly, it is possible that therapeutic intervention at this regulatory level may be possible in the future.
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PMID:Central regulation of food intake in ageing. 1722 84

Taranabant is a novel cannabinoid CB-1 receptor (CB1R) inverse agonist in clinical development for the treatment of obesity. This double-blind, randomized, placebo-controlled, single oral dose study evaluated the safety, tolerability, pharmacokinetics, and pharmacodynamics of taranabant (0.5-600 mg) in 24 healthy male volunteers. Single-dose AUC(0-infinity) and C(max) values for taranabant increased approximately linearly with dose up to 200 mg, with slightly less than dose-proportional increases in AUC(0-infinity) and C(max) values for doses >200 mg. Plasma taranabant had a biphasic disposition, with a median t(max) of 1 to 2.5 hours and a terminal elimination t((1/2)) of 38 to 69 hours. Coadministration of taranabant with a high-fat meal led to a 14% increase in C(max) and a 74% increase in AUC(0-infinity). Clinical adverse experiences associated with single doses of taranabant were generally mild and transient. Of the 198 clinical adverse experiences reported, the most common drug-related ones were nausea (36), headache (22), drowsiness (14), abdominal discomfort/abdominal pain/stomachache (14), hiccups (9), dizziness (8), decreased appetite (7), increased bowel movement (7), mood change (6), tiredness (4), vomiting (4), and sweating increased (4). Taranabant has pharmacokinetic characteristics suitable for a once-daily dosing regimen.
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PMID:Safety, tolerability, pharmacokinetics, and pharmacodynamic properties of taranabant, a novel selective cannabinoid-1 receptor inverse agonist, for the treatment of obesity: results from a double-blind, placebo-controlled, single oral dose study in healthy volunteers. 1825 50

The prevalence of pediatric obstructive sleep apnea syndrome (OSAS) is approximately 3% in children. Adenotonsillar hypertrophy is the most common cause of OSAS in children, and obesity, hypotonic neuromuscular diseases, and craniofacial anomalies are other major risk factors. Snoring is the most common presenting complaint in children with OSAS, but the clinical presentation varies according to age. Agitated sleep with frequent postural changes, excessive sweating, or abnormal sleep positions such as hyperextension of neck or abnormal prone position may suggest a sleep-disordered breathing. Night terror, sleepwalking, and enuresis are frequently associated, during slow-wave sleep, with sleep-disordered breathing. Excessive daytime sleepiness becomes apparent in older children, whereas hyperactivity or inattention is usually predominant in younger children. Morning headache and poor appetite may also be present. As the cortical arousal threshold is higher in children, arousals are not easily developed and their sleep architectures are usually more conserved than those of adults. Untreated OSAS in children may result in various problems such as cognitive deficits, attention deficit/hyperactivity disorder, poor academic achievement, and emotional instability. Mild pulmonary hypertension is not uncommon. Rarely, cardiovascular complications such as cor pulmonale, heart failure, and systemic hypertension may develop in untreated cases. Failure to thrive and delayed development are serious problems in younger children with OSAS. Diagnosis of pediatric OSAS should be based on snoring, relevant history of sleep disruption, findings of any narrow or collapsible portions of upper airway, and confirmed by polysomnography. Early diagnosis of pediatric OSAS is critical to prevent complications with appropriate interventions.
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PMID:Obstructive sleep apnea syndrome in children: Epidemiology, pathophysiology, diagnosis and sequelae. 2118 56


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