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cocaine/lihavuus

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Sivu 1 alkaen 349 tuloksia

Cocaine and desipramine elicit distinct striatal noradrenergic and behavioral responses in selectively bred obesity-resistant and obesity-prone rats.

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Previous studies have demonstrated a role for norepinephrine (NE) in energy regulation and feeding, and basal differences have been observed in hypothalamic NE systems in obesity-prone vs. obesity-resistant rats. Differences in the function of brain reward circuits, including in the nucleus

Pre-existing differences in motivation for food and sensitivity to cocaine-induced locomotion in obesity-prone rats.

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Obesity is a significant problem in the United States, with roughly one third of adults having a body mass index (BMI) over thirty. Recent evidence from human studies suggests that pre-existing differences in the function of mesolimbic circuits that mediate motivational processes may promote obesity

Cocaine abuse and sleep apnea in severe obesity.

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Obesity is a cause of sleep breathing disorders that result in excessive daytime sleepiness. We describe the adaptive strategy used by an obese person who started to snort cocaine to remedy incoercible drowsiness affecting his working financial skills. Clinical workup documented severe sleep apnea,

Treating Cocaine Addiction, Obesity, and Emotional Disorders by Viral Gene Transfer of Butyrylcholinesterase.

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Butyrylcholinesterase (BChE), a plasma enzyme that hydrolyses the neurotransmitter, acetylcholine relatively well, with far lower efficiency than acetylcholinesterase (AChE) but with the capability to degrade a broad range of bioactive esters. AChE is universally understood as essential to

Potential anti-obesity effects of a long-acting cocaine hydrolase.

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A long-acting cocaine hydrolase, known as CocH3-Fc(M3), engineered from human butyrylcholinesterase (BChE) was tested, in this study, for its potential anti-obesity effects. Mice on a high-fat diet gained significantly less body weight when treated weekly with 1 mg/kg CocH3-Fc(M3) compared to

Cocaine and amphetamine regulated transcript and brain-derived neurotrophic factor in morbid obesity. One-year follow-up after gastric bypass.

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BACKGROUND The identification of biomarkers associated with obesity and response to treatment could represent an important advance to design more effective and personalized therapeutic strategies. The complexity of morbid obesity could be explained as the combination of genetic, biochemical,

Cocaine- and amphetamine-regulated transcript peptide immunoreactivity in the brain of the CCK-1 receptor deficient obese OLETF rat.

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Cocaine- and amphetamine-regulated transcript (CART) peptide is expressed in brain areas involved in homeostatic regulation and reward. CART has been shown to reduce food intake, but the underlying mechanisms and the relevance of this effect on obesity yet remain unknown. Therefore, we used

Sequence variants in the human cocaine and amphetamine-regulated transcript (CART) gene in subjects with early onset obesity.

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OBJECTIVE The cocaine and amphetamine-regulated transcript (CART) is expressed in the brain of rodents and humans, and intracerebroventricular injection of the peptide in rats reduces food intake. The objective of the present study was to chromosomally map the CART gene and to examine the coding

Cocaine and amphetamine-regulated transcript mRNA regulation in the hypothalamus in lean and obese rodents.

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Cocaine and amphetamine-regulated transcript (CART) mRNA and immunoreactivity are expressed abundantly in the hypothalamus. Central administration of various fragments of this neuropeptide decreases food intake in rodents. To find out whether CART might play a role in the physiological regulation of

Comparison of cocaine reinforcement in lean and obese Zucker rats: Relative potency and reinstatement of extinguished operant responding.

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Evidence indicates that obese individuals exhibit alterations in brain-reward function that are anatomically and functionally similar to what has been observed in drug addicts, which could theoretically make obese individuals vulnerable to drug abuse and drug abusers vulnerable to overeating.
Monosodium glutamate (MSG) treatment of neonatal mice results in a selective damage to the arcuate nucleus (ARC) and development of obesity with increased adiposity at sustained body weight in the adulthood. Feeding pattern of the MSG obese mice is unusual. Our previous results showed that after
OBJECTIVE We tested the hypothesis that polymorphisms in the cocaine- and amphetamine-regulated-transcript (CART) gene is associated with the development of obesity. METHODS Five-hundred and twenty-eight subjects (325 men and 203 women) aged 49.6+/-11.0 y with body mass index (BMI) of
Nesfatin-1, processed from nucleobindin-2 (NUCB2), is a potent anorexigenic peptide being expressed in rodent hypothalamic nuclei and involved in the regulation of feeding behavior and body weight in animals. The present study aimed to investigate NUCB2/nesfatin-1 protein expression in
Epidemiologic studies show that cocaine- and amphetamine-regulated transcript prepropeptide (CARTPT) gene polymorphism modifies diet-obesity relationships. However, the interaction between CARTPT gene polymorphism and diet quality indices have not been investigated yet. The current

Chronic central infusion of cocaine- and amphetamine-regulated transcript (CART 55-102): effects on body weight homeostasis in lean and high-fat-fed obese rats.

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BACKGROUND Cocaine- and amphetamine-regulated transcript (CART) is expressed within hypothalamic nuclei implicated in the regulation of feeding behaviour. It is up-regulated by leptin, and CART-derived peptides acutely inhibit food intake. OBJECTIVE The present study was designed to assess the
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