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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypothalamic regulatory system of body weight which develops in rats during critical periods of early postnatal life seems to express plastic changes depending on nutrition at that time. Adult rats previously exposed to early postnatal overnutrition by raising them in small litters become persistently predisposed to overweight, hyperphagia and hyperleptinaemia. The hypothesis was raised that feeding-related peptides could be involved through altered effects on neuronal activity of the regulatory systems of such rats. This was studied on brain slices of small-litter rats and normal-weight controls between days 60 and 120 of life. Neurons of the medial parvocellular part of the paraventricular nucleus were significantly activated by the adiposity signals leptin, insulin and amylin in controls. This is a kind of negative feedback, because activation of these neurons is known to be followed in vivo by increased energy expenditure. GABAergic mechanisms seem to affect these neuronal responses because the activating effects of insulin and amylin were reduced in the presence of a GABA(A) receptor antagonist. In overweight small-litter rats, however, the neuronal responses to the adiposity signals were significantly changed; activating effects were reduced and inhibitory effects increased. By means of blockade of GABA(A) receptors, significant alterations in the neuronal responses to leptin, insulin and amylin in small-litter rats were prevented. Responses to the peptides were reversed and now resembled those of controls. In conclusion, changes in neuronal wiring with GABAergic interneurons seem to contribute to a persistently reduced negative feedback of adiposity signals in early postnatally overfed rats.
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PMID:GABAA receptor antagonists prevent abnormalities in leptin, insulin and amylin actions on paraventricular hypothalamic neurons of overweight rats. 1655 87

In this paper, we consider the control of energy balance in animals and man. We argue that patterns of mammalian feeding have evolved to control energy balance in uncertain environments. It is, therefore, expected that, under sedentary conditions in which the diet is rich in nutrients and abundantly available, animals and man will overeat. This suggests that no physiological defects are needed to induce overweight and ultimately obesity in man. Several considerations arise from these observations. The time period over which energy balance is controlled is far longer than allowed by most experiments. Physiological models of energy balance control often treat excess energy intake as a defect of regulation; ecological models view the same behaviour as part of normal energy balance control in environments where resources are uncertain. We apply these considerations to common patterns of human and animal feeding. We believe that the ecological perspective gives a more accurate explanation for the functionality of excess fat and the need to defend nutrient balance and avoid gross imbalances, as well as explaining hyperphagia in the face of plenty. By emphasising the common features of energy balance control in different mammalian species, the importance of changes in behaviour to accommodate changes in the environment becomes apparent. This also opens up possibilities for the control of body weight and the treatment of obesity in man.
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PMID:Control of energy balance in relation to energy intake and energy expenditure in animals and man: an ecological perspective. 1657 Nov 45

In our obesogenic environment, self-control might be necessary in order to prevent overeating. Impulsivity is supposed to make it more difficult to resist the temptation to eat too much and can thereby contribute to overweight. In the present study, the hypotheses is tested that obese individuals are more impulsive. Thirty-one obese and 28 lean women, sampled from the normal population, are tested on a behavioural measure and three self-report measures of impulsivity. The obese women appeared more impulsive on the last part of the behavioural task, but not on the self-report measures. Implications of the results are discussed.
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PMID:Impulsivity in obese women. 1678 31

Treatment for obesity is still running short, particularly on the long term. However, some people do take advantage of treatments and are able to retain their weight loss. What makes the difference between those who can keep their weight loss and those who cannot? One possible predictor of relapse in obesity treatment is impulsivity. Overall, obese people are found to be more impulsive than lean people, especially obese binge eaters. Intuitively, it would make sense that the most impulsive people are less able to keep control over eating behaviour. Therefore, impulsivity could serve as an obstacle for treatment. In the present study impulsivity was measured with a behavioural task (the stop signal task) in 26 obese children. Overweight of the children was measured before and after treatment and at 6 and 12 months follow ups. The results show that impulsivity was related to overweight at all moments: The most impulsive children were the most overweight ones; even after 12 months. Moreover, impulsivity predicted therapy success: the most impulsive children lost less weight. Impulsivity appears to contribute to the difference between succeeding or failing in attempts to lose weight.
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PMID:Impulsivity predicts treatment outcome in obese children. 1682 53

Obesity is a major global epidemic, with over 300 million obese people worldwide, and nearly 1 billion overweight adults. Being overweight carries significant health risks, reduced quality of life, and impaired socioeconomic success, with profound consequences for health expenditure. The most successful treatment for obesity is gastric bypass surgery, which acts in part by reducing appetite through alterations in gut hormones. Circulating gut hormones, secreted or suppressed after eating food, act in the brain, particularly the hypothalamus, to alter hunger and fullness. Stomach-derived ghrelin increases food intake even in those with anorexia from chronic illness, while pancreatic polypeptide (PP), intestinal peptide YY 3-36 (PYY), oxyntomodulin, and other hormones reduce food intake and appetite. While obese subjects have appropriate reductions in orexigenic ghrelin, other gut-hormone disturbances may contribute to obesity such as reduced anorexigenic PYY and PP. Prader-Willi syndrome (PWS) arises from the loss of paternally inherited genes on chromosome 15q11-13, leading to life-threatening insatiable hunger and obesity from early childhood, through developmental brain, particularly hypothalamic defects. The study of genetically homogenous causes of abnormal-feeding behavior helps our understanding of appetite regulation. PWS subjects have inappropriately elevated plasma ghrelin for their obesity, at least partly explained by preserved insulin sensitivity. It remains unproven if their hyperghrelinemia or other gut-hormone abnormalities contribute to the hyperphagia in PWS, in addition to brain defects. Postmortem human hypothalamic studies and generation of animal models of PWS can also provide insight into the pathophysiology of abnormal-feeding behavior. Changes in orexigenic NPY and AGRP hypothalamic neurons, or anorexigenic oxytocin neurons have been found in illness and PWS. Functional neuroimaging studies, using PET and fMRI, will also allow us to tease apart the hormonal and brain pathways responsible for controlling human appetite, and their defects in obesity.
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PMID:The hypothalamus, hormones, and hunger: alterations in human obesity and illness. 1687 68

Excessive weight gain is directly related to a positive energy balance which is due to both a decreased physical activity and overeating. Obesity prevalence is increasing since thirty years and the treatment of obesities is particularly necessary to solve this public health and economical problem. The receptors of numerous hypothalamic neuropeptides are potential targets for such drug treatments. Hormones of the gastro-intestinal tract or produced by the adipose tissue directly interact with these central pathways to regulate feeding behavior. The use of leptin, an adipose tissue hormone that inhibits food intake, has not been conclusive because of the development of leptin resistance in obese subjects. Similar disappointing results have been obtained with antagonists of neuropeptide Y (NPY), one of the most potent orexigenic peptide. This was linked to the complexity and redundancy of the circuits involved in feeding regulation. Consequently, a multitherapy targeting several pathways simultaneously is probably the best option to cure obesity. Among these pathways, PYY 3-36 has been tested in man and some encouraging data have been obtained in animals with antagonists of some other orexigenic peptides such as orexins and melanin-concentrating hormone. A few gene therapy trials in the rat brain have restored interest for the leptin and NPY pathways. Their general use is however not planed in a next future. According to the type of obesity, these new treatments might be associated with either current (or almost current) drugs acting either on serotoninergic/catecholaminergic or cannabinoid pathways, or with surgery. Behavioral changes (food intake, exercise) and preventive actions during early life (in utero, young children) will remain for a while the best solutions to limit overweight development. The new treatments will help obese people to adhere to these behavioral changes by improving their efficiency to induce weight loss.
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PMID:[Feeding regulatory peptides: hopes and limits for the treatment of obesities]. 1714 57

With the worldwide epidemic of metabolic syndrome (MetS), the proportion of women that are overweight/obese and overfed during pregnancy has increased. The resulting abnormal uterine environment may have deleterious effects on fetal metabolic programming and lead to MetS in adulthood. A balanced/restricted diet and/or physical exercise often improve metabolic abnormalities in individuals with obesity and type 2 diabetes mellitus (T2D). We investigated whether reducing fat intake during the periconceptual/gestation/lactation period in mothers with high-fat diet (HFD)-induced obesity could be used to modify fetal/neonatal MetS programming positively, thereby preventing MetS. First generation (F1) C57BL/6J female mice with HFD-induced obesity and T2D were crossed with F1 males on control diet (CD). These F1 females were switched to a CD during the periconceptual/gestation/lactation period. At weaning, both male and female second generation (F2) mice were fed a HFD. Weight, caloric intake, lipid parameters, glucose, and insulin sensitivity were assessed. Sensitivity/resistance to the HFD differed significantly between generations and sexes. A similar proportion of the F1 and F2 males (80%) developed hyperphagia, obesity, and T2D. In contrast, a significantly higher proportion of the F2 females (43%) than of the previous F1 generation (17%) were resistant (P<0.01). Despite having free access to the HFD, these female mice were no longer hyperphagic and remained lean, with normal insulin sensitivity and glycemia but mild hypercholesterolemia and glucose intolerance, thus displaying a "satiety phenotype." This suggests that an appropriate dietary fatty acid profile and intake during the periconceptual/gestation/lactation period helps the female offspring to cope with deleterious intrauterine conditions.
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PMID:Resistance to high-fat diet in the female progeny of obese mice fed a control diet during the periconceptual, gestation, and lactation periods. 1716 37

Palatability and variety of foods are major reasons for "hedonic" eating, and hence for overeating and obesity. Palatable food and drugs of abuse share a common reward mechanism, and compounds that block the reinforcing effect of drugs of abuse preferentially suppress the intake of palatable foods. This research was aimed at studying the influence of the gamma-hydroxybutyrate analogue N-(4-trifluoromethylbenzyl)-4-methoxybutanamide (GET73) - that inhibits alcohol consumption - on consumption and reinforcing effect of palatable food. Adult male rats were used. For place preference conditioning, sweetened corn flakes were used as the reinforcer, and GET73 (50, 100 and 200mgkg(-1)) or vehicle were orally (p.o.) administered either 30min before each training session and the test session, or only before the test session. To study the influence on consumption, GET73 was given p.o. at the same doses once daily for 12 days to rats given free access to both palatable and varied food (cafeteria diet) or to standard chow. Both acquisition and expression of palatable food-induced conditioned place preference were inhibited by GET73, either administered throughout the conditioning period or only before the test session. GET73 reduced also the consumption of cafeteria food, while that of standard chow was increased. At these doses, GET73 had no detrimental effect on open-field behaviour. GET73 seems to specifically attenuate the gratification produced by varied and palatable food, without affecting the consumption of not particularly palatable chow. Since, overweight and obesity are mostly due to the overeating of palatable and varied foods, drugs like GET73 could represent a somewhat ideal and rational approach to obesity treatment.
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PMID:Preference for palatable food is reduced by the gamma-hydroxybutyrate analogue GET73, in rats. 1724 Jan 59

Obesity and overweight have become one of the most concerning health problems in Japan. Japan has been keeping the longest life expectancy in the last decade after the very rapid economic growth. However, the increases in chronic degenerative diseases that are partly due to over-nutrition and obesity will be a large burden in an aging society. Also in Japan, the increase of obese and overweight population is not only due to over eating but also to less exercise and daily activities. In this paper, the situation of the obese and overweight people and the trends of obesity from 1947 to 2000 in adults and children as well as the food intake tendencies during the past 50 years are summarized.
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PMID:The situation of the epidemiology and management of obesity in Japan. 1724 90

Previous research has linked overeating and overweight/obesity to impulsivity. To find out whether impulsivity causes overeating and hence overweight and obesity, we attempted to prime the concept of impulsivity in healthy participants. In a within-subjects design one sample participated in two conditions. In both conditions participants did a priming task that either hinted subtly at the concept of impulsivity or that was neutral in content. Each time the priming task was followed by a bogus taste test. Trait impulsivity was measured by means of a behavioural task and self-report. Firstly, we hypothesized that participants would eat more during the taste test after they had been primed with the concept "impulsivity" compared to after the control session. Secondly, we expected that a more impulsive personality would predict a heightened food intake. Thirdly, we expected that impulsivity would predict food intake better than restraint. The results showed that both the self-report measure of impulsivity and the behavioural task predicted food intake. Restraint did not significantly predict food intake. Primed impulsivity did not increase food intake, possibly because the priming effect did not last long enough.
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PMID:The influence of trait and induced state impulsivity on food intake in normal-weight healthy women. 1726 43


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