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

Most weight control programs facilitate weight loss by encouraging participants to adopt healthy eating patterns and increase physical activity. There is a need for a relatively brief measure of eating habits and physical activity that could be used to evaluate changes in behavior during weight loss treatment. The purpose of this series of four studies was to develop and validate such a measure, which was subsequently named the Weight Loss Behavior Scale (WLBS). Study 1 (n = 533) included item and scale development and examination of the WLBS's factor structure and internal consistency. Study 2 (n = 226) evaluated the test-retest reliability and convergent validity of its subscales. Study 3 examined their reliability and internal consistency scales in a predominantly overweight sample (n = 36). Study 4 evaluated the WLBS as a treatment outcome measure in a weight loss intervention (n = 50). Study 1 found that the WLBS contained five internally consistent and stable factors: 1) Concern with Dieting and Weight, 2) Exercise, 3) Overeating, 4) Avoidance of Fattening Foods and Sweets, and 5) Emotional Eating. Study 2 found convergent validity for the WLBS by assessing the correlation of its factors/scales with established inventories of comparable constructs, e.g., dietary restraint, disinhibited eating, and physical activity. Test-retest reliability of the five scales was also supported in this second study. In Study 3, support for the internal consistency and test-retest reliability of the WLBS among overweight individuals was found. Study 4 found that all scales significantly changed in the expected directions after a 5-month behavioral weight loss treatment. The findings from this series of studies suggest that the WLBS is a reliable and valid self-report inventory of cognitive and behavioral scales associated with weight control that can be utilized as an outcome measure for weight loss interventions.
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PMID:Psychometric development of a multidimensional measure of weight-related attitudes and behaviors. 1094 5

The central melanocortin system is critical for the long term regulation of energy homeostasis. Null mutations of the melanocortin-4 receptor (MC4-R) are associated with hyperphagia, obesity, and accelerated longitudinal growth in mice and humans. However, little is known about the function of another central melanocortin receptor, the MC3-R. To assess the role of the MC3-R in energy homeostasis, the majority of the mc3r coding sequence was deleted from the mouse genome. In contrast to the MC4-R knockout, which exhibits increased food intake, increased somatic growth, and defects in metabolism, mc3r-/- mice exhibit an exclusively metabolic syndrome. Homozygous null mc3r mice, while not significantly overweight, exhibit an approximately 50% to 60% increase in adipose mass. Mc3r-/- mice also exhibit an unusual increase in respiratory quotient when transferred onto high fat chow, suggesting a reduced ratio of fat/carbohydrate oxidation. Furthermore, male mc3r-/- mice also exhibit an approximately 50% reduction in locomotory behavior on the running wheel, suggesting reduced energy expenditure.
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PMID:A unique metabolic syndrome causes obesity in the melanocortin-3 receptor-deficient mouse. 1096 27

Rats neonatally overnourished due to a reduced litter size develop persisting overweight throughout life. A presumed mechanism leading to this 'malprogramming' consists of an acquired change of the responsiveness to leptin of the neuronal system regulating feeding behavior. The study reports significant differences in the effects of leptin on single unit activity of the arcuate nucleus in brain slices of normal compared with early postnatally overfed juvenile rats. The firing rate of arcuate neurons in normal rats was inhibited by leptin (Wilcoxon test p < 0.0001, n = 42), whereas it was not changed in obese rats (Wt p = 0.24, n = 35). The reduced inhibition by leptin of arcuate neurons in neonatally overfed rats might indicate an acquired hypothalamic leptin resistance contributing to persistent hyperphagia and overweight.
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PMID:Decreased inhibition by leptin of hypothalamic arcuate neurons in neonatally overfed young rats. 1097 65

The aim of the present study was to determine whether the anorexic and thermogenic effects of leptin were attenuated in overweight aged rats following intracerebroventricular (i.c.v.) injection of murine leptin. Male F344/BN rats of two ages (6 months: young (n=20) and 24 months: old (n=18)) were divided into three groups (control, pair-fed and leptin) and were treated with either vehicle (artificial cerebrospinal fluid) or leptin (15.6 microgram/day) for 3 days. There was an age-related increase in basal food intake (20+/-2%), serum leptin levels (363+/-106%) and leptin (OB) mRNA (72+/-16%) in perirenal white adipose tissue (PWAT). In contrast, basal expression of hypothalamic NPY mRNA and brown adipose tissue (BAT) uncoupling protein 1 (UCP1) mRNA was reduced significantly (-35+/-4% and -51+/-5%, respectively) with age. I.c.v. leptin treatment had a significantly greater effect in reducing food intake (-42+/-5% vs. -23+/-4%), serum leptin levels (-55+/-7% vs. 10+/-2%) and PWAT OB mRNA (-46+/-2% vs. 10+/-5%) in young than in old rats. Similarly, central leptin treatment also had a greater effect in suppressing hypothalamic NPY mRNA expression in young (-23+/-4%) than in old (-8+/-4%) rats compared with their age-matched pair-fed treated rats. The stimulatory effect of i.c.v. leptin treatment on BAT UCP1 mRNA expression was also significantly greater in young rats (45+/-8%) than in old rats (10+/-6%) compared with age-matched pair-fed rats. Our previous report indicated that these overweight aged rats were resistant to peripheral administered leptin. The present data extend those findings and demonstrate that the impaired anorexic and metabolic effects of leptin are centrally mediated. This leptin resistance may be due to either the elevated obesity and serum leptin with age or due to age itself or both. The development of leptin resistance with age may contribute to the hyperphagia, hyperleptinemia and impaired energy balance with age.
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PMID:Resistance to the anorexic and thermogenic effects of centrally administrated leptin in obese aged rats. 1102 67

Leptin is crucially involved in the central nervous regulation of body weight. Neurons of the ventromedial hypothalamic nucleus (VMH) express leptin receptors and signal satiety with increase in their firing. Normally, leptin mainly activates VMH neurons. Rats grown up in small litters (SL) develop persistent hyperphagia and obesity throughout life. We studied single unit activity in hypothalamic brain slices of juvenile SL rats overweight due to early postnatal overfeeding (Mann-Whitney U-test, P < 0.001). VMH neurons of normal rats were mainly activated by leptin (Wilcoxon test, P < 0.05, n = 39), whereas neurons of overweight SL rats were mainly inhibited (Wt, P < 0.001, n = 33). This clearly altered response to leptin in neonatally overnourished rats might contribute to their persistent overweight throughout life.
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PMID:Different responses of ventromedial hypothalamic neurons to leptin in normal and early postnatally overfed rats. 1106 28

This study presents the development and testing of the Overeating Tension Scale. Overeating tension was defined operationally as the total discrepancy score resulting from differences between subjects' ratings of actual and desired feelings before overeating. The 32-item Overeating Tension Scale, derived from Apter's Reversal Theory, measures reported overall tension and motivation-specific tension. The scale initially included 48 items, six items for each of eight motivational states. After two instrument development studies (N = 373, N = 208), items were refined and reduced to a total of 32, or four for each of eight motivational states. The final version of the instrument was tested in two additional studies (N = 330, N = 130) that provided evidence to support the internal consistency reliability of the Overeating Tension Scale. There was support for construct validity using contrasted groups (overweight and normal weight subjects), convergent validity, and factor analysis.
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PMID:Reliability and validity of the Overeating Tension Scale. 1122 81

The decision to eat, and to eat particular foods, varies for different individuals and situations. Individual differences in food likes and desires develop throughout life because of differing food experiences and attitudes. There are many internal and external cues, not just stimulation from foods or hunger, which can trigger the immediate desire to eat or orient eating toward certain foods. Food desires and intake are an outcome of interactions between these cues and more stable individual physiological and psychological characteristics. Overweight and obese individuals show a tendency toward greater liking and selection of energy-dense foods, which may contribute to development and maintenance of these conditions. However, although liking (pleasure from eating) is an important part of food choice, it may make only a modest contribution to overall variation in food choice and eating behaviors. Indeed, difficulties of weight control may reflect problems with cues and motivations to eat, rather than with heightened pleasure derived from eating. Paradoxically, individuals highly concerned with food intake and weight control may be particularly susceptible to thoughts, emotions, and situational cues that can prompt overeating and undermine their attempts to restrain eating. Repeat dieting, high day-to-day fluctuations in intakes, and attempts to enforce highly rigid control over eating all seem to be counterproductive to weight control efforts and may disrupt more appropriate food choice behaviors. Longer-term weight maintenance solutions and programs that offer a degree of structuring of the personal food environment, while retaining flexibility in choices, therefore, may be particularly beneficial in weight management.
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PMID:Determinants of food choice: relationships with obesity and weight control. 1170 50

Single unit activity was studied in brain slices of normal and overweight adolescent rats, the latter grown up until weaning in small litters of three pups per mother (SL). Significantly fewer neurons of the ventromedial hypothalamic nucleus (VMN) were activated by insulin in overweight SL rats than in normal (NL) rats (chi2 p < 0.01). Although there is no significant difference between NL and SL rats in the number of VMN neurons responsive to insulin, the neurons differ in the type of reaction. In overweight SL rats neurons were mainly inhibited by insulin (Wilcoxon test p < 0.0001, n = 45). This altered response to the satiety signal insulin in postnatally overnourished rats might contribute to their persisting hyperphagia and overweight.
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PMID:Inhibition by insulin of hypothalamic VMN neurons in rats overweight due to postnatal overfeeding. 1171 56

Melanocortins, e.g. alpha-melanocyte stimulating hormone, are involved in the central nervous regulation of body weight. Agouti-related peptide (AGRP) as an endogenous melanocortin receptor antagonist induces feeding. Overexpression leads to obesity. Rats that grow up in small litters develop persistent hyperphagia and are overweight throughout life. Changes in the neuronal activity of the ventromedial hypothalamic nucleus (VMH) that signals satiety with activation might be involved. We studied single unit activity in hypothalamic brain slices. Melanocortins activated or inhibited similarly in control and small litter rats. AGRP mainly inhibited VMH neurons of overweight rats (t-test, P < 0.005, n = 33), whereas it also activated neurons of controls. This increased inhibition of VMH neurons by AGRP in early postnatally overnourished rats might contribute to the changed regulation leading to a persistent overweight condition throughout life.
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PMID:Increased inhibition by agouti-related peptide of ventromedial hypothalamic neurons in rats overweight due to early postnatal overfeeding. 1221 28

Neuronal responses to neuropeptide Y and dopamine were recorded in brain slices of hypothalamic paraventricular (PVH) and ventromedial (VMH) nuclei in normal and hyperphagic overweight rats reared in small litters of three pups. NPY significantly activated PVH neurons of normal rats, but inhibited neurons of overweight rats. In the VMH, a significantly higher coincidence of inhibition induced by NPY and dopamine was found in overweight rats. Similar neuronal responses were evoked by a NPY Y5 receptor agonist. Effects of NPY could be blocked by a Y1 receptor antagonist. The altered response of PVH neurons to the feeding-inducing NPY and the increased inhibition by NPY and dopamine in the VMH might contribute to the persisting hyperphagia and overweight of postnatally overnourished rats.
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PMID:Differential response to NPY of PVH and dopamine-responsive VMH neurons in overweight rats. 1221 98


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