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This study was designed to determine the effect of ingesting three preexercise meals on energy metabolism during exercise and recovery and to relate metabolic perturbations to subjective and objective measurements associated with central fatigue. Twelve subjects consumed isoenergetic meals consisting of oat, wheat, or corn cereals 90 min before cycling. A fasting trial served as the control. Blood samples and cognitive function, perceived hunger, and sleepiness measurements were obtained before and after feeding and during recovery when self-selected food intake was also measured. After meal ingestion, plasma insulin was lower for oat than for wheat or corn whereas the ratio of tryptophan to large neutral amino acids (LNAAs) for corn was less than for all others. During exercise, the tryptophan-LNAA ratio increased from preexercise values for the fasting and wheat trials, but exercise performance was unaffected. During recovery, tryptophan:LNAA increased from postexercise values in fasting trials. Also, hunger and fatigue ratings were greater in fasted subjects, but self-selected food intake measured at the end of the recovery period was not different among groups. We conclude that preexercise meal consumption affected tryptophan:LNAA before, during, and after exercise, but these changes were not sufficient to alter physical and cognitive performance.
Am J Clin Nutr 1996 Nov
PMID:Preexercise meal composition alters plasma large neutral amino acid responses during exercise and recovery. 890 1

The profound self-destructiveness and tenacity of eating disorders found among women abused and neglected in childhood become comprehensible when understood within a complex posttraumatic conceptualization as desperate attempts to regulate overwhelming affective states and construct a coherent sense of self and system of meaning. Trauma leads to the predictable consequences of dysregulation of the arousal system, avoidance, and constriction of affect; coherence of self and world are shattered. Abused patients' childhood experiences teach them that to need is to expose oneself to the pain of abandonment and betrayal at the hands of individuals responsible for their care. Consequently, needs-psychological, physical, and spiritual-come to be perceived as dangerous, and human relationships are simultaneously yearned for and feared. Robbed of the opportunity to develop a cohesive self and a coherent system of meaning and faith to sustain from within, the traumatized eating-disorder patient turns to the culture to tell her who to be and how to live; she learns that to conquer rather than satisfy needs and to be "in control" (an internal state of equanimity manifested externally in a thin body) will bring meaning and purpose. Binge eating, purging, and starving become apt metaphors for the boundless hunger, the wish to fulfill needs together with the wish to rid oneself forever of need, the desire to "purify" the damaged psychic and physical self, and the hope of restoring meaning. The treatment of the traumatized eating disorder patient is complex. Individual therapy provides the opportunity for intensive relational work that begins to restore faith in human connection and that provides a "safe base" from which to examine the trauma and separate past from present. Therapy groups for eating-disordered women and trauma survivors provide relief from isolation, valuable perspectives from others who have "been there," and the opportunity to contribute to others' healing as one heals. Ultimately, these patients must be willing to leave the world of obsession with food and weight, which guarantees safety from interpersonal hurt while it simultaneously guarantees that hope will not be restored. Though reconnecting with humanity carries the risk of further pain, it opens up the opportunity for connection, healing, and growth.
Psychiatr Clin North Am 1996 Dec
PMID:Histories of childhood trauma and complex post-traumatic sequelae in women with eating disorders. 893 8

This article has examined the control of food intake as a physiologically complex, motivated behavioral system. During the past four decades, considerable progress has been made in understanding putative signals for hunger, satiation, and satiety, although hunger signals have proven to be more difficult to identify. The putative physiologic controls of food intake include positive and negative sensory feedback; gastric and intestinal distension; the effects of nutrients, nutrient reserves, and metabolism in producing signals to the liver or brain; and peptides and hormones released in the gastrointestinal tract or the brain. However, food intake is not influenced solely by physiologic signals for hunger, satiation, and satiety. To comprehend feeding behavior more thoroughly, current physiologic models must be extended to include modulating factors such as feeding-associated responses adapted through learning processes and the influence of circadian rhythms, which can be dominating over hunger, satiation, and satiety signals.
Endocrinol Metab Clin North Am 1996 Dec
PMID:Control of food intake. A physiologically complex, motivated behavioral system. 897 47

An increase in the sensation of hunger and overeating after a period of chronic energy deprivation can be part of an autoregulatory phenomenon attempting to restore body weight. To gain insights into the role of fat and lean tissue depletion as determinants of such a hyperphagic response in humans, we reanalyzed the individual data on food intake and body composition available for the 12 starved and refed men in the classical Minnesota Experiment after a shift from a 12-wk period of restricted refeeding to an ad libitum refeeding period of 8 wk. For each individual, the following were determined: 1) the total hyperphagic response during the ad libitum refeeding period, calculated as the energy intake in excess of that during the prestarvation (control) period; 2) the degree of fat recovery and that of fat-free-mass (FFM) recovery before ad libitum refeeding, calculated as the deviation in fat and FFM from their respective prestarvation values (ie, the amount of fat or FFM before ad libitum refeeding as a percentage of fat or FFM during the control period); and 3) the deficit in energy intake before ad libitum refeeding, calculated as the difference between the energy intake during the period of restricted refeeding and that during the control period. The results indicate that 1) the total hyperphagic response is inversely correlated with the degree of fat recovery (r = -0.6) as well as with that of FFM recovery (r = -0.5), 2) the correlation between hyperphagia and FFM recovery persists after adjustment for fat recovery, and 3) the correlations between hyperphagia and fat recovery or FFM recovery persist after adjustment for the variance in the energy deficit during the preceding period of restricted refeeding. Taken together, these results in humans suggest that poststarvation hyperphagia is determined to a large extent by autoregulatory feedback mechanisms from both fat and lean tissues. These findings, which have implications for both the treatment of obesity and for nutritional rehabilitation after malnutrition and cachexia, have been integrated into a compartmental model of autoregulation of body composition, and can be used to explain the phenomenon of poststarvation overshoot in body fat.
Am J Clin Nutr 1997 Mar
PMID:Poststarvation hyperphagia and body fat overshooting in humans: a role for feedback signals from lean and fat tissues. 906 20

The sweet taste of nonnutritive sweeteners has been reported to increase hunger and food intake through the mechanism of cephalic-phase insulin release (CPIR). We investigated the effect of oral sensation of sweetness on CPIR and other indexes associated with glucose metabolism using nutritive and nonnutritive sweetened tablets as stimuli. At lunchtime, 12 normal-weight men sucked for 5 min a sucrose, an aspartame-polydextrose, or an unsweetened polydextrose tablet (3 g) with no added flavor. The three stimuli were administered in a counterbalanced order, each on a separate day at 1-wk intervals. Blood was drawn continuously for 45 min before and 25 min after the beginning of sucking and samples were collected at 1-min intervals. Spontaneous oscillations in glucose, insulin, and glucagon concentrations were assessed as were increments (slopes) of fatty acid concentrations during the baseline period. The nature of the baseline (oscillations: glucose, insulin, and glucagon; and slopes: fatty acids) was taken into account in the analyses of postexposure events. No CPIR and no significant effect on plasma glucagon or fatty acid concentrations were observed after the three stimuli. However, there was a significant decrease in plasma glucose and insulin after all three stimuli. Only the consumption of the sucrose tablet was followed by a postabsorptive increase in plasma glucose and insulin concentrations starting 17 and 19 min, respectively, after the beginning of sucking. In conclusion, this study suggested that oral stimulation provided by sweet nonflavored tablets is not sufficient for inducing CPIR.
Am J Clin Nutr 1997 Mar
PMID:Cephalic phase responses to sweet taste. 906 23

In response to evidence linking obesity and high amounts of dietary fat, the food industry has developed numerous reduced-fat and nonfat food items. These items frequently derive a relatively large percentage of their energy from sugars and the effect of these sugars on weight regulation is not well known. We studied the comparative effects of high- and low-sucrose, low-fat, hypoenergetic diets on a variety of metabolic and behavioral indexes in a 6-wk weight-loss program. Both diets contained approximately 4606 kJ energy/d with 11% of energy as fat, 19% as protein, and 71% as carbohydrate. The high-sucrose diet contained 43% of the total daily energy intake as sucrose; the low-sucrose diet contained 4% of the total daily energy intake as sucrose. Twenty women aged 40.6 +/- 8.2 y (mean +/- SD) with a body mass index (in kg/m2) of 35.93 +/- 4.8 consumed the high-sucrose diet; 22 women aged 40.3 +/- 7.3 y with a body mass index of 34.93 +/- 4.4 consumed the low-sucrose diet. Mixed-design analysis of variance showed a main effect of time (P < 0.01), with both diet groups showing decreases in weight, blood pressure, resting energy expenditure, percentage body fat, free triiodothyronine (FT3), urinary norepinephrine, and plasma lipids. Small but significant interactions were found between group and time in total cholesterol (P = 0.009) and low-density lipoprotein (LDL) (P = 0.01). Both groups showed decreases in depression, hunger, and negative mood, and increases in vigilance and positive mood with time (P < 0.01). Results showed that a high sucrose content in a hypoenergetic, low-fat diet did not adversely affect weight loss, metabolism, plasma lipids, or emotional affect.
Am J Clin Nutr 1997 Apr
PMID:Metabolic and behavioral effects of a high-sucrose diet during weight loss. 944 Mar 91

Accumulating evidence suggest that a good way to compare the satiety power of meals with different compositions or energy contents is to measure the onset latency of the next meal when freely requested by subjects deprived of any time cues. This study was performed in normal-weight young men (aged 19-24 y) isolated from time cues. At sessions 1 and 2, we studied the effects of two high-carbohydrate pasta lunchs with either 50 g low-energy butter substitute (lunch A) or 50 g butter (lunch B) on hunger ratings, on the latency of the dinner request, and on energy and nutrient intakes at the offered ad libitum dinner. Sessions 3 and 4 were designed to examine the effects of the two lunchs on the postlunch and predinner profiles of plasma glucose, insulin, glucagon, and lipids; consequences on the metabolic and hormonal responses to the fixed dinner offered on request also were tested. The addition of 1588 kJ butter to the pasta lunch compared with the addition of 67 kJ butter substitute had no effect on hunger ratings but significantly delayed the onset of dinner by approximately 38 min; however, neither energy intake nor nutrient intakes were different. The high-fat lunch led to a slightly different postlunch plasma glucose concentration profile but, as expected, to higher plasma triacylglycerol and fatty acid concentrations. The high-fat lunch also led to postdinner glucose intolerance with normal insulin and high fatty acid concentrations that may help explain the partial and delayed adjustment in energy intake after a high-fat meal as reported by some studies.
Am J Clin Nutr 1997 May
PMID:Satiety power of dietary fat: a new appraisal. 912 70

1. Leptin is generally thought to play a key role in the regulation of eating. However, its real role in human eating behaviour is still poorly known. Therefore, the role of leptin in the regulation of eating was examined in obese binge- and non-binge-eating women during exposure to food and food-related stimuli. 2. Eleven binge- and ten non-binge-eating obese women took part in the study. In addition to serum leptin, serum insulin, non-esterified fatty acids, plasma glucose, salivation, the feeling of hunger and the desire to eat were repeatedly measured during the experiment. 3. Serum leptin levels did not differ between the binge- and non-binge-eating women. Neither were leptin levels associated with the feeling of hunger or the desire to eat food, nor with the amount or composition of food eaten. During food exposure leptin levels did not change, whereas at the same time serum insulin levels increased and serum non-esterified fatty acid levels decreased. The change in salivation during food exposure was inversely associated with the fasting leptin level. 4. This study indicates that serum leptin does not play a role in the regulation of eating in obese women, at least not in the short term. Furthermore, leptin levels are not different in obese binge-eating women as compared with obese non-binge-eating women. Interestingly, high fasting leptin levels may be associated with a decreased salivation response in the presence of food and food-related stimuli.
Clin Sci (Lond) 1997 Jun
PMID:Serum leptin and short-term regulation of eating in obese women. 920 17

The object of this study was to examine whether eating behavior, food preference, gastric emptying, and gut hormone patterns are altered after jejunoileal bypass (JIB) in patients with severe obesity. Eight obese [mean (+/- SD) body mass index (BMI; in kg/m2) 42.9 +/- 4] subjects were studied prospectively before and 9 mo after JIB with eight age- and sex-matched normal-weight control subjects. Total energy intake, data from the universal eating monitor (VIKTOR), eating motivation measured by visual analog scales, a food-preference checklist, a forced-choice list, solid-phase gastric emptying, and postprandial concentrations of cholecystokinin, motilin, and neurotensin were studied. BMI was reduced by 29% after JIB. Compared with normal subjects, the JIB patients showed a reduced desire to eat, decreased hunger, and reduced prospective consumption before a test meal. After surgery, obese subjects selected fewer food items and showed a reduced preference for high-carbohydrate and high-fat items before a test meal. There was a trend from an accelerated toward a decelerated eating pattern in obese subjects after JIB. After JIB, gastric emptying of obese subjects was slowed and similar to that in control subjects. Obese subjects had lower postprandial cholecystokinin concentrations that were lower than those of control subjects both before and after JIB. Postprandial concentrations of neurotensin were higher after JIB. We conclude that after JIB, the desire to eat and preference for high-carbohydrate and high-fat items is reduced, resulting in decreased energy intake. That gastric emptying is prolonged and gut hormone patterns are altered with low postprandial plasma cholecystokinin and high neurotensin plasma concentrations may at least partly account for these observations.
Am J Clin Nutr 1997 Jul
PMID:Reduced food intake after jejunoileal bypass: a possible association with prolonged gastric emptying and altered gut hormone patterns. 920 88

The factors influencing appetite in humans are poorly understood. There is a weak relation between appetite and gastric emptying in normal subjects. Recent studies have shown that fasting and postprandial antral areas increase in patients with functional dyspepsia compared with normal subjects. We evaluated the hypothesis that antral area, and hence antral distention, is a significant determinant of postprandial fullness. Fourteen normal subjects had simultaneous measurements of gastric emptying by scintigraphy and antral area by ultrasound after ingestion of 350 mL 20% glucose. Fullness and hunger were assessed by visual analog scales. Measurements of the gastric-emptying half time (t1/2) by scintigraphy and ultrasound were not significantly different (129.6 +/- 11.8 min compared with 115.6 +/- 11.4 min). Fullness increased (P < 0.001) and hunger decreased (P < 0.001) after the drink. Both fullness and the magnitude of the increase in fullness after the drink were related to antral area (r > 0.56, P < 0.05), the increase in antral area (r > 0.59, P < 0.05), and the scintigraphic content of the distal stomach (r > 0.57, P < 0.05), but not to the ultrasound or scintigraphic t1/2 values. In contrast, hunger and the magnitude of the decrease in hunger after the drink were not related to either antral area, the increase in antral area, or the rate of gastric emptying. We conclude that postprandial fullness, but not hunger, was closely related to antral distention in normal subjects.
Am J Clin Nutr 1997 Jul
PMID:Relation between postprandial satiation and antral area in normal subjects. 920 80


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