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Query: UMLS:C0020175 (hunger)
 5,670 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Serum leptin and short-term regulation of eating in obese women. 920 17

1. This study aimed to investigate the possible role of leptin in post-traumatic anorexia by making pre- and post-operative (0-8 days) measurements of circulating leptin concentrations in six patients undergoing elective total hip replacement for osteoarthritis. 2. Mean daily hunger rating (four categories) and food intake (assessed by food record charts) were measured pre-operatively, as well as post-operatively for the first 5 days (days 0-5). Leptin concentrations, circulating metabolites [glucose, non-esterified fatty acids, glutamine and 3-hydroxybutyrate] and insulin and cortisol concentrations were measured pre-operatively (day 0) and post-operatively (days 1, 2, 3, 5 and 8). 3. Mean leptin concentrations were significantly increased only on day 1 (56% increase compared with pre-operative values, P < 0.009), whereas food intake (only 0.6 MJ on day 0) and hunger (5/6 patients 'not hungry' on day 0) only gradually improved over the next few days. (The energy intake over the first 5 days was 56% of the pre-operative value.) 4. Circulating insulin and cortisol concentrations were elevated on day 1 compared with pre-operative values on day 0 (P < 0.05). Of the measured metabolites implicated in the control of food intake, circulating non-esterified fatty acids and 3-hydroxybutyrate were not significantly altered in the post-operative period, but significant hyperglycaemia was noted on day 1 compared with day 0 pre-operatively (8.8 compared with 6.4 mmol/l glucose; P < 0.01). 5. It is concluded that circulating leptin is involved in the early (< 24 h) acute-phase response after moderately severe surgical trauma (characterized biochemically by a substantial acute-phase protein response, hypoalbuminaemia, hyperglycaemia and hypoglutaminaemia). Therefore, leptin may be implicated in post-traumatic anorexia, although other factors are likely to be involved, especially after the first 24 h when circulating leptin concentrations are no longer elevated.
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PMID:Plasma leptin, energy intake and hunger following total hip replacement surgery. 930 25

Leptin, the ob gene product, is considered as a signal involved in the regulation of energy stores through centrally mediated effects on ingestive behavior and metabolism. To investigate the relationships between appetite-related sensations and circulating leptin in humans, 12 healthy male volunteers were served two test lunches (1200 kcal, 38% carbohydrate, 50% fat, 12% protein) with comparable palatability but resulting in different postprandial hunger ratings, and plasma leptin concentrations were monitored during 8 h after meal ingestion. Whereas postprandial hunger ratings (assessed by visual analog scales) and plasma insulin patterns differed significantly between meals, no significant difference in postprandial plasma leptin concentrations was observed between the two meals. A moderate but significant increase in mean plasma leptin was found over time. We conclude that postprandial plasma leptin concentrations do not significantly differ between two meals inducing different effects on hunger subjective feelings. These data are in agreement with a role for leptin in the regulation of energy balance as a long-term adiposity-related signal rather than a short-term meal-related factor.
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PMID:Plasma leptin and hunger ratings in healthy humans. 957 48

In insulin resistant subjects with android obesity the leptin levels are, as compared with non-obese subjects, elevated in proportion to their BMI, WHR and their percentage of body fat. Generally independent on obesity, leptin levels are significantly higher in women than in men as in women the percentage of adipose tissue is higher. After administration of 2 mg nicotine in Nicorette chewing gum to 36 android obese non-smokers the elevated baseline values of leptin did not change and thus the observation that cigarettes suppress hunger or that smoking promotes weight reduction is untrue or else this effect is not mediated by nicotine stimulation of leptin secretion or formation in adipose tissue, leptin being the adipose tissue hormone which controls food intake, the sensation of satiety and via neuropeptide Y also other hypothalamic functions such as muscular and sexual activity, gonadoliberin output, thermoregulation etc. Leptin thus offers no alibi to smokers. Conversely smoking in android obese hyperinsulinaemic hyperleptinaemic subjects with syndrome X (5H) potentiates significantly the risk of cardiovascular death.
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PMID:[The effects of nicotine on leptin levels in patients with android obesity]. 975 Apr 63

To assess the impact of the macronutrient content of a meal on the postprandial leptin response and its relationship with postprandial satiety, 22 young healthy subjects (11 men and 11 women) were given, in a randomized order, an isoenergetic meal [carbohydrate (81%) or fat (79%)] or remained fasting. Blood sampling and hunger and satiety scores were collected hourly during 9 h after the meal. Spontaneous intake was measured at a buffet meal at 9 h postprandially. In both genders, leptin response was higher after the carbohydrate meal than after the fat meal and while fasting. In women, leptin levels were higher after the fat meal than while fasting. Leptin response was significantly correlated to insulin response (r = 0.51, P < 0.0001). Hunger and satiety ratings and subsequent energy intake were not different after carbohydrate or fat intake. In conclusion, a carbohydrate meal induces higher postprandial leptin levels than an isoenergetic fat meal. Short-term regulation of postprandial satiety and food intake is not influenced by circulating leptin.
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PMID:Leptin response to carbohydrate or fat meal and association with subsequent satiety and energy intake. 1056 12

Leptin is a 16-kDa cytokine secreted in humans primarily but not exclusively by adipose tissues. Its concentration in blood is usually proportional to body fat mass, but is higher in women than in men not only because of a different distribution of and greater fat mass in women, but also because testosterone reduces its level in men. Leptin features in different ways during the life span. It is synthesized in the ovary, transported in the oocyte, and made by both fetus and placenta, particularly during the last month of gestation. It is made by the lactating mammary gland and ingested by the newborn infant in its milk. The prime importance of leptin is realized at puberty when it is necessary for progression to a normal adult reproductive status in females. Fasting and chronic undernutrition result in a lower level of leptin in the blood. Lack of leptin results in hunger, ensuring that the individual eat to survive, and also inhibition of reproduction, until such time as food and fat stores are adequate to supply energy for pregnancy and lactation. Thus, leptin is important for survival of the individual and survival of the species. Although an extremely rare genetic absence of leptin induces hyperphagia and obesity in humans, as it does in mice, there appears to be little role for leptin in humans in ensuring that fat stores are not in excess of adequate, that is, in preventing obesity. The mouse differs from humans in many respects, in particular in the far more drastic ways it conserves energy when it very rapidly adapts to lack of food. These include not only suppression of reproduction but also lowering of its body temperature (torpor), suppressing its thyroid function, suppressing its growth, and increasing secretion of stress hormones (from the adrenal). This review concentrates on roles of leptin in human physiology and pathophysiology but also discusses why some observations on actions of leptin in mice are not applicable to humans.
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PMID:Physiological roles of the leptin endocrine system: differences between mice and humans. 1065 40

Feeding is a complex process responsive to sensory information related to sight and smell of food, previous feeding experiences, satiety signals elicited by ingestion and hormonal signals related to energy balance. Dopamine released in specific brain regions is associated with pleasurable and rewarding events and may reinforce positive aspects of feeding. Dopamine also influences initiation and coordination of motor activity and is required for sensorimotor functions. Thus, dopamine may facilitate integration of sensory cues related to hunger, initiating the search for food and its consumption. Dopaminergic neurons in the substantia nigra and ventral tegmental area project to the caudate putamen and nucleus accumbens, where they modulate movement and reward. There are projections from the nucleus accumbens to the lateral hypothalamus that regulate feeding. Dopamine-deficient mice (Dbh(Th/+), Th-/-; hereafter DD mice) cannot synthesize dopamine in dopaminergic neurons. They gradually become aphagic and die of starvation. Daily treatment of DD mice with L-3,4-dihydroxyphenylalanine (L-DOPA) transiently restores brain dopamine, locomotion and feeding. Leptin-null (Lep(ob/ob)) mice exhibit obesity, decreased energy expenditure and hyperphagia. As the hypothalamic leptin-melanocortin pathway appears to regulate appetite and metabolism, we generated mice lacking both dopamine and leptin (DD x Lep(ob/ob)) to determine if leptin deficiency overcomes the aphagia of DD mice. DD x Lep(ob/ob) mice became obese when treated daily with L-DOPA, but when L-DOPA treatment was terminated the double mutants were capable of movement, but did not feed. Our data show that dopamine is required for feeding in leptin-null mice.
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PMID:Dopamine is required for hyperphagia in Lep(ob/ob) mice. 1080 66

Appetite control involves an integration of the drive signals arising form energy stores in the body with the satiety signals generated by periodic episodes of food consumption. Serotonin (5-hydroxytryptamine, 5-HT) has been implicated in the processes of within-meal satiation and postmeal satiety (5-HT1B and 5-HT2C postsynaptic receptors) which are concerned with the signals arising form the pattern of food intake. Central nervous system (CNS) 5-HT is sensitive to circulating levels of the precursor tryptophan, certain macronutrients and peripheral satiety factors such as cholecystokinin (CCK) and enterostatin. Hypothalamic 5-HT receptor systems inhibit neuropeptide Y (NPY), a potent stimulator of hunger and food intake. In contrast to the linking of 5-HT with the consequences of food ingestion, the hormone leptin (OB protein) is regarded as a signal linking adipose tissue status with a number of key CNS circuits. Leptin itself stimulates CNS leptin receptors (OB-r receptor) which link with pro-opiomelanocortin (POMC)/ MC-4 receptors. The effects of leptin may also be modulated by factors such as the corticotrophin-releasing factor (CRF), cocaine and amphetamine-regulated transcript (CART), orexins and galanin. Very little evidence exists to support any direct link between the actions of 5-HT and leptin, suggesting that they are separate systems. 5-HT is a part of an integrated network for short-acting satiety signals (episodic in nature), and leptin is a hormonal indicator of long-term (tonic) energy reserves. At a conceptual level, these may represent the distinction between 'satiety' and 'drive'. Interestingly, both 5-HT and leptin modulate the action of NPY, which may form a part of a common output pathway for the expression of appetite.
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PMID:Separate systems for serotonin and leptin in appetite control. 1082 29

Adipose tissue performs complex metabolic and endocrine functions. Among the endocrine products produced by adipose tissue are tumour necrosis factor alpha, interleukin 6, acylation-stimulating protein and leptin. The present review will focus primarily on mechanisms regulating leptin production and leptin action, and the implications of this regulation in the control of energy balance. Leptin acts in the central nervous system where it interacts with a number of hypothalamic neuropeptide systems to regulate feeding behaviour and energy expenditure. The presence of extreme obesity in animals and human subjects with mutations of the leptin gene or the leptin receptor demonstrates that normal leptin production and action are critical for maintaining energy balance. Insulin is the major regulator of leptin production by adipose tissue. Insulin infusions increase circulating leptin concentrations in human subjects. Plasma leptin levels are markedly decreased in insulin-deficient diabetic rodents, and the low leptin levels contribute to diabetic hyperphagia. Based on in vitro studies, the effect of insulin to stimulate leptin production appears to involve increased glucose metabolism. Blockade of glucose transport or glycolysis inhibits leptin expression and secretion in isolated adipocytes. Evidence suggests that anaerobic metabolism of glucose to lactate does not stimulate leptin production. Alterations in insulin-mediated glucose metabolism in adipose tissue are likely to mediate the effects of energy restriction to decrease, and refeeding to increase, circulating leptin levels. Changes in glucose metabolism may also explain the observation that high-fat meals lower 24h circulating leptin levels relative to high-carbohydrate meals in human subjects, suggesting a mechanism that may contribute to the effects that high-fat diets have in promoting increased energy intake, weight gain and obesity. The decreased circulating leptin observed during energy restriction is related to increased sensations of hunger in human subjects. Thus, decreases in leptin during energy-restricted weight-loss regimens may contribute to the strong propensity for weight regain. A better understanding of the precise mechanisms regulating leptin production and leptin action may lead to new approaches for managing obesity.
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PMID:Role of adipose tissue in body-weight regulation: mechanisms regulating leptin production and energy balance. 1099 52

Food intake is a regulated system. Afferent signals provide information to the central nervous system, which is the centre for the control of satiety or food seeking. Such signals can begin even before food is ingested through visual, auditory and olfactory stimuli. One of the recent interesting findings is the demonstration that there are selective fatty acid taste receptors on the tongue of rodents. The suppression of food intake by essential fatty acids infused into the stomach and the suppression of electrical signals in taste buds reflect activation of a K rectifier channel (K 1.5). In animals that become fat eating a high-fat diet the suppression of this current by linoleic acid is less than that in animals that are resistant to obesity induced by dietary fat. Inhibition of fatty acid oxidation with either mercaptoacetate (which blocks acetyl-CoA dehydrogenase) or methylpalmoxirate will increase food intake. When animals have a choice of food, mercaptoacetate stimulates the intake of protein and carbohydrate, but not fat. Afferent gut signals also signal satiety. The first of these gut signals to be identified was cholecystokinin (CCK). When CCK acts on CCK-A receptors in the gastrointestinal tract, food intake is suppressed. These signals are transmitted by the vagus nerve to the nucleus tractus solitarius and thence to higher centres including the lateral parabrachial nucleus, amygdala, and other sites. Rats that lack the CCK-A receptor become obese, but transgenic mice lacking CCK-A receptors do not become obese. CCK inhibits food intake in human subjects. Enterostatin, the pentapeptide produced when pancreatic colipase is cleaved in the gut, has been shown to reduce food intake. This peptide differs in its action from CCK by selectively reducing fat intake. Enterostatin reduces hunger ratings in human subjects. Bombesin and its human analogue, gastrin inhibitory peptide (also gastrin-insulin peptide), reduce food intake in obese and lean subjects. Animals lacking bombesin-3 receptor become obese, suggesting that this peptide may also be important. Circulating glucose concentrations show a dip before the onset of most meals in human subjects and rodents. When the glucose dip is prevented, the next meal is delayed. The dip in glucose is preceded by a rise in insulin, and stimulating insulin release will decrease circulating glucose and lead to food intake. Pyruvate and lactate inhibit food intake differently in animals that become obese compared with lean animals. Leptin released from fat cells is an important peripheral signal from fat stores which modulates food intake. Leptin deficiency or leptin receptor defects produce massive obesity. This peptide signals a variety of central mechanisms by acting on receptors in the arcuate nucleus and hypothalamus. Pancreatic hormones including glucagon, amylin and pancreatic polypeptide reduce food intake. Four pituitary peptides also modify food intake. Vasopressin decreases feeding. In contrast, injections of desacetyl melanocyte-stimulating hormone, growth hormone and prolactin are associated with increased food intake. Finally, there are a group of miscellaneous peptides that modulate feeding. beta-Casomorphin, a heptapeptide produced during the hydrolysis of casein, stimulates food intake in experimental animals. In contrast, the other peptides in this group, including calcitonin, apolipoprotein A-IV, the cyclized form of histidyl-proline, several cytokines and thyrotropin-releasing hormone, all decrease food intake. Many of these peptides act on gastrointestinal or hepatic receptors that relay messages to the brain via the afferent vagus nerve. As a group they provide a number of leads for potential drug development.
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PMID:Afferent signals regulating food intake. 1099 53


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