Satiety values of isocaloric diets for reducing, with special reference to the glucostatic theory of appetite control.
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The 5-HT1A agonist 8-OH-DPAT was shown to diminish the water and 1.8% NaCl solution consumption, whereas its antagonist pMPPI--to enhance the water intake in rats. Another agonist: CGS-12066A enhanced water intake or exerted no effect on drinking behaviour and diminished salt intake. Other substances under study exerted various effects. The data obtained suggest that the 5-HT receptors are involved in regulation of water and salt intake, even though the mechanisms of the effects are different. Apparently 5-HT1B and 5-HT2A receptors play an activating role in regulation of water intake, whereas 5-HT1A, 5-HT2C and 5-HT3 receptors act as inhibitory ones. Only three of the receptors under study seem to regulate salt intake by inhibiting the salt appetite.
As endogenous opiates are known to be involved in regulation of appetite, an obese patient with panhypopituitarism and frequent episodes of ravenous hunger was treated with the oral opiate antagonist naltrexone for 13 months. This resulted in loss of body weight and attacks of severe hunger. The increased serum prolactin concentration and the dose of vasopressin required for substitution could be reduced. Long-term application of opiate antagonists may be useful in related cases.
Leptin inhibits food intake and increase energy expenditure via an interaction with specific leptin receptors located in the hypothalamus. Leptin receptors have been identified in cocaine and amphetamine-regulated transcript(CART), neuropeptide Y(NPY), galanin-containing neurons of the arcuate nucleus, respectively, and in corticotropin-releasing hormone(CRH)-containing neurons of the paraventricular nucleus, suggesting that these peptides are mediators of leptin's action in the hypothalamus. Anabolic pathways such as those including NPY and galanin promote feeding and are inhibited by leptin, whereas catabolic pathways which include CART and CRH have the opposite effect and are stimulated by leptin. In the current review we examine the significant role of the CART, CRH, NPY and galanin in the regulation of energy balance.
Obesity is a multifactorial pathology currently considered one of the main public health problems. Its prevalence is increasing dramatically in the last decades, reaching huge rates in Brazil and many other countries. Regardless of the factors associated with genetic predisposition, this pathology is often associated with abnormal food intake, and also with high consumption of caloric foods and sedentary habits. Thus, obesity is the result of an imbalance between food intake and energy expenditure. One of the greatest research interests in nutrition has currently been the dietetic determinants that may exert an influence on the process of food intake, as well as the role of foods on physiological, physical and chemical factors most related to the processes of satiation and satiety. Based on these aspects, this paper analyzes several research works to gain a better insight of the dietetic factors affecting food intake and body weight regulation.
There is a growing literature on the role of leptin in appetite and neuroendocrine regulation in domestic ruminants. Circulating leptin concentration is higher in fat than in thin sheep, is reduced by chronic underfeeding and is higher in sheep subjected to long-day rather than short-day photoperiods. Leptin is reduced acutely by fasting and increases after meals so that there are long- and short-term components to the systemic leptin signal. Nutritional stimulation of reproductive neuroendocrine output is associated with increased circulating concentrations of leptin; peripheral leptin administration restores LH secretion in fasted sheep, and leptin is permissive (although not a trigger) for puberty. Intracerebroventricular (i.c.v.) pharmacological leptin infusion stimulates LH in underfed but not in well-fed sheep, and reduces food intake in well-fed sheep. A single i.c.v. pharmacological injection or physiological infusion of leptin stimulates LH in well-fed sheep, with or without a concomitant decrease in appetite. Furthermore, these appetite and LH responses are differentially affected by photoperiod, indicating that different neuronal pathways may mediate the two responses. Hypothalamic leptin receptors co-localize with orexigenic and anorexigenic neurones, some of which contact GnRH cells, but the confluence of leptin signalling with photoperiod (melatonin) signalling remains unresolved. Photoperiod-entrained sheep provide potential models of altered central leptin sensitivity, in which downstream mechanisms regulating appetite and GnRH may be dissociated.
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BACKGROUND: The serotonergic system is implicated in the pathophysiology of posttraumatic stress disorder (PTSD) and depression. The present study focused on platelet serotonin (5-HT) concentration and symptoms of comorbid depression in war veterans with or without PTSD. METHODS: PTSD and depression were evaluated using Clinician Administered PTSD Scale, Davidson Trauma Scale, Montgomery-Asberg Depression Rating Scale and Hamilton Anxiety Scale. Sixty-five male drug-free war veterans (48 with PTSD and 17 without PTSD) and 65 age- and sex-matched healthy controls were studied. RESULTS: Comorbid depression occurred in 54 and 31% of war veterans with PTSD and without PTSD, respectively. Platelet 5-HT concentration was similar in the groups of depressed and nondepressed war veterans with or without PTSD and healthy controls. Platelet 5-HT concentration was found to differ between war veterans with various degrees of appetite loss. A positive correlation was observed between platelet 5-HT concentration and severity of appetite loss in veterans with PTSD. There was no relationship between platelet 5-HT concentration and severity of other symptoms of PTSD or depression. LIMITATIONS: War veterans included in the study were outpatients. CONCLUSIONS: War veterans with PTSD had a high incidence of comorbid depression, that was not related to platelet 5-HT concentration. The marked relationship between platelet 5-HT concentration and severity of appetite loss, suggested that 5-HT system is involved in the regulation of appetite, at least in depressed war veterans with PTSD.
OBJECTIVE: Drinking ethanol stimulates the appetite, producing a positive energy balance. The mechanism by which ethanol regulates the appetite in the central nervous system, however, has not been fully understood. The aim of this study is to investigate the interaction of ethanol with the satiety effect of leptin, a hormone which suppresses the appetite in the hypothalamic region. DESIGN: : Leptin (7.5 micro g) or the same dose of phosphate buffer saline (PBS) was administered into the third ventricle (i.c.v.), 30 min after an intraperitoneal injection (i.p.) of ethanol (0.5 g/kg body weight) or the same dose of PBS. MATERIALS: Adult male Sprague-Dawley rats weighing 290-320 g were used. MEASUREMENTS: Food intake was measured 2, 12 and 24 h after leptin i.c.v. infusion. The tyrosine phosphorylation of signal transducer and activator transcription factor 3 (STAT3) in the hypothalamus was analyzed by Western blotting. RESULTS: The cumulative food intakes in the saline/leptin group (saline i.p.+leptin i.c.v.) were markedly reduced to about 45% of the saline/PBS group (saline i.p.+PBS i.c.v.) at 2, 12 and 24 h time points (P<0.05, 0.001, and 0.005, respectively). As compared with the saline/leptin group, those of the ethanol/leptin group (ethanol i.p.+leptin i.c.v.) were significantly increased to the level seen in the saline/PBS group at 12 and 24 h time points (P<0.05, and P<0.005 vs the saline/leptin group, respectively). Ethanol administration resulted in about a 50% reduction of the leptin-induced STAT3 tyrosine phosphorylation seen in the hypothalamic protein as compared to that of the saline/leptin group. CONCLUSION: These findings suggest that ethanol-induced enhancement of the appetite may, in part, result from leptin resistance transiently caused by ethanol to attenuate the leptin signal transduction.
BACKGROUND: In patients with chronic renal failure, rHuEpo therapy ameliorates anaemia and improves wellbeing, exercise tolerance, and appetite. Both leptin and neuropeptide Y play an important role in regulation of appetite and energy balance in humans. METHODS: The present study aimed to assess the influence of 12 months rHuEpo therapy on plasma leptin and neuropeptide Y concentrations in 15 haemodialysed patients (HDP) (6F, 9M; mean age 40.8+/-2.9 years; mean BMI 23.6+/-1.1 kg/m2; mean duration of HD 3.3+/-0.6 months) (Epo group). A second group (No-Epo group) consisted of 17 HDP (9F, 8M; mean age 44+/-3.2 years; mean BMI 24.3+/-1.0 kg/m2; mean duration of HD 2.5+/-0.4 months) not treated with rHuEpo for 12 months. Basal plasma leptin and neuropeptide Y concentrations were estimated by RIA at the beginning and after 3, 6, 9 and 12 months of rHuEpo therapy (Epo group) or clinical observation (No-Epo group). The control group consisted of 30 healthy subjects (15 females, 15 males, mean age=38.2+/-1.7 years, mean BMI 24.5+/-0.7 kg/m2). RESULTS: Baseline plasma leptin concentrations in HDP were higher, although statistically not significant than leptinaemia in healthy subjects. After 3, 6, and 12 months of rHuEpo therapy plasma leptin concentrations were significantly lower than at the beginning of the study. Baseline plasma neuropeptide Y concentrations in HDP did not differ significantly from controls. After 3 and 6 months of the study period plasma neuropeptide Y concentrations increased significantly in patients of both the Epo and No-Epo group. This increase was, however, significantly higher in rHuEpo-treated than in untreated patients. CONCLUSIONS: (1) rHuEpo treatment in haemodialysed patients with chronic renal failure is followed by a significant decline of leptinaemia and disappearance of the physiological positive BMI/leptinaemia relationship. (2) Suppression of leptinaemia induced by rHuEpo may be of clinical relevance in haemodialysed patients with chronic renal failure.
Impaired appetite and weight changes are commonly seen in patients with depression, but the pathophysiology behind this imbalance between energy intake and energy expenditure remains largely unknown. The aim of this paper is to review the literature regarding a possible role for cytokines in the regulation of appetite and body weight, with special emphasis on depression. There now exists a substantial amount of evidence that depressed patients show signs of immune activation including increased levels of proinflammatory cytokines. Cytokines, which by themselves have anorectic properties, stimulate the release of the cytokine-like anorexogenic peptide leptin. In addition to their anorectic properties, both proinflammatory cytokines and leptin interact with the hypothalamic-pituitary-adrenal (HPA) axis, the sympathetic nervous system (SNS) and the immune system. In turn, these systems regulate energy balance as well as they are dysfunctional in depression. Furthermore, both proinflammatory cytokines and leptin can induce anhedonia, one of the cardinal symptoms of depression. In view of the different effects on appetite and/or body weight observed in melancholic versus atypical depression, we suggest that cytokines are differentially altered in these subtypes of depression, and that this may explain some of the inconsistency in the reported findings of cytokine as well as leptin levels in depressed patients. Finally, we propose that the immune system uses the interoceptive pathway projecting to the insular cortex, a brain region where cytokine-induced changes in appetite could be partly mediated, and that this pathway is activated in depression.
Endogenous cannabinoid systems have been implicated in the physiological regulation of appetite by the ability of cannabinoid receptor agonists to induce hyperphagia. Both the exogenous cannabinoid Delta9-THC and the endocannabinoid arachidonoyl ethanolamide (anandamide) stimulate eating in rats. However, there has been no detailed analysis of the adjustments to feeding behaviour underlying this action. We used observational methods to determine the specific components of feeding affected by these compounds. Two groups (n=6) of presatiated, male, Lister hooded rats received either Delta9-THC (0, 0.5, 1.0 or 2.0 mg/kg) or anandamide (0, 1.0, 5.0 or 10.0 mg/kg sc), and their behaviour in an open field was recorded for 45 min. Behaviour (eating, drinking, rearing, grooming, sniffing, locomotion, resting/inactivity, sleeping) was continuously monitored to provide data on the latency, temporal distribution, duration and frequency of each category. Under control conditions, a minority of animals ate small quantities of lab chow, with feeding beginning only after a long latency. Both Delta9-THC and anandamide selectively stimulated feeding, with a marked reduction in latency. Apart from its rapid onset, cannabinoid-induced eating retained the normal, species-typical sequence, characteristic of untreated, free-feeding rats. Our data suggest that exogenously administered cannabinoids promote eating by increasing the incentive value of food and support a role for endocannabinoids in the regulation of the appetitive aspects of feeding motivation.