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PubMed1985

Cerebrospinal fluid sodium concentration and salt appetite.

Infusion into a lateral brain ventricle (IVT) of different hypertonic (0.7 M) saccharide solutions decreased [Na+] of cerebrospinal fluid (CSF). Increased Na appetite of moderately Na-deplete sheep was observed during infusion of mannitol, L-glucose or L-fucose, while no change was observed during infusion of D-glucose, D-fucose, D-mannose, 2-deoxy-D-glucose, 3-O-methyl-glucose or fructose. In other experiments, increased Na appetite was observed during infusion of 2.3 mM phlorizin (a relatively specific blocker of Na-coupled glucose transport into cells) or 2.3 mM phlorizin plus 0.7 M D-glucose. In addition, phlorizin eliminated the characteristic decrease in Na appetite but did not affect the increase in water intake caused by IVT infusion of hypertonic NaCl which increased [Na+] of CSF. The results suggest that: (a) there are sensors within the neuropil which respond to change of [Na+] and influence Na appetite, and that these changes of [Na+] are induced deep within the neuropil by those saccharides which do not cross the blood-brain barrier or enter cells; change of CSF[Na+] alone is not sufficient to alter appetite but a change in brain extracellular fluid (ECF)[Na+] is probably necessary; (b) the theory is advanced that the stimulus for altered Na intake could be altered brain ECF[Na+] producing a change in cerebral intracellular fluid (ICF)[Na+] of the sensors; and (c) phlorizin, in reducing or blocking Na-coupled glucose transport, could increase Na appetite by producing a fall in ICF[Na+] of the specific neurones subserving sodium appetite or prevent a decrease in Na appetite caused by IVT infusion of hypertonic NaCl by preventing an increase in ICF[Na+] of this same neuronal system.

Animals↗
PubMed2004

Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite.

BACKGROUND: Total sleep deprivation in rodents and in humans has been associated with hyperphagia. Over the past 40 years, self-reported sleep duration in the United States has decreased by almost 2 hours. OBJECTIVE: To determine whether partial sleep curtailment, an increasingly prevalent behavior, alters appetite regulation. DESIGN: Randomized, 2-period, 2-condition crossover clinical study. SETTING: Clinical Research Center, University of Chicago, Chicago, Illinois. PATIENTS: 12 healthy men (mean age [+/-SD], 22 +/- 2 years; mean body mass index [+/-SD], 23.6 +/- 2.0 kg/m2). MEASUREMENTS: Daytime profiles of plasma leptin and ghrelin levels and subjective ratings of hunger and appetite. INTERVENTION: 2 days of sleep restriction and 2 days of sleep extension under controlled conditions of caloric intake and physical activity. RESULTS: Sleep restriction was associated with average reductions in the anorexigenic hormone leptin (decrease, 18%; P = 0.04), elevations in the orexigenic factor ghrelin (increase, 28%; P < 0.04), and increased hunger (increase, 24%; P < 0.01) and appetite (increase, 23%; P = 0.01), especially for calorie-dense foods with high carbohydrate content (increase, 33% to 45%; P = 0.02). LIMITATIONS: The study included only 12 young men and did not measure energy expenditure. CONCLUSIONS: Short sleep duration in young, healthy men is associated with decreased leptin levels, increased ghrelin levels, and increased hunger and appetite.

Adult↗
PubMed2000

Conjugated linoleic acid supplementation in humans: effects on circulating leptin concentrations and appetite.

Conjugated linoleic acid (CLA) has been demonstrated to reduce body fat in animals. However, the mechanism by which this reduction occurs is unknown. Leptin may mediate the effect of CLA to decrease body fat. We assessed the effects of 64 d of CLA supplementation (3 g/d) on circulating leptin, insulin, glucose, and lactate concentrations in healthy women. Appetite was assessed as a physiological correlate of changes in circulating leptin levels. Analysis of plasma leptin concentrations adjusted for adiposity by using fat mass as a covariate showed that CLA supplementation significantly decreased circulating leptin concentrations in the absence of any changes of fat mass. Mean leptin levels decreased over the first 7 wk and then returned to baseline levels over the last 2 wk of the study in the CLA-treated group. Appetite parameters measured at around the time when the greatest decreases in leptin levels were observed showed no significant differences between supplementation and baseline determinations in the CLA-supplemented group or between the CLA and placebo-supplemented groups. There was a nonsignificant trend for mean insulin levels to increase toward the end of the supplementation period in CLA-treated subjects. CLA did not affect plasma glucose and lactate over the treatment period. Thus, 64 d of CLA supplementation in women produced a transient decrease in leptin levels but did not alter appetite. CLA did not affect these parameters in a manner that promoted decreases of adiposity.

Adipose Tissue↗
PubMedDate not supplied

Intestinal transit and body weight responses to ovarian hormones and dietary fiber in rats.

A two-part experimental design was used to study the effects of ovarian hormone cessation, hormone supplementation, and dietary fiber composition on body weight, appetite, and intestinal transit. In Part 1, effects of ovarian hormone status on body weight and baseline and stimulated intestinal transit were measured in chow-fed rats. Sprague-Dawley rats were ovariectomized (OVX), then injected daily (22 days) with estrogen (E), progesterone (P), the combination (E + P), or placebo. Controls were sham operated and placebo injected. Among OVX rats, E and E + P had the least body weight gain (9%, 6%); placebo and P had the greatest (36%, 34%). In OVX-P, baseline intestinal transit (measured in anesthetized rats as distance traveled by a charcoal marker) was relatively low, but vagal stimulation via centrally administered thyrotropin-releasing hormone evoked an increase significantly larger than that in other groups. In Part 2, experiments probed the interacting effects of ovarian hormone cessation and dietary fiber composition on body weight and baseline intestinal transit. Caloric intake was measured to determine the contribution of altered appetite. Rats were OVX or sham operated, then fed liquid diets with or without dietary fiber (25 days). OVX fiber-fed rats had significantly higher caloric intake, weight gain, and baseline intestinal transit than other groups. Caloric intake did not fully account for group differences. These results demonstrate modulation of GI function by ovarian hormones and dietary fiber.

Animals↗
PubMed1978

Effect of diazepam on food consumption in rats.

Diazepam significantly increased milk consumption in rats that had never been exposed to this food before but not in rats trained to drink milk. Diazepam failed to increase lever-pressing for food reward except when this behavior had been previously suppressed by the simultaneous administration of electric shock. These data suggest that diazepam does not alter appetite, but enhances the expression of motivation suppressed by instinct or training.

Animals↗
PubMed2006

Nonalcoholic Fatty Liver Disease (NAFLD): Approach in the Adolescent Patient.

Nonalcoholic fatty liver disease (NAFLD) is a spectrum of liver disease whose hallmark is the accumulation of large-droplet fat in hepatocytes. This metabolic disorder occurs mainly in overweight or obese individuals. The disease mechanism involves hyperinsulinemia and hepatic insulin resistance, not ethanol abuse. NAFLD may be the hepatic manifestation of the "metabolic syndrome" classically associated with type 2 diabetes mellitus and cardiovascular disease. NAFLD ranges from simple steatosis, which is the least rapidly progressing disorder, to nonalcoholic steatohepatitis to cirrhosis, which can evolve to chronic liver failure. The high prevalence of NAFLD in children has been recognized only in the past 5 to 10 years, as rates of childhood obesity have soared. Accordingly, the best strategies for diagnosis and treatment of childhood NAFLD are a work in progress and remain controversial. Weight reduction through a healthy diet and regular medium-intensity exercise is the mainstay of current treatment. Few research data are available to guide pharmacologic therapy. Certain points regarding management of childhood NAFLD require emphasis: It is a serious liver disease that requires detailed clinical investigation. Other liver diseases causing fatty liver and/or abnormal liver tests, notably Wilson disease and chronic viral hepatitis, need to be excluded. Liver biopsy can provide critical diagnostic and staging information. Associated genetic or endocrine disorders need to be identified. Treatment should begin with a low-glycemic index diet that provides adequate nutrients but is low in harmful fats and eliminates foods causing postprandial hyperglycemia. Initially, this can target two to three problem foods so that it is easy for the adolescent to follow. Regular exercise suited to the capabilities and interests of the teenager should be added to the daily routine. Where possible, a team approach, including a dietician and psychologist, should be utilized, as adolescents do better in a supportive atmosphere. Optimal drug treatment requires further research: current front-runners are vitamin E and metformin. The roles of drugs that alter appetite and bariatric surgery for adolescents with NAFLD have not been determined.

Journal Article↗
PubMed2003

Paroxetine does not improve symptoms and impairs cognition in frontotemporal dementia: a double-blind randomized controlled trial.

RATIONALE: Patients with frontal variant frontotemporal dementia (fvFTD) present with disinhibition, impulsiveness, apathy, altered appetite and stereotypic behaviors. A non-randomized clinical trial found improvement in these symptoms after treatment with a selective serotonin reuptake inhibitor (SSRI). OBJECTIVES: We aimed to subject a SSRI, paroxetine, to a more rigorous test of its efficacy using a double-blind, placebo-controlled experimental design. METHODS: Ten subjects meeting the consensus criteria for FTD were entered into a double-blind, placebo-controlled crossover trial. Doses of paroxetine were progressively increased to 40 mg daily. The same regimen was used for placebo capsules. Subjects were assessed with a battery of cognitive tests in the sixth week of paroxetine and placebo treatment. At each assessment, caregivers were interviewed using the Neuropsychiatric Inventory and asked to complete the Cambridge Behavioral Inventory. RESULTS: There were no significant differences on the Neuropsychiatric Inventory or the Cambridge Behavioral Inventory. Paroxetine caused a decrease in accuracy on the paired associates learning task, reversal learning and a delayed pattern recognition task. There were no changes on the decision-making task, in spatial span, spatial recognition, spatial working memory, digit span and verbal fluency. CONCLUSIONS: This study finds no evidence for the efficacy of paroxetine in the treatment of fvFTD. The results suggest that a chronic course of paroxetine may selectively impair paired associates learning, reversal learning and delayed pattern recognition. This pattern of deficits closely resembles that seen after tryptophan depletion. Results are discussed with respect to current theories on serotonergic modulation of orbitofrontal/ventromedial prefrontal cortex.

Aged↗
PubMed1990

What do we mean when we say "palatable food"?

The word palatability and related words have not been used in a consistent way. Palatability may be a property of a food, of the organism eating the food, or both. Investigators have failed to distinguish different possible meanings of the statement: "palatable foods increase intake". This may indicate: (1) a simple observation that some foods stimulate more intake than others, (2) an innate response to the taste of foods that alters appetite, (3) a correlate of food intake that does not itself affect intake, and (4) a link in a causal chain involving prior associations between foods and their postingestive consequences.

Appetite↗
PubMed2006

Anorexia in chronic obstructive pulmonary disease--association to cachexia and hormonal derangement.

BACKGROUND: In patients with chronic obstructive pulmonary disease (COPD) weight loss frequently occurs that may ultimately lead to cachexia as a serious co-morbidity, indicating severely impaired functional capacity, health status and increased mortality. Increased energy expenditure due to mechanic and metabolic inefficiency and systemic inflammation are determinants of a hypermetabolic state that is not balanced by dietary intake. Anorexia may importantly contribute to weight loss in COPD, however, the association between immune and hormonal derangement and altered appetite has not been studied in detail. AIM: The aim of the present study was to investigate whether anorexia in COPD is related to inflammation and hormonal derangement in association to weight loss. METHODS: We prospectively enrolled 103 consecutive patients with COPD (age 59.8+/-1.3 years, 35% female, mean FEV1 38.3+/-1.7%) in comparison to healthy controls of similar age (n=15). RESULTS: In 34 patients (33%) cachexia was diagnosed (weight loss >7.5%, BMI < or = 24 kg/m2). Cachectic COPD patients had lower BMI (19.0+/-0.5 vs 25.6+/-0.7 kg/m2) and impaired lung function (FEV1 31+/-2% vs 42+/-2%, FVC 51+/-3 vs 59+/-3%, both p<0.001). Inflammatory immune activation (IL-6 and IL-6/IL-10 ratio) was significantly higher in cachectic COPD patients. Analysis of the extent of anorexia (visual analogue scale) revealed that cachectic COPD patients had significantly decreased subjective desire to eat compared to non-cachectic patients (3.5+/-0.3 vs 6.3+/-0.2, p<0.001). Patients with COPD and cachexia showed evidence of acquired GH resistance (decreased IGF-1/GH ratio) and insulin resistance (HOMA). Anorexia showed a direct correlation with the IGF-1/GH ratio (r=0.34, p<0.05) and was further related to BMI and % weight loss (both p<0.001). CONCLUSION: In COPD anorexia relates to hormonal derangement and inflammatory immune activation. Anorexia contributes to development of cachexia. The concept of appetite stimulating therapy emerges as a novel therapeutic option in cachectic COPD patients.

Anorexia↗
PubMedDate not supplied

Intake of trans fatty acid-rich hydrogenated fat during pregnancy and lactation inhibits the hypophagic effect of central insulin in the adult offspring.

OBJECTIVE: Using rats we examined whether maternal intake of hydrogenated fat rich in trans fatty acids affects brain fatty acid profile, hypothalamic content of insulin receptor and insulin receptor substrate-1 proteins, and the hypophagic effect of centrally administered insulin in 3-mo-old male progeny. METHODS: Throughout pregnancy and lactation, Wistar rats ate isocaloric/normolipidic diets with soybean oil (control) or soybean oil-derived hydrogenated fat (trans diet) as a fat source. Upon weaning, the trans offspring continued on the trans diet (trans group) or were switched to a control diet (trans-control group). RESULTS: Compared with control rats, trans rats had lower brain levels of eicosapentaenoic acid. Compared with trans rats, trans-control rats had increased levels of total polyunsaturated fatty acids and arachidonic acid and decreased levels of trans fatty acids, saturated fatty acids, and monounsaturated fatty acids. Insulin receptor and insulin receptor substrate-1 levels were significantly lower (44% and 38%, respectively) in trans than in control rats. In trans-control rats, insulin receptor was 26% lower (P < 0.05), whereas insulin receptor substrate-1 was 50% lower, than in control rats. Insulin decreased 24-h feeding in control (27%) and trans (38%) rats but failed to do so in trans-control rats. The latter group had increased serum glucose levels. CONCLUSIONS: The data suggest that the early (intrauterine/perinatal) exposure to hydrogenated fat rich in trans fatty acids programmed the hypothalamic feeding control mechanisms. As young adults, only trans-control animals showed loss of insulin-induced hypophagia, indicating that the mismatch between early and later nutritional environments was relevant. However, the trans group also showed signs of altered appetite signaling mechanisms, suggesting that the early adaptations may have deleterious consequences later in life.

Animals↗
PubMed2002

Recreational Ecstasy/MDMA, the serotonin syndrome, and serotonergic neurotoxicity.

The ring-substituted amphetamine derivative 3,4-methylenedioxymethamphetamine (MDMA) or "Ecstasy" is widely used a recreational drug. It stimulates the release and inhibits the reuptake of serotonin (5-HT) and other neurotransmitters such as dopamine to a lesser extent. The acute boost in monoamine activity can generate feelings of elation, emotional closeness, and sensory pleasure. In the hot and crowded conditions of raves/dances, mild versions of the serotonin syndrome often develop, when hyperthermia, mental confusion, and hyperkinesia predominate. Rest in a cooler environment generally reverses these problems, although they can develop into medical emergencies, which occasionally prove fatal. This acute serotonergic overactivity is exacerbated by the high ambient temperatures, overcrowding (aggregate toxicity), and use of other stimulant drugs. The on-drug experience is generally followed by negative moods, with 80--90% of weekend Ecstasy users reporting 'midweek blues', due probably to monoaminergic depletion. Single doses of MDMA can cause serotonergic nerve damage in laboratory animals, with repeated doses causing extensive loss of distal axon terminals. Huether's explanatory model for this 5-HT neurotoxicity will be briefly described. There is an increasing body of evidence for equivalent neuropsychobiological damage in humans. Abstinent regular Ecstasy users often show: reduced cerebrospinal 5-HIAA, reduced density of 5-HT transporters, blunted response to a fenfluramine challenge, memory problems, higher cognitive deficits, various psychiatric disorders, altered appetite, and loss of sexual interest. Functional deficits may remain long after drug use has ceased and are consistent with serotonergic axonal loss in higher brain regions.

Animals↗
PubMed2000

Psychobiological problems in heavy 'ecstasy' (MDMA) polydrug users.

Twelve heavy recreational ecstasy drug users (30-1000 occasions), 16 light ecstasy users (1-20 occasions) and 22 non ecstasy user controls, with group mean ages around 21 years, were compared. Three self-rating questionnaires were completed when drug-free: the SCL-90 (an outpatient psychiatric symptom checklist), the impulsiveness venturesomeness and empathy (IVE) scale; and the uplifts, hassles, stresses and cognitive failures questionnaire. Heavy Ecstasy users reported significantly higher scores than controls on the following SCL-90 factors: paranoid ideation, psychoticism, somatisation, obsessionality, anxiety, hostility, phobic anxiety, altered appetite and restless sleep, together with greater IVE impulsiveness. Light ecstasy users generally produced intermediate scores, with significantly higher scores than controls on two factors and significantly lower scores than heavy ecstasy users on another two. Previous reports have described various psychiatric and psychobiological disorders in recreational ecstasy users, but it is not known how typical they are, being mainly based on individual case studies. This is the first study to describe psychological problems in a non clinical sample of young recreational ecstasy users. However, our ecstasy users were polydrug users, with both groups showing significantly greater usage of amphetamine, LSD and cocaine, than the controls. These other illicit drugs probably contributed to their adverse psychobiological profiles, while there is also the possibility of pre-existing differences between ecstasy users and non users. However, since repeated MDMA can cause serotonergic neurotoxicity in laboratory animals and man, these problems may reflect reduced serotonin activity induced by regular ecstasy use.

Adolescent↗
PubMed2000

Brain-derived neurotrophic factor regulates glucose metabolism by modulating energy balance in diabetic mice.

We previously reported that brain-derived neurotrophic factor (BDNF) regulates both food intake and blood glucose metabolism in rodent obese diabetic models such as C57BL/KsJ-lepr(db)/lepr(db) (db/db) mice. To elucidate the effect of BDNF on glucose metabolism, we designed a novel pellet pair-feeding apparatus to eliminate the effect of appetite alteration on glucose metabolism. The apparatus was used to synchronize food intake precisely between BDNF-treated and vehicle-treated db/db mice. It was shown using this pellet pair-feeding apparatus that BDNF administered daily (20 mg x kg(-1) x day(-1)) to db/db mice significantly lowered blood glucose compared with pellet pair-fed db/db mice. To evaluate the effect of BDNF on insulin action, we used streptozotocin-induced type 1 diabetic mice. In this case, BDNF did not lower blood glucose concentration but rather enhanced the hypoglycemic action of insulin. In hyperglycemic db/db mice, pancreatic insulin content was reduced and glucagon content was increased compared with normoglycemic db/m mice. BDNF administered to db/db mice significantly restored both pancreatic insulin and glucagon content. Histological observations of aldehyde-fuchsin staining and immunostaining with anti-insulin indicated that insulin-positive pancreatic beta-cells were extensively regranulated by BDNF administration. We also studied the effect of BDNF on KK mice, normoglycemic animals with impaired glucose tolerance. In these mice, BDNF administration improved insulin resistance in the oral glucose tolerance test. To elucidate how blood glucose was metabolized in BDNF-treated animals, we investigated the effect of BDNF on the energy metabolism of db/db mice. Body temperature and oxygen consumption of the pellet pair-fed vehicle-treated mice were remarkably lower than the ad libitum-fed vehicle-treated mice. Daily BDNF administration for 3 weeks completely ameliorated both of the reductions. Finally, to clarify its action mechanism, the effect of intracerebroventricular administration of BDNF on db/db mice was examined. Here, a small dose of BDNF was found to be effective in lowering blood glucose concentration. This indicates that BDNF regulates glucose metabolism by acting directly on the brain.

Animals↗
PubMedDate not supplied

The use of intradialytic parenteral nutrition to treat malnutrition: a case study.

Protein energy malnutrition in dialysis patients has been well-described in the literature. Most malnourished patients with end stage renal disease (ESRD) suffer from a mixed marasmus-kwashiorkor type of malnutrition with loss of both somatic and visceral protein mass. Malnutrition is associated with increased risk of morbidity and mortality. Up to 50% of patients on dialysis have protein energy malnutrition (Mortelmans & Vanholder, 1999). Malnutrition may be under-recognized and under-reported in dialysis patients. Malnutrition may result from inadequate food intake secondary to the uremic condition, nausea, vomiting, loss of appetite, altered taste and other physiologic conditions that impede food intake or metabolism. The usual indices of nutritional assessment--body weight, body mass index (BMI), anthropometrics, etc., may be inaccurate in patients with ESRD, as the results are often skewed by fluid retention. Therefore, we often rely on weight loss, bloodwork, a pre-dialysis low serum potassium, phosphorus and urea, as early signs of a decreased food intake. When patients are malnourished, measures such as oral supplements and/or tube feedings may be used to augment protein and calorie intake. However, when these interventions are inadequate to reverse the malnutrition condition, intradialytic parenteral nutrition (IDPN) should be implemented. Although there is no definite supportive data to show that the use of IDPN improves morbidity and mortality of dialysis patients, there are data to support that IDPN has positive effects on numerous nutritional parameters (Acchiardo, 2000; Capelli et al., 1994; Foulks, 1999; Hiroshige et al., 1998; Ikizler et al., 1995; Korzets et al., 1999; Mortelmans & Vanholder, 1999; Saunders et al., 1999; Smolle et al., 1995). In this article, we will discuss the causes of malnutrition in dialysis patients, the use of IDPN on one of our patients, and the potential complications associated with IDPN.

Body Weight↗
PubMedDate not supplied

[Behavioural disorders in Alzheimer's disease. Data from a populational study].

AIMS: The purpose of this work was to study the characteristics of the behavioural disorders (non-cognitive or neuropsychiatric symptoms) presented by subjects with Alzheimer's disease from a sample of the population together with their relation to the cognitive and functional impairment suffered by these patients. PATIENTS AND METHODS: NEDICES is a longitudinal populational study based on the census of neurological diseases in subjects above the age of 64. In 2001, a study was conducted of the situation of 83 subjects who had started suffering from Alzheimer's disease between 1994 and 1997. Due to death and a number of other reasons, only 32 of them could be examined. Patients were administered a structured interview with scales referring to the cognitive state, functional capacity, severity of the dementia and the presence and severity of neuropsychiatric disorders. RESULTS: All the patients studied presented some non-cognitive symptom. Apathy was the most frequent (93.8%), followed by irritability (81.1%), anxiety (75.0%), dysphoria (71.8%) and agitation-aggressiveness (56.2%). The least frequent were deliria (50.2%), altered nocturnal behaviour and aberrant motor activity (37.6%), altered appetite and eating, and hallucinations (24.9%), disinhibition (21.8%) and euphoria (21.6%). The degree of cognitive impairment and the presence of non-cognitive symptoms exerted a similar and independent effect on functional capacity. Only 56.3% of the patients were treated with some kind of anticholinesterase or psychotropic medication. CONCLUSIONS: Our census-based populational study confirmed the high prevalence rate of non-cognitive symptoms in patients with Alzheimer's disease. These data confirm the notion that these symptoms are intrinsic manifestations of the disease.

Aged↗
PubMed2001

The actual, but not labelled, fat content of a soup preload alters short-term appetite in healthy men.

The effects of the actual and labelled fat content of a soup preload on appetite at a test meal 30 min later were assessed in 16 healthy men. Each participant ate lunch on four occasions, combining two levels of fat energy (Low, 265 kJ or High, 1510 kJ) and two types of label (Low-fat or High-fat), presented as fictitious soup brand names. Preliminary work established that the Low-fat labels produced an expectation of reduced fat content and lower anticipated hedonic ratings, whereas the High-fat labels generated expectations of a high-fat content and above average hedonic ratings. These expectancies were confirmed in the main experiment, with the soups labelled as high fat rated as both more pleasant and creamy than those labelled low-fat, independent of actual fat content. However, intake at the test meal was unaffected by the preload label, but instead reflected the actual fat (hence, energy) content of the soup, with significantly lower food intake after the high-fat soup regardless of the food label. Rated hunger was lower, and fullness higher, at the start of the meal after the high-fat preloads regardless of how they were labelled, while the pattern of appetite change during the test meal was unaffected by preload. These results suggest that realistic food labels can modify the immediate experience of a consumed food, but do not alter appetite 30 min later in healthy men.

Adult↗
PubMed1991

Relationships between weight and caloric intake of men who stop smoking: the Multiple Risk Factor Intervention Trial.

Data from 6,569 middle-aged men in the Multiple Risk Factor Intervention Trial were analyzed to determine whether the weight change associated with smoking cessation resulted primarily from appetite or metabolic alterations. The appetite hypothesis attributes weight gain to an enhanced appetite and subsequent increase in caloric intake. The metabolic change hypothesis attributes weight gain to a metabolic alteration and subsequent decrease in basic caloric needs. Caloric intake and weight changes were tabulated for men who quit smoking and were compared to similar changes in men who continued smoking over 12 months. The difference between caloric intake changes in men quitting smoking versus men continuing smoking, controlled for weight change, was attributed to the metabolic change hypothesis. Men who quit smoking consumed 103 calories per day less (95% confidence interval = 29 to 177) than men who continued smoking with similar body weight changes. The decrease in caloric intake attributed to smoking cessation was proportional to the number of cigarettes smoked prior to cessation [corrected].

Adult↗
PubMed1997

Altered concentrations of appetite regulators may contribute to the development and maintenance of HIV-associated wasting.

OBJECTIVE: To examine the relation of circulating appetite neuropeptides, CCK-8 sulphate (CCK-8s) and beta-endorphin, and the tumour necrosis factor-alpha (TNF-alpha) and soluble TNF receptors (sTNFR) to the anorexia and wasting associated with HIV-infection. DESIGN: Cross-sectional analysis. SETTING: A university-based HIV/AIDS ambulatory clinic in Madrid, Spain. PARTICIPANTS: Thirty-six randomly selected AIDS patients without concomitant diseases or secondary infections were classified into two groups: 19 patients with wasting and 17 with normal body weight, and 18 healthy controls. MEASUREMENTS: Nutritional status was evaluated by anthropometry, laboratory parameters and self-report of appetite. Plasma levels of TNF-alpha and sTNFR proteins p55 (sTNFR-p55) and p75 (sTNFR-p75) were determined by enzyme immunoassay, whereas CCK-8s and beta-endorphin levels were measured by radioimmunoassay. RESULTS: AIDS patients with wasting had significantly higher plasma concentrations of CCK-8s, but lower levels of beta-endorphin when compared to well-nourished AIDS patients (P < 0.01) or controls (P < 0.001). Mean levels of TNF-alpha, and sTNFR-p55 and sTNFR-p75 were greater in AIDS patients with wasting than in asymptomatic AIDS patients or in controls. No significant association was observed between any of these circulating peptides and the parameters of malnutrition. CONCLUSIONS: An activation of the TNF system, together with reciprocal changes in plasma concentrations of two neuropeptides with opposing appetite regulation, that is increased concentrations of CCK-8s but lower levels of beta-endorphin, are associated with the presence of HIV wasting. We hypothesize that these changes may contribute to the development of HIV wasting by producing a pathological inhibition of appetite.

Acquired Immunodeficiency Syndrome↗