[Obesity as a disorder of appetite behavior. II. Psychosocial and psychodynamic aspect of obesity].
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Adolescent↗
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Leptin and reproductive function in males.
Leptin is a circulating protein produced by adipocytes that has been implicated in control of body weight through appetite regulation and control of reproduction, most likely through an effect on the central nervous system. From studies in mice, it is clear that the genetic background of the animal on which the mutation in the leptin gene is placed can influence how that mutation is expressed. Although the effects of leptin have been more thoroughly documented in nonprimate species than in primates, a few human families with genetic mutations of the gene for leptin or the leptin receptor show obesity and impaired fertility. There is conflicting evidence regarding the effects of leptin in male primates, but it appears that the metabolic and reproductive effects of low leptin levels caused by reduced energy intake in adult animals can be more readily alleviated by administration of energy substrates than by administration of leptin.
Adipocytes↗
Obesity and related metabolic abnormalities during antipsychotic drug administration: mechanisms, management and research perspectives.
Excessive body weight gain (BWG) is a common side effect of some typical and atypical antipsychotic drugs (APs). Convergent evidence suggests a hierarchy in the magnitude of BWG that may be induced by diverse agents, being very high for clozapine and olanzapine; high for quetiapine, zotepin, chlorpromazine, and thioridazine; moderate for risperidone and sertindole; and low for ziprazidone, amisulpiride, haloperidol, fluphenazine, pimozide, and molindone. BWG may be related to increased appetite that is due to drug interaction with the brain monoaminergic and cholinergic systems and to the metabolic/endocrine effects of hyperprolactinemia. Subjects with schizophrenia and bipolar disorders manifested a significantly high prevalence of diabetes, even before the introduction of atypical APs. However, clozapine and olanzapine appear to display a high propensity to induce glucose dysregulation and dyslipidemia. Sudden BWG, insulin resistance, increased appetite, and related endocrine changes also may be involved in the development of glucose intolerance and dyslipidemia in predisposed individuals. Patients should be informed of these side effects in order to prevent excessive BWG, and their blood glucose and lipids should be monitored before treatment and then at regular intervals. Nutritional advice must be given and regular physical exercise recommended. An appropriate selection of APs ought to be based on drug efficacy for specific patients and assessment of relevant risk factors such as propensity to gain weight; family or personal history of diabetes or hyperlipidemia; and elevated fasting serum glucose, lipid, or insulin levels. At present, there is no standardized pharmacological treatment for AP-induced BWG. Some studies have assessed the effects of agents such as amantadine, orlistat, metformin, nizatidine, and topiramate on AP-induced BWG. Further studies will provide tools to identify patients at high risk for obesity and metabolic abnormalities during AP administration. Excessive body weight gain (BWG), glucose intolerance, and dyslipidemia during treatment with antipsychotic drugs (APs) were reported in the late 1950s [14,101]. However, after 1990, interest in these problems increased noticeably, mainly because of the high propensity of some new atypical APs to induce these side effects (Fig.1). The APs are currently used in diverse mental disorders. Hence, excessive BWG and metabolic dysfunction are not exclusive of subjects with schizophrenia. In the case of bipolar disorders, AP-induced BWG may be additive to that induced by mood stabilizers [14,48,101]. The clinical features [2,14,24,133,139,140] and mechanisms [14,34,68,87,93,101,130] of BWG and metabolic dysfunction have been previously reviewed. In this article, we focus on a unified theory to explain these side effects, based on the interaction of APs with brain neurotransmitters involved in appetite regulation. This review comprises the following sections: 1) the clinical features of AP-induced BWG; 2) the effects of APs on carbohydrate and lipid metabolism in humans and experimental animals; 3) mechanisms involved in BWG, glucose, and lipid dysregulation; 4) strategies for prevention and treatment of these side effects; and 5) research perspectives in the field. The following sources were consulted: MEDLINE, Cochrane database system, and PsychINFO. Numerous articles referred to in leading articles also were consulted. The literature on this subject has increased so rapidly that it was impossible to include all the data recently published. For the first two sections, references that illustrate current controversies in the field were selected.
Animals↗
Regulation of food intake and body weight by cobalt porphyrins in animals.
Cobalt-substituted protoporphyrin administered subcutaneously to normal adult rats elicited prompt decreases in food intake and sustained decreases in body weight. Repetitive parenteral administration of small doses of this synthetic heme analogue resulted in dose-related diminutions of carcass fat content without changes in carcass protein content. Direct injection of the compound into the third ventricle of the brain produced changes in food intake and body weight that were quantitatively similar to those observed after parenteral treatment but required only 1-2% of the parenteral dose. The effects of intracerebroventricularly administered cobalt protoporphyrin on body weight were dose-related and were not produced by inorganic cobalt, heme, and a number of other metal-substituted protoporphyrins. Differential body weights between control and treated animals persisted for at least 300 days after intracerebroventricular injections of a single dose (0.2 or 0.4 mumol/kg of body weight) of the compound. Similar effects were observed after subcutaneous administration of the metalloporphyrin to genetically obese Zucker (fa/fa) rats and normal and genetically obese (ob/ob) mice as well as chickens and dogs. Cobalt-substituted mesoporphyrin elicited comparable effects on food intake and body weight. The results of these studies define a new biological action of cobalt protoporphyrin and demonstrate that this and certain other cobalt porphyrins can act, at least in part, in the central nervous system to regulate appetite and to produce long-sustained diminutions in body weight and carcass content of fat in animals.
Animals↗
Specific sequences in the N and C termini of apolipoprotein A-IV modulate its conformation and lipid association.
Apolipoprotein (apoA-IV) is a 376-residue exchangeable apolipoprotein that may play a number of important roles in lipid metabolism, including chylomicron assembly, reverse cholesterol transport, and appetite regulation. In vivo, apoA-IV exists in both lipid-poor and lipid-associated forms, and the balance between these states may determine its function. We examined the structural elements that modulate apoA-IV lipid binding by producing a series of deletion mutants and determining their ability to interact with phospholipid liposomes. We found that the deletion of residues 333-343 strongly increased the lipid association rate versus native apoA-IV. Additional mutagenesis revealed that two phenylalanine residues at positions 334 and 335 mediated this lipid binding inhibitory effect. We also observed that residues 11-20 in the N terminus were required for the enhanced lipid affinity induced by deletion of the C-terminal sequence. We propose a structural model in which these sequences can modulate the conformation and lipid affinity of apoA-IV.
Amino Acid Sequence↗
Clinical treatment of obesity: are drugs and surgery the answer?
Obesity treatment remains a 'Cinderella' of all clinical management programmes, but generally without a happy ending. The great expectation for new therapeutic agents has not been fulfilled in clinical practice, whilst the restriction of eating through surgical division of the upper bowel seems strange in an age of advanced and sophisticated technology. The better understanding of the neuro-regulation of appetite, and its application as part of evidence-based clinical interventions, could lead to a more coherent approach to obesity treatment. Nevertheless, investigation of potential neuroendocrine targets for appetite suppression suggests redundancy in the systems, which make development of effective agents against single receptors impractical. Importantly, the progressive rise in the prevalence of obesity will inevitably mean that only a small proportion of afflicted patients will actually be treated by long-term drugs and surgery. Drugs and surgery are not currently the answer for the majority of obese individuals. What is required is a better way of identifying patients who may particularly benefit from such approaches. However, the major emphasis must be the development of effective population-wide interventions that halt the increase in fatness and ensure that future generations maintain and enjoy a healthy body weight.
Anti-Obesity Agents↗
Effect of bipiperidyl mustard and gold thioglucose on the hypothalamus and growth of the hatchling chick and duckling.
Following a 48 h fasting period after hatching, male Cobb broiler chicks were injected with either bipiperidyl mustard (intraperitoneally; 0.01 and 0.02 mg/g body weight) or goldthioglucose (intracardially; 0.25 mg/g body weight). The influence of these obesifying agents on growth was compared to control injections of physiological saline. Bi-weekly body weights, and eight week live, carcass, and abdominal fat plus carcass weights were depressed in chicks injected with bipiperidyl mustard, the depression being significant for eight-week abdominal fat weights. In birds injected with gold thioglucose all weights were significantly depressed. In a separate investigation, histological evidence of generalised hypothalmic lesions was observed in both chicks (Gallus domesticus) and ducklings (Anas platyrhynchos) injected with bipiperidyl mustard or gold thioglucose. Similar lesions were absent in control chicks and ducklings. The possibility of the existence of a sex-steroid-mediated endorphinergic-glucostatic mechanism for appetite regulation in birds is discussed.
Adipose Tissue↗
Gastric capacity, gastric emptying, and test-meal intake in normal and bulimic women.
The role of the stomach in regulating appetite in bulimia nervosa was examined. Subjects were nine normal and nine bulimic women of similar age, height, and weight. Gastric capacity was estimated by filling a balloon in the stomach. The mean stomach capacity of bulimic subjects was significantly larger than that of normal subjects, as revealed by the larger balloon volume tolerated (P less than 0.01) and by the larger volume needed to produce a 5 cm H2O increase in intragastric pressure (P = 0.07). The intake of a liquid meal was also significantly larger for the bulimic subjects. Gastric-emptying rate of a liquid meal was significantly delayed in the bulimic subjects during the initial 5-15 min. In all subjects, test-meal intake correlated significantly with gastric capacity (r = 0.53). In the bulimic subjects, self-reported binge intake (J) also correlated significantly with gastric capacity (r = 0.75). Binge eating in bulimic subjects may enlarge gastric capacity, which could then promote even larger binges through positive feedback.
Adult↗
Changes in childhood food consumption patterns: a cause for concern in light of increasing body weights.
Childhood obesity is currently at its highest: recent statistics show that 16% of children between the ages of 6 and 11 y are overweight [> or =95th percentile of body mass index (BMI; in kg/m(2)) for age] and that an additional 14.3% are at risk of becoming overweight (> or =85th percentile but < 95th percentile of BMI for age). As children's body weights have increased, so has their consumption of fast foods and soft drinks. The proportion of foods that children consumed from restaurants and fast food outlets increased by nearly 300% between 1977 and 1996. Children's soft drink consumption has also increased during those years, and now soft drinks provide soft drink consumers 188 kcal/d beyond the energy intake of nonconsumers. These changes in food intakes among children may partly explain the rise in childhood obesity observed in the past few years. Although the mechanism of appetite regulation will not be explored in this report, it is hypothesized that the greater energy intakes in children who consume large amounts of soft drinks and fast foods are not compensated for by increased physical activity or decreased energy intakes. Furthermore, overweight and obesity in childhood may predispose persons to morbidity in adulthood. Blood pressure and fasting insulin and cholesterol concentrations are higher in overweight children than in normal-weight children. This review focuses on current food patterns and eating habits of children, in an attempt to explain their increasing BMI. In addition, a critical review of food service and political practices regarding food choices for children at school is included.
Body Mass Index↗
Alcohol intake, tumour necrosis factor-alpha, leptin and craving: factors of a possibly vicious circle?
AIMS: Since the appetite-regulating peptide leptin was recently found to be highly correlated with both craving for alcohol and lifetime ethanol intake, the aim of our study was to test the hypothesis whether tumour necrosis factor-alpha (TNF-alpha) might be the factor that links alcohol intake with elevated leptin levels. METHODS: TNF-alpha, leptin, and alcohol craving were assessed in male alcohol addicts at the onset of alcohol withdrawal and in matched controls. RESULTS: Increased leptin plasma levels in alcohol addicts correlated significantly with an enhanced secretion of TNF-alpha, which was itself related to the duration of alcohol misuse. CONCLUSIONS: Since leptin was shown to be associated with alcohol craving, a possible vicious circle is suggested, including the components: alcohol intake, increase of TNF-alpha, enhanced leptin secretion, enhanced alcohol craving, and consecutively increased alcohol intake.
Adult↗
Molecular-based therapeutic approaches in treatment of anorexia of aging and cancer cachexia.
Loss of appetite, or anorexia, has profound implications for older persons, altering social interactions, reducing quality of life, and leading to weight loss with grave health consequences. Two conditions associated with anorexia considered in this article are the multidetermined anorexia of aging and the wasting syndrome termed cachexia induced by cancer. Nutritional interventions may have some benefit in the former, but are of limited value in the latter. Emerging studies at the molecular level relating to appetite regulation and energy balance may offer new approaches to arrest progressive weight loss in the anorexia of aging and cancer cachexia.
Aged↗
Leptin directly stimulates aromatase activity in human luteinized granulosa cells.
Leptin, the obese (ob) gene product, is secreted by adipocytes and regulates appetite through interaction with hypothalamic leptin receptors. Leptin may also have a stimulatory effect on reproductive function. Furthermore, leptin receptor mRNA is expressed in the ovary, suggesting a direct effect on its function. The present study examines the direct role of leptin on the oestrogen-producing activity in human luteinized granulosa cells. The cells were obtained from in-vitro fertilization pre-ovulatory follicles, precultured for 24 h in the presence of 5% charcoal-treated serum, and incubated for 48-96 h in a serum-free medium containing recombinant human leptin, follicle stimulating hormone (FSH), and/or insulin-like growth factor-I (IGF-I). A single addition of leptin (0. 5-10 ng/ml) stimulated aromatase activity with the incubation time of up to 96 h. The addition of leptin (1 ng/ml) further augmented the stimulation by a single addition of FSH (100 ng/ml) or IGF-I (100 ng/ml), or a combination of both. A single addition of leptin (1 ng/ml) or a combination of leptin (1 ng/ml), FSH (100 ng/ml), and IGF-I (100 ng/ml) gave rise to an increase in each parameter of oestrogen-producing activity measured, i.e. P450arom mRNA level, P450arom protein level, aromatase specific activity, and the oestradiol concentration in the culture supernatant. However, the production of progesterone did not change. These results indicate that leptin stimulates oestrogen production by increasing P450arom mRNA and P450arom protein expression and, consequently, aromatase activity by its direct action on the human luteinized granulosa cells.
Aromatase↗
Plasma leptin concentrations and lipid profiles during nicotine abstinence.
BACKGROUND: Weight gain is a frequent consequence of smoking cessation. Leptin, the protein product of the obese gene, seems to regulate appetite and body fat stores. The purpose of this study was to assess changes in circulating leptin levels and lipid metabolism during nicotine abstinence (NA) and their role in postcessation weight gain. METHODS: Six sedentary, weight-stable, nonobese adult smokers were studied before and after 7 days of NA while following a weight-maintenance diet of standard composition. All subjects refrained from smoking overnight (as assessed by breath CO) and were instructed to chew nicotine polacrilex gum (4 mg) hourly from 7:00 AM to 8:00 PM [nicotine intake (NI) day]. Venous blood samples were collected at 7:00 AM (after an overnight fast) and 5:00 PM (pre-supper) on NI day and again after 7 days of NA. RESULTS: Body weight did not change after 7 days of NA (72.0 +/- 2.8 versus 71.8 +/- 2.7 kg). Serum cotinine levels declined from 207 +/- 40 ng/mL during NI to undetectable levels during NA (P < 0.01). Fasting plasma leptin was similar during NI and NA (5.7 +/- 1.4 versus 6.4 +/- 1.9 ng/mL; P = NS). Moreover, plasma concentrations of glucose, insulin, and free fatty acids were unaffected by 7 days of NA. Although plasma triglycerides, total cholesterol, and low-density lipoprotein cholesterol were similar during NI and NA, high-density lipoprotein cholesterol increased by 15% after 7 days of NA (P < 0.05). CONCLUSIONS: In this group of nonobese, adult smokers consuming an isocaloric diet, NA for 7 days did not affect body weight or circulating concentrations of leptin, glucose, insulin, or free fatty acids. In contrast, HDL cholesterol increased significantly after NA. These results indicate that under controlled dietary conditions, changes in leptin expression do not contribute to the weight gain that commonly accompanies smoking cessation.
Cholesterol, HDL↗
Orexin A immunoreactivity and preproorexin mRNA in the brain of Zucker and WKY rats.
The primary role of the orexins was originally believed to be appetite regulation, but is now believed to be the regulation of sleep, arousal and locomotor activity. Orexin A immunoreactivity (orexin A-IR) and prepro-orexin mRNA were measured in the CNS of obese and lean Zucker rats. There were no differences in orexin A-IR or prepro-orexin mRNA levels between obese and lean Zucker rats. The orexins are therefore unlikely to be important in this model of obesity. Levels of orexin A-IR and prepro-orexin mRNA were measured in the CNS of Wistar-Kyoto (WKY) rats, which are hypoactive and have abnormal sleep architecture. Compared to Wistar rats, WKY rats had significantly lower orexin A-IR (with differences of up to 100% in some brain regions) and prepro-orexin mRNA levels. These observations suggest that the sleep and activity phenotype of the WKY strain may be related to orexin deficiency and that this strain may be a useful model of partial orexin deficiency.
Animals↗
Contrasting blood pressure effects of obesity in leptin-deficient ob/ob mice and agouti yellow obese mice.
OBJECTIVE: Recent advances in understanding the neuroendocrine pathways regulating appetite, metabolism and body weight afford an opportunity to explore further the mechanisms by which obesity influences arterial pressure. ob/ob(Lep(ob)/Lep(ob)) mice have a mutation in the ob gene and are leptin-deficient. Leptin possesses pressor actions and has been shown to increase arterial pressure when infused chronically or over-expressed transgenically. In contrast, agouti yellow obese(Ay) mice have overexpression of an agouti peptide that blocks melanocortin receptors. Stimulation of melanocortin receptors by alpha-melanocyte-stimulating hormone decreases arterial pressure. DESIGN AND METHODS: This study measured arterial pressure in leptin-deficient ob/ob mice, agouti yellow obese mice and their lean controls to test the hypothesis that the effects of obesity on arterial pressure are importantly influenced by the genetic and neuroendocrine mechanisms causing the obesity. We measured arterial pressure directly in conscious ob/ob mice (n = 14), agouti yellow obese mice (n = 6) and the same number of lean littermates. RESULTS: Body weight was nearly twice as high in ob/ob mice as in their lean controls, but mean arterial pressure was significantly lower in ob/ob mice (92+/-3 mmHg) compared with their lean controls (106+/-2 mmHg; P = 0.00017). In contrast, mean arterial pressure was significantly higher in agouti yellow obese mice (124+/-3 mmHg) than in their lean controls (99+/-1 mmHg; P = 0.000002) despite the fact that the agouti mice had milder obesity. CONCLUSIONS: This study prompts three conclusions: (1) leptin-deficient ob/ob mice and agouti yellow obese mice have contrasting blood pressure responses to obesity, (2) obesity does not invariably increase arterial pressure in mice, and (3) the arterial pressure response to obesity may depend critically on the underlying genetic and neuroendocrine mechanisms.
Animals↗
A multicomponent behavioral program for oral aversion in children dependent on gastrostomy feedings.
OBJECTIVES: Describe outcomes in nine children with Nissen fundoplication and feeding gastrostomy treated in a multicomponent feeding program. The importance of comprehensive evaluation, appetite regulation, and family-focused intervention within a behavioral feeding program are discussed. METHODS: Prospective clinical intervention with dependent measures evaluated before treatment, after treatment, and at follow-up. RESULTS: Nine children (4 girls; mean age, 3.1 +/- 1.2 years; range, 1.8-5.5 years) and their mothers were admitted for intensive treatment (mean duration, 11.4 +/- 1.7 days; range, 5-16 days). At discharge, 4 of 9 (44%) children were weaned completely from gastrostomy feedings. The mean oral intake of all patients increased 50% from pretreatment to posttreatment assessment. At a mean of 3.1 +/- 0.5 months (range, 2.4-3.6 months) after treatment, six of nine children were weaned completely from gastrostomy feedings. The percent of daily nutritional needs consumed orally increased from a pretreatment mean of 14.6% +/- 21.2% (range, 0%-67%) to a posttreatment mean of 63.4% +/- 18.3% (range, 34%-85%) and a follow-up mean of 88.1% +/- 25.1% (range, 30%-100%). The mean percent ideal body weight for height was not compromised during intensive treatment. CONCLUSIONS: Short-term intensive biobehavioral treatment was successful in improving oral intake and weaning from gastrostomy tube feeding in children with Nissen fundoplication and feeding gastrostomy.
Behavior Therapy↗
Leptin and cytokines levels in children with failure to thrive.
BACKGROUND: The majority of cases of failure to thrive (FTT) are non-organic. Many of these patients present with significant decreased caloric intake. It appears as if the appetite regulation center in the hypothalamus is not attuned to the calorie requirements of the infant. OBJECTIVE: Our hypothesis was that some cases of non-organic FTT might be caused by abnormalities in hunger/satiety control secondary to neuroendocrine or cytokine imbalance. The aim of this study was to investigate which hormonal/cytokine profiles could be assigned to a defined category of FTT, namely organic, psychosocial and idiopathic subgroups. STUDY DESIGN: 34 patients were enrolled and 32 completed the study (12 controls, 12 idiopathic FTT, 5 organic FTT, and 3 psychosocial FTT). Each child was assessed by a pediatric gastroenterologist, dietician, and social worker and underwent appropriate laboratory investigation during which leptin, IL1, IL6 and TNF-alpha levels were determined. The Mann-Whitney U test was used to compare the groups. RESULTS: IL6 was the only cytokine that showed significant differences between FTT patients (4.06 +/- 6.3 pg/ml) and normal controls (0.0 pg/ml (p = 0.028). Leptin values were significantly higher in the normal control group (1632 +/- 483 pg/ml) as compared to FTT patients (685 +/- 687 pg/ml) (p = 0.001). CONCLUSIONS: Our results indicate that leptin does not play a role in the pathogenesis of anorexia in children with FTT. It is however, possible that IL6 may be an important factor in the etiology of anorexia in patients with FTT.
Anorexia↗
Energy and fluid metabolism in microgravity.
Astronauts lose body mass when exploring space. The mechanism was considered to be an upward fluid shift inducing diuresis and natriuresis (the Henry-Gauer mechanism) during the first few days in microgravity. However, recent space missions have shown that neither diuresis nor natriuresis occurs in space missions. In contrast, a sodium-retaining status was shown, which led to positive metabolic sodium balances without fluid retention. Energy intake was consistently reduced whereas energy needs were unchanged, resulting in a negative energy balance of 20%. The reasons for this are many, although proper studies on appetite regulation have not been carried out. Despite numerous countermeasures, bone mass is lost in microgravity situations. These are body composition changes that need to be challenged before humans can be sent to space for extra-long missions.
Body Fluids↗