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PubMed1978

Pharmacological treatment of obesity.

Obesity results when the ingestion of energy exceeds its utilization, leading to an excessive expansion of the adipose tissue mass. Current pharmacological therapy for the obese patient focuses primarily on reducing energy intake. Anorectic agents reduce food consumption by modifying central systems in the brain which are involved in appetite regulation. These agents are reviewed in terms of mechanism of action, and clinical safety and efficacy in suppressing appetite and promoting weight loss. Newer anorectic agents which are being evaluated currently in clinical and animal studies are described. Clinical assessments of therapeutic regimens utilizing the thyroid hormones and human chorionic gonadotropin are evaluated. Finally, an overview of novel pharmacological approaches to the treatment of obesity is presented.

Appetite Depressants↗

PubMed2001

Hepatic monitoring of essential amino acid availability may regulate IGF-I activity, thermogenesis, and fatty acid oxidation/synthesis.

Diets that are low in certain essential amino acids (EAAs), whether owing to low protein content or poor protein quality, tend to down-regulate systemic IGF-I activity, boost thermogenesis, and suppress hepatic capacity for lipogenesis, while promoting hepatic fatty acid oxidation. It is proposed that for each EAA there is a regulatory protein in hepatocytes whose activity is repressed by adequate levels of its EAA; if one (or more) of these regulatory proteins is active, it serves as a signal of EAA deficiency which then mediates the aforementioned effects on IGF-I activity, thermogenesis, and hepatic fatty acid metabolism. Mechanisms which monitor EAA availability likewise play a role in appetite regulation, thus accounting for the fact that spontaneous calorie consumption tends to be lower on high-protein diets. Diets low in protein quantity or quality may decrease insulin secretion, an effect which should contribute to their impact on IGF-I activity and lipid metabolism. The fact that vegans ingest diets that tend to be relatively low in certain EAAs may play a key role in their characteristic leanness and their decreased risk for diabetes, coronary disease, and cancer.

Amino Acids, Essential↗

PubMed2003

Influence of housing conditions on the effects of serotonergic drugs on feeding behavior in non-deprived rats.

Serotonin plays an important role in the regulation of food and water intake, and drugs that inhibit the uptake of this neurotransmitter have been used as appetite suppressors. As the clinical usage of anorectics necessarily involves chronic drug administration, the effects of chronic treatment in animals are likely to be of greater clinical relevance than acute drug effects. Besides, little effort has been made to examine whether these effects interact with stressful situations, such as isolation. We have therefore examined the effects of fluoxetine, a selective 5-HT reuptake inhibitor, and gepirone, a 5-HT1A agonist, on body weight in isolated and in group-housed rats during 3 weeks of daily treatment. Gepirone caused an increase in body weight only in isolated rats. On the other hand, fluoxetine caused a significant reduction in body weight in both singly- and group-housed animals. The effects of these serotonergic agents were more prominent during the first week of treatment. From the data obtained in this study, it is suggested that increased 5-HT transmission produced by fluoxetine during chronic administration seems to be crucial for the appetite-regulating action of 5-HT, and this hypophagic effect does not seem to be dependent on the activation of 5-HT1A receptors since it was not shared by gepirone. Moreover, a concomitant stressful situation, such as isolation, interferes with the action of gepirone on feeding behavior. The hyperphagic effects of chronic regimen with gepirone in isolated animals are probably due to the concurrent reduction of the 5-HT transmission caused by this anxiogenic condition at the earlier stages of treatment. On the other hand, the anorectic effects of fluoxetine do not seem to interact with the stressful situations caused by isolation.

Animals↗

PubMed1999

Neuropeptide Y, leptin, galanin and insulin in women with polycystic ovary syndrome.

It has been reported that polycystic ovary syndrome (PCOS) is very frequently associated with obesity, insulin resistance and hyperinsulinemia. However, metabolic disorders may lead to suppression of reproductive hormone secretion during undernutrition and in obesity. Some neuropeptides, such as neuropeptide Y (NPY) and galanin, modulate the control of appetite and play an important role in the mechanism of luteinizing hormone-releasing hormone (LHRH) secretion. NPY and galanin regulate appetite via both central and peripheral mechanisms. The interaction between central and peripheral signals for the control of food intake is due to leptin. Leptin can modulate the activity of NPY and other peptides in the hypothalamus that are known to affect eating behavior. In order to evaluate the relationship between NPY, galanin and leptin, 28 women with PCOS, 32 obese women (non-PCOS) and 19 lean healthy women (control group) were investigated. Obese women with PCOS were divided into two groups: PCOS (A) overweight (body mass index, BMI 26-30 kg/m2), and PCOS (B) obese (BMI 31-40 kg/m2). Plasma NPY, galanin and leptin concentrations were measured by radioimmunoassay. Plasma leptin levels in obese women with PCOS (groups A and B) were significantly higher than those in the control group (p < 0.05, p < 0.05, respectively). A significant positive correlation between plasma leptin and BMI in women with PCOS was found (r = 0.427, p < 0.01). A positive correlation was demonstrated between leptin and testosterone in PCOS (r = 0.461, p < 0.01). Plasma galanin concentrations in PCOS were higher than in the control group but the differences were not significant. Plasma NPY levels were significantly elevated in both non-obese (normal) and obese women with PCOS (group A) (p < 0.01, p < 0.005, respectively). However, in obese non-PCOS women plasma NPY levels gradually increased with increase in BMI. No significant correlations were found between galanin, NPY and percentage change in response of LH to LHRH, as well as between NPY and insulin, and galanin and testosterone. Plasma insulin concentrations in women with PCOS (group B) were significantly higher than in the control group (p < 0.001). Increased plasma NPY levels are found in both obese and non-obese women with PCOS. The increase in NPY is independent of the increase in BMI. In obese women with PCOS, plasma leptin is increased compared with control lean women. Serum insulin concentration is increased in obese women with PCOS. A positive correlation exists between leptin and BMI as well as between leptin and testosterone in women with PCOS. These results may suggest that the feedback system in the interaction between leptin and NPY is disturbed in PCOS.

Adolescent↗

PubMed2003

Future directions in weight control. Molecular and genetic discoveries pave the way.

Obesity is the result of a long-standing imbalance between energy intake and energy expenditure, aided by a complex biologic system that regulates appetite and favors intake. New knowledge about substances that stimulate or inhibit appetite offers hope that drug-based solutions will be found for the current high prevalence of obesity in the United States. In this article, Dr Bessesen highlights some of the new molecular and genetic discoveries related to obesity and outlines the hypothalamic neural pathways involved in regulating food intake.

Animals↗

PubMed2005

Relationships between gastric accommodation and gastrointestinal sensations in healthy volunteers. A study using the barostat technique and two- and three-dimensional ultrasonography.

The origin of postprandial gastrointestinal sensations and their relation to gastric accommodation remain unclear. Our aim was to investigate the relation between antral and fundal accommodation and sensations. (A) In eight healthy volunteers fundus accommodation was measured using a barostat after a 200-ml (300-kcal) liquid nutrient. Antral area (AA) was measured using ultrasound. Data on bag volumes, AA, and sensations were assessed. (B) In another eight healthy volunteers gastric volume was measured after a 500-ml (300-kcal) liquid nutrient using 2-D/3-D ultrasound. Sensations were scored using VAS. Distal and proximal volumes were calculated from 3-D datasets. (A) Fullness was correlated with AA (r = 0.48, P = 0.002). Fullness and bag volume were not correlated. (B) Fullness was correlated with AA (r = 0.77, P < 0.001) and distal volume (r = 0.75, P < 0.001). Proximal volume was not correlated with fullness (r = 0.10, P = NS). We conclude that fullness is related to antral volume and area rather than proximal volume. The gastric antrum may play a key role in normal appetite regulation.

Adolescent↗

PubMed2000

Zinc and nitric oxide synthase inhibitor L-NAME attenuate NPY-induced feeding in mice.

The influences of zinc (Zn) and the nitric oxide synthase (NOS) inhibitor L-NAME on peripheral neuropeptide Y (NPY)-induced feeding in mice were investigated. Male mice received NPY (200 ng/d/mouse subcutaneously) and were separated into four groups based on cotreatments (with or without Zn [0.1 mg/mL]) and with or without L-NAME [0.2 mg/mL]) administered in drinking water for 10 d. A control group that received saline injection was also studied. The results showed that NPY, with or without any studied chemicals, did not affect body weight gain or body fat content. However, the mice that were administered NPY alone had increased energy intakes, higher serum triglyceride and free fatty acid, and lower serum glucose than saline-injected controls. NPY-treated mice that were given Zn and L-NAME cotreatments had compatible results of determined variables in comparison with control mice. This study showed that Zn and L-NAME attenuated NPY-mediated feeding and selected serum variables in mice. However, the mechanisms of the interactions among NPY, Zn and NOS, and their effects on appetite regulation, remain to be elucidated.

Animals↗

PubMed2026

Effects of intensive lifestyle interventions with calorie-carbohydrate-restricted diet versus time-restricted eating on appetite and binge eating in type 2 diabetes: A randomized controlled trial.

The impact of intensive lifestyle interventions on appetite regulation and binge eating in individuals with type 2 diabetes (T2D) remains unclear. This study evaluated the effects of combined lifestyle interventions on appetite responses and binge eating in overweight or obese adults with T2D. In a randomized trial, 120 participants with T2D were allocated to three groups (n = 40 each): (1) Calorie-carbohydrate restriction (CCR), (2) Time-restricted eating with CCR (TRE + CCR), or (3) Control. Intervention groups received structured exercise and behavioral education based on the Information-Motivation-Behavioral Skills model. Appetite perceptions (hunger, satiety, desire to eat, and prospective food consumption) and binge eating (Binge Eating Scale; BES and objective binge episodes) were evaluated at baseline, week 12, and week 24 using linear mixed models. Both CCR and TRE + CCR significantly improved subjective appetite compared with the control group at 12 and 24 weeks (all p < 0.01). At 24 weeks, hunger decreased by -24.1 mm (95% CI: -35.8, -12.5) in the CCR group and -32.7 mm (95% CI: -44.2, -21.3) in the TRE + CCR group. Satiety also increased by 21.7 mm (95% CI: 9.46, 33.9) and 29.4 mm (95% CI: 17.4, 41.4), respectively. Significant reductions were observed for desire to eat and prospective food consumption. In contrast, changes in BES and objective binge episodes were not significantly different between groups at any time point. No significant differences were detected between the CCR and the TRE + CCR groups. Intensive lifestyle interventions incorporating CCR or TRE + CCR effectively reduced appetite in adults with T2D but did not significantly affect binge eating. Future research should target individuals with higher baseline BES scores to clarify potential benefits for binge eating behavior.

Humans↗

PubMed2005

Melanocortin-4 receptors, beta-MSH and leptin: key elements in the satiety pathway.

This paper reviews aspects of our research, focusing on the role of the melanocortin system in the central regulation of feeding and energy balance, which was begun in 1997. It describes data from successive physiological studies, concerning the identity of the appetite-regulating melanocortin receptor, melanocortin-4 receptor (MC4R) regulation with altered nutritional status, the role of MC4R in dietary obesity and the identity of the endogenous MC4R ligand.

Animals↗

PubMed2003

No effect of physiological concentrations of glucagon-like peptide-2 on appetite and energy intake in normal weight subjects.

OBJECTIVE: To examine the effect of a GLP-2 infusion on appetite sensations and ad libitum energy intake in healthy, normal weight humans. DESIGN: The experiment was performed in a randomised, blinded, and placebo-controlled crossover design. Placebo or GLP-2 was infused (infusion rate of 25 pmol/kg body wth) for 4.5 h. SUBJECTS: A total of 18 healthy, normal weight young subjects participated; eight women and 10 men. MEASUREMENTS: During the infusion, subjects recorded their appetite sensations every 30 min using visual analogue scales, and blood was sampled frequently. After 2 h of infusion, an ad libitum meal, consisting of sandwiches, was served. RESULTS: The concentration of GLP-2 was significantly higher during the GLP-2 infusion compared with placebo (P<0.0001) and increased further in both conditions in response to the meal. Neither appetite sensations, nor palatability of the test meals, or energy intake were different on the two occasions. Glucose, GLP-1, insulin, and GIP responses were also unaffected by the infusion, whereas glucagon levels were higher during the GLP-2 treatment (P<0.05). CONCLUSION: Circulating GLP-2 in physiological concentrations does not seem to play a significant role in human appetite regulation.

Adult↗

PubMed2002

Weight in the balance.

The adage 'we are what we eat' is taking on a new meaning in our well-fed and increasingly sedentary culture, as many of us convert much of our excess food into body fat; in the USA, 60% of the population is now considered to be overweight. Obesity brings with it an increased risk of developing type II diabetes, hypertension and heart disease, so the mechanisms that control food intake and body weight are of considerable importance for public health and clinical medicine. The mass of body fat is now known to be regulated by several hormones and neuropeptides. Two of these, the circulating peptide hormones leptin and ghrelin have actions that include reciprocal effects on appetite-regulating neurons in the hypothalamus. This article reviews data discussed at a recent meeting(1), where an overview of recent developments in research into leptin and ghrelin was presented. Topics covered are the roles of leptin and ghrelin in the regulation of food intake and energy production; the integration of food intake with other energy-regulated processes, such as growth, sexual maturation and reproduction, sleep and the immune response; and pathological conditions, ranging from diabetes to psychiatric disorders.1 This report summarizes conclusions of the meeting 'Brain Somatic Cross-Talk and the Central Metabolism' held in Paris on January 28, 2002.

Body Weight↗

PubMed1999

State-of-the-art-lecture: Obesity-induced hypertension: new concepts from the emerging biology of obesity.

offsity is associated with an increased risk of hypertension. In the past 5 years there have been dramatic advances into the genetic and neurobiological mechanisms of obesity with the discovery of leptin and novel neuropeptide pathways regulating appetite and metabolism. In this brief review, we argue that these mounting advances into the neurobiology of obesity have and will continue to provide new insights into the regulation of arterial pressure in obesity. We focus our comments on the sympathetic, vascular, and renal mechanisms of leptin and melanocortin receptor agonists and on the regulation of arterial pressure in rodent models of genetic obesity. We suggest 3 concepts. First, the effect of obesity on blood pressure may depend critically on the genetic-neurobiological mechanisms underlying the obesity. Second, obesity is not consistently associated with increased blood pressure, at least in rodent models. Third, the blood pressure response to obesity may be critically influenced by modifying alleles in the genetic background.

Animals↗

PubMed2001

The role of postprandial releases of insulin and incretin hormones in meal-induced satiety--effect of obesity and weight reduction.

BACKGROUND: Previous studies have indicated that the secretion of the intestinal satiety hormone glucagon-like peptide-1 (GLP-1) is attenuated in obese subjects. OBJECTIVE: To compare meal-induced response of GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) in obese and lean male subjects, to investigate the effect of a major weight reduction in the obese subjects, and to look for an association between these hormones and ad libitum food intake. METHOD: Plasma concentrations of intestinal hormones and appetite sensations were measured prior to, and every 30 min for 180 min after, ingestion of a 2.5 MJ solid test meal. Gastric emptying was estimated scintigraphically. An ad libitum lunch was served 3 h after the test meal. SUBJECTS: Nineteen non-diabetic obese (body mass index (BMI) 34.1--43.8 kg/m(2)) and 12 lean (BMI 20.4--24.7 kg/m(2)) males. All obese subjects were re-examined after a mean stabilised weight loss of 18.8 kg (95% CI 14.4--23.2). RESULTS: Total area under the GLP-1 response curve (AUC(total, GLP-1)) was lower in obese before and after the weight loss compared to lean subjects (P<0.05), although weight loss improved the response from 80 to 88% of that of the lean subjects (P=0.003). The GIP response was similar in obese and lean subjects. However, after the weight loss both AUC(total, GIP) and AUC(incremental, GIP) were lowered (P<0.05). An inverse correlation was observed between AUC(incremental, GIP) and energy intake at the subsequent ad libitum meal in all groups. In lean subjects ad libitum energy intake was largely predicted by the insulin response to the preceding meal (r(2)=0.67, P=0.001). CONCLUSION: Our study confirmed previous findings of a reduced postprandial GLP-1 response in severely obese subjects. Following weight reduction, GLP-1 response in the obese subjects apparently rose to a level between that of obese and lean subjects. The data suggests that postprandial insulin and GIP responses are key players in short-term appetite regulation.

Absorptiometry, Photon↗

PubMed2004

Clinical endocrinology and metabolism. Ghrelin, a novel growth-hormone-releasing and appetite-stimulating peptide from stomach.

Recent identification of novel appetite-regulating hormones has revealed the complex interactions of these humoral factors in the regulation of feeding behavior in mammals. One of these hormones, ghrelin, a natural ligand of the orphan receptor GHS-R, purified from stomach, is able to stimulate growth hormone release from pituitary cells. Ghrelin is a 28 amino acid peptide containing an n-octanoylated serine 3 residue that is essential for its activity. Ghrelin stimulates appetite by acting on the hypothalamic arcuate nucleus, the region known to control food intake. As an orexigenic peptide, ghrelin is therefore an endogenous regulator of feeding behavior from the peripheral tissues to the central nervous system.

Amino Acid Sequence↗

PubMed2006

Mechanism of oleoylethanolamide on fatty acid uptake in small intestine after food intake and body weight reduction.

The increase in the prevalence of human obesity highlights the need to identify molecular and cellular mechanisms involved in control of feeding and energy balance. Oleoylethanolamide (OEA), an endogenous lipid produced primarily in the small intestine, has been identified to play an important role in the regulation of animal food intake and body weight. Previous studies indicated that OEA activates peroxisome proliferator-activated receptor-alpha, which is required to mediate the effects of appetite suppression, reduces blood lipid levels, and enhances peripheral fatty acid catabolism. However, the effect of OEA on enterocyte function is unclear. In this study, we have examined the effect of OEA on intestinal fatty acid uptake and FAT/CD36 expression in vivo and in vitro. We intraperitoneally administered OEA to rats and examined FAT/CD36 mRNA level and fatty acid uptake in enterocytes isolated from the proximal small intestine, as well as in adipocytes. Our results indicate that OEA treatment significantly increased FAT/CD36 mRNA expression in intestinal mucosa and isolated jejunal enterocytes. In addition, we also found that OEA treatment significantly increases fatty acid uptake in isolated enterocytes in vitro. These results suggest that in addition to appetite regulation, OEA may regulate body weight by altered peripheral lipid metabolism, including increased lipolysis in adipocytes and enhanced fatty acid uptake in enterocytes, both in conjunction with increased expression of FAT/CD36. This study may have important implications in understanding the mechanism of OEA in the regulation of fatty acid absorption in human physiological and pathophysiological conditions.

Adipocytes↗

PubMed2006

Enhanced activation of reward mediating prefrontal regions in response to food stimuli in Prader-Willi syndrome.

BACKGROUND: Individuals with Prader-Willi syndrome (PWS) exhibit severe disturbances in appetite regulation, including delayed meal termination, early return of hunger after a meal, seeking and hoarding food and eating of non-food substances. Brain pathways involved in the control of appetite in humans are thought to include the hypothalamus, frontal cortex (including the orbitofrontal, ventromedial prefrontal, dorsolateral prefrontal and anterior cingulate areas), insula, and limbic and paralimbic areas. We hypothesised that the abnormal appetite in PWS results from aberrant reward processing of food stimuli in these neural pathways. METHODS: We compared functional MRI blood oxygen level dependent (BOLD) responses while viewing pictures of food in eight adults with PWS and eight normal weight adults after ingestion of an oral glucose load. RESULTS: Subjects with PWS demonstrated significantly greater BOLD activation in the ventromedial prefrontal cortex than controls when viewing food pictures. No significant differences were found in serum insulin, glucose or triglyceride levels between the groups at the time of the scan. CONCLUSIONS: Individuals with PWS had an increased BOLD response in the ventromedial prefrontal cortex compared with normal weight controls when viewing pictures of food after an oral glucose load. These findings suggest that an increased reward value for food may underlie the excessive hunger in PWS, and support the significance of the frontal cortex in modulating the response to food in humans. Our findings in the extreme appetite phenotype of PWS support the importance of the neural pathways that guide reward related behaviour in modulating the response to food in humans.

Adult↗

PubMed2004

Excretion of electrolytes in Brown Norway and Fischer 344 rats: effects of adrenalectomy and of mineralocorticoid and glucocorticoid receptor ligands.

Our previous studies showed that adrenalectomy (ADX) has surprisingly no effect on body weight and fluid intake in the Brown Norway rat strain, suggesting that mineralocorticoid receptor (MR)-mediated effects are present even in absence of corticosteroids in this strain. Moreover, glucocorticoid receptor (GR)-mediated mechanisms are more effective in Brown Norway than in Fischer 344 rats. Such functional differences in corticosteroid receptor pathways between Brown Norway and Fischer 344 rats led us to compare the effect of ADX and MR/GR-mediated actions on sodium and potassium excretion between these two rat strains. To this end, we first measured the effect of an acute high dose of aldosterone on the urinary Na+/K+ concentration ratio in intact and ADX Brown Norway and Fischer 344 rats. Second, to discriminate mineralocorticoid from glucocorticoid actions, we treated chronically ADX rats with increasing doses of aldosterone or RU28362, a pure GR agonist, in the drinking fluid. As sodium homeostasis involves salt appetite regulation, behaviour under mineralocorticoid control, we also measured saline preference in Brown Norway and Fischer 344 rats. Our data illustrate: (1) the very limited effect of ADX on body weight, food and fluid intake, diuresis, natriuresis, kaliuresis and salt appetite in Brown Norway rats, supporting the presence of MR signalling pathways in the absence of adrenal steroids in these rats; (2) the insensitivity of MR to aldosterone in intact Brown Norway rats, and the reduced sensitivity of MR to aldosterone in ADX Brown Norway rats compared with ADX Fischer 344 rats; and (3) the greater sensitivity of GR-related mechanisms to RU28362 in Brown Norway than in Fischer 344 rats in terms of body weight gain and electrolyte excretion. Considering that both MRs and GRs regulate hypothalamic-pituitary-adrenal axis processes, such functional differences in corticosteroid receptors could be at the origin, at least partly, of the strain differences in corticotropic activity/reactivity to stress previously described.

Adrenalectomy↗

PubMed2007

Serotonergic drugs : effects on appetite expression and use for the treatment of obesity.

Over 35 years of research suggests that endogenous hypothalamic serotonin (5-hydroxytryptamine) plays an important part in within-meal satiation and post-meal satiety processes. Thus, the serotonin system has provided a viable target for weight control, critical to the action of at least two effective anti-obesity treatments, both producing clinically significant weight loss over a year or more. Numerous serotonin receptor subtypes have been identified; of these, serotonin 5-HT1B and 5-HT2C receptors have been specifically recognised as mediators of serotonin-induced satiety.A number of serotonergic drugs, including selective serotonin reuptake inhibitors (SSRIs), dexfenfluramine and 5-HT2C receptor agonists, have been shown to significantly attenuate rodent bodyweight gain. This effect is strongly associated with marked hypophagia and is probably mediated by the hypothalamic melanocortin system. Additionally, sibutramine, dexfenfluramine, fluoxetine and the 5-HT2C receptor agonist chlorophenylpiperazine (mCPP) have all been shown to modify appetite in both lean and obese humans, resulting in reduced caloric intake. Clinical studies demonstrate serotonergic drugs specifically reduce appetite prior to and following the consumption of fixed caloric loads, and cause a reduction in pre-meal appetite and caloric intake at ad libitum meals. Weight loss in the obese has also been produced by treatment with both the serotonin precursor 5-hydroxytryptophan and the preferential 5-HT2C receptor agonist mCPP.A new generation of 5-HT2C receptor selective agonists have been developed and at least one, lorcaserin (APD356), is currently undergoing clinical trials. In addition, 5-HT6 receptor antagonists such as PRX-07034 and BVT74316 have been shown to potently reduce food intake and bodyweight gain in rodent models and have recently entered clinical trials. However, the role of the 5-HT6 receptor in the expression of appetite remains to be determined. The hope is that these drugs will not only be free of their predecessors' adverse effect profiles, but will also be equally or more effective at regulating appetite and controlling bodyweight.

Animals↗