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PubMed1986

Medial hypothalamic serotonin: effects on deprivation and norepinephrine-induced eating.

Evidence to date suggests an inhibitory role for serotonin (5-HT) in the regulation of feeding behavior. In the present study, hypothalamic 5-HT was investigated for its anorexic potency under different feeding conditions. In fasted rats, 5-HT (1.1-4.4 micrograms) injected into the hypothalamic paraventricular nucleus (PVN), produced a reliable dose-dependent reduction in food consumption. Under satiated conditions, this inhibitory effect was significantly larger and apparent at lower doses (down to 0.1 micrograms), in animals induced to eat by PVN injection of norepinephrine (NE). Tests with receptor antagonists, injected into the PVN immediately prior to 5-HT, revealed a dose-dependent blockade of 5-HT's action by the serotonergic blockers, metergoline, methysergide and cinanserin. While the effect of 5-HT was somewhat attenuated by administration of certain beta-adrenergic and phenothiazine-type dopamine receptor antagonists, 5-HT was totally resistant to the actions of more selective dopamine blockers and of the cholinergic and histaminergic antagonists, atropine and dexbrompheniramine. PVN injection of various serotonergic compounds, known to inhibit feeding when peripherally administered, also suppressed NE-induced feeding in a dose-related manner (fluoxetine = dl-norfenfluramine greater than quipazine greater than chlorimipramine greater than dl-fenfluramine). Further tests with PVN administration of the dextro isomer and metabolite of fenfluramine showed a considerably stronger inhibitory effect with d-norfenfluramine as compared to dexfenfluramine, and a particular effectiveness of peripherally injected dexfenfluramine in NE-injected rats, at doses at least 10-fold higher than centrally effective doses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Temporal trends and drug exposures in pulmonary hypertension: an American experience.

BACKGROUND: Reports have linked anorexigen intake to an increased risk of pulmonary arterial hypertension (PAH). With the rise in anorexigen use in the latter half of the last decade, we established a surveillance network within the United States to monitor temporal trends in the number of reported cases of PAH. We also studied whether use of anorexigens and other drugs differed among patients with pulmonary hypertension of different etiologies. METHODS: Newly diagnosed subjects (N = 1335) at 13 tertiary pulmonary hypertension centers were enrolled between January 1998 and June 2001. Patient-reported medication use was obtained by a telephone interview. Patients were classified as to the type of pulmonary hypertension. Poisson regression models were fitted to monthly case counts, and logistic regression methods were used to assess the association between type of pulmonary hypertension and medication use. RESULTS: The average monthly number of reported cases of PAH and other categories of pulmonary hypertension did not change over the study period. Fenfluramine or dexfenfluramine use during the 5 years before the time of the interview was preferentially associated with PAH. Fenfluramine/dexfenfluramine use was particularly common in cases referred but found not to have pulmonary hypertension. CONCLUSIONS: No epidemic of anorexigen-related PAH was evident during the study period. As persons who had taken fenfluramine or dexfenfluramine were particularly likely to be referred for evaluation of pulmonary hypertension, it is unlikely that the failure to detect an anorexigen-induced rise in primary pulmonary hypertension was because of underascertainment. The association between fenfluramine derivatives and PAH is consistent with the risk elevations previously reported.

Adolescent↗
PubMed1998

Chronic d-fenfluramine treatment reduces fat intake independent of macronutrient preference.

We investigated the effect of chronic dexfenfluramine (DFEN) treatment on macronutrient selection in a three-choice diet paradigm using Sprague-Dawley rats. Baseline macronutrient intakes were measured for several days before the initiation of treatment. In Experiment 1, daily intraperitoneal injections of DFEN (1.5 mg/kg) or saline were administered 60 min before dark onset for 12 consecutive days and 24 h macronutrient intakes were measured. DFEN significantly reduced absolute fat intake (kcal) by 30% and relative fat intake (% of total energy) by 14% in animals that received dexfenfluramine treatment compared to controls over the 12-day period. Absolute carbohydrate intake was increased 24% compared to controls, but this difference was not significant. These changes in food intake resulted in a 10% lower total energy intake. Upon discontinuation of the drug, fat intake of the DFEN-treated rats rebounded to control levels within 24 h. In Experiment 2, rats were assigned to carbohydrate- or fat-preferring groups based on the ratio of their average daily carbohydrate to fat intake (kcal). All animals then received DFEN. During DFEN treatment, fat-preferring rats reduced their daily fat intake from 62 to 53% of total energy. The low baseline fat intake of carbohydrate-preferring rats was reduced even further by DFEN (from 24 to 15% of total energy). These corresponding effects of DFEN on macronutrient selection in both fat- and carbohydrate-preferring rats indicate that chronic DFEN treatment selectively suppressed fat intake independent of the preferred macronutrient diet.

Animals↗
PubMed2001

Low risk of significant echocardiographic valvulopathy in patients treated with anorectic drugs.

BACKGROUND: Phentermine--fenfluramine and dexfenfluramine use for weight loss has been previously associated with increased prevalence of valvular heart disease. This association was initially based on small numbers of patients, limited data on dose and duration of drug therapy, and no correlation with matched controls. METHODS: Our investigation involved 343 obese subjects enrolled in a prospective, strict weight loss, research protocol from September 1994 to September 1997. All subjects underwent transthoracic echocardiography for significant valvular lesions within a mean of 121 days from the manufacturer's announcement of the voluntary withdrawal of fenfluramine and dexfenfluramine from the market. All echocardiograms were interpreted by 2 independent readers. RESULTS: The study population included 281 females and 62 males with a mean age of 46.7+/-9.1 years and mean initial body mass index of 40.1+/-8.1 kg/m(2). Using the Food and Drug Administration's criteria, only 21 subjects (6.1%) had significant valvular lesions. Aortic regurgitation was detected in 18 subjects, mitral regurgitation in 3 subjects, and both aortic and mitral regurgitation in 1 subject; no one had severe regurgitation. Significant valvular disease did not correlate with age, gender, initial/ending body mass index, the drug dose, duration of drug therapy, or serotonin reuptake inhibitors. CONCLUSIONS: Anorexigen therapy is associated with a low prevalence of significant valvular regurgitation. Late valvular abnormalities from drug treatment await long term prospective studies.

Aortic Valve Insufficiency↗
PubMed2003

[Valvular heart disease associated with benfluorex].

We report the first case of valvular heart disease due to benfluorex. A 50-year-old woman who had been taking the anorectic agent benfluorex intermittently for one year developed severe fibrosis and regurgitation of the mitral, aortic and tricuspid valves. Clinical, echocardiographic and histopathological findings were analogous to those reported with fenfluramine and dexfenfluramine. The similarity between the histopathological lesion documented in patients treated with the appetite suppressants fenfluramine, dexfenfluramine and benfluorex and the valvular lesions reported in valve disease associated with ergot alkaloid use and carcinoid heart disease suggest a common pathophysiological mechanism and a central role for serotonin in the development of the disease.

Appetite Depressants↗
PubMed1997

Pulmonary hypertension, family and environment.

The focus of interest on pulmonary hypertension (PH) has come through recent therapeutic advances which prolong and improve quality of life. From this interest, recent observations form family studies indicate that a gene located on chromosome 2 is associated with PH. Environmental factors, the use of an anorectic agent, dexfenfluramine, has been associated with a risk of developing primary PH. A link with hypoxic induced PH has emerged in that a strain of rat, the fawn-hooded rat (FHR) which has a susceptibility to developing PH with mild hypoxia has an inherited storage defect to serotonin. Dexfenfluramine, by inhibiting the serotonin transporter, produces a similar pattern of disturbance of biogenic amine metabolism. This observation provides some insight into potential mechanisms for this complex disorder.

Animals↗
PubMed1997

Intensity dependence of the cortical auditory evoked potentials as a surrogate marker of central nervous system serotonin transmission in man: demonstration of a central effect for the 5HT1B/1D agonist zolmitriptan (311C90, Zomig).

As shown in animal studies, 5HT1B/D agonists can inhibit activity in the trigeminal nucleus caudalis, which may be advantageous for their antimigraine effect. To demonstrate a possible central nervous system (CNS) action of these compounds in man we studied their effect on the intensity dependence of the cortical auditory evoked potentials (IDAPs), thought to be inversely related to central serotonergic transmission. An amplitude/stimulus intensity function (ASF) slope was computed in healthy volunteers and migraine patients between attacks before and 2 h after oral 311C90 (zolmitriptan "Zomig") 10 mg (n=14), 311C90 5 mg (n=7), sumatriptan 100 mg (n=14), dexfenfluramine 15 mg (n=4), lorazepam 1.25 mg (n=4) and placebo (n=14). 311C90 10 mg and, to a lesser degree, 5 mg significantly increased the mean ASF slope (p=0.007 and 0.05 vs placebo). There was a significant positive correlation between plasma levels of 311C90 and ASF slope changes. Sumatriptan and lorazepam had little effect, but dexfenfluramine produced a significant ASF slope decrease. 311C90 is able to modify a CNS activity that is modulated by serotonin, i.e. the IDAP. This effect is probably the consequence of its superior lipophilicity compared to sumatriptan and of activation of prejunctional 5HT1B/D autoreceptors, which lowers central serotonin release and thus the preactivation level of sensory cortices.

Adult↗
PubMed2000

Recent progress in obesity pharmacotherapy.

Interest in obesity pharmacotherapy is intense, sparked by the public health threat of increases in obesity rates, as well as by increased knowledge of the biology underlying food intake and energy balance. After a hiatus of more than 20 years, three new medications approved by the US Food and Drug Administration for obesity treatment recently reached the marketplace. One of these, dexfenfluramine, has been withdrawn because of fenfluramine's and its isomer's association with valvular regurgitation. Sibutramine, a centrally acting reuptake inhibitor of monoamines, and orlistat, a pancreatic lipase inhibitor, have been approved for long-term obesity treatment. This review covers recent publications documenting clinical trial experience with these two agents and updates the evidence associating dexfenfluramine and fenfluramine with valvulopathy. As obesity rates increase throughout the world and as knowledge expands regarding the biology of obesity, an expansion of pharmacologic options for obesity treatment is certain.

Journal Article↗
PubMed1993

Neurochemical mechanism of action of anorectic drugs.

Studies with dexfenfluramine, an anorectic agent which releases 5-hydroxytryptamine (5-HT) from nerve terminals and inhibits its reuptake, have considerably increased our knowledge of the role of 5-HT in feeding control. 5-HT1B receptors mediate the satiating effect of dexfenfluramine, whereas the mechanism by which 5-HT uptake inhibitors such as fluoxetine and sertraline cause anorexia is not clear. Anorexia induced by (+)-amphetamine, phentermine, diethylpropion and phenylpropanolamine seems to be the result of their ability to increase the release of noradrenaline and/or dopamine from nerve terminals and inhibit their reuptake or, in the case of phenylpropanolamine, to stimulate directly alpha 1-adrenoceptors. It has been suggested that beta- and alpha 1-adrenoceptors and D1 dopamine receptors are involved in their effect on food intake. The difficulties of extrapolation across species limit our knowledge of the mechanism of the anorectic action in humans. Significant advances in the treatment of feeding pathology will be linked to identifying new receptor types and subtypes for neurotransmitters and quantifying and modelling eating disorders such as binge-eating and food craving.

Animals↗
PubMed2005

Pergolide is an inhibitor of voltage-gated potassium channels, including Kv1.5, and causes pulmonary vasoconstriction.

BACKGROUND: Pergolide produces clinical benefit in Parkinson disease by stimulating dopamine D1 and D2 receptors. An increased incidence of carcinoid-like heart valve disease (CLHVD) has been noted in pergolide users, reminiscent of that induced by certain anorexigens used for weight reduction. Anorexigens that modulate serotonin release and reuptake, such as dexfenfluramine, were withdrawn from sale because of CLHVD. Interestingly, the anorexigens also caused pulmonary arterial hypertension (PAH). Anorexigens were shown to enhance hypoxic pulmonary vasoconstriction, in part by inhibiting voltage-gated K+ channels (Kv) in pulmonary artery smooth muscle cells (PASMCs). Although PAH has not been associated with pergolide use, we hypothesized that pergolide might have similar effects on hypoxic pulmonary vasoconstriction and Kv channels. METHODS AND RESULTS: Pergolide enhanced hypoxic pulmonary vasoconstriction in the isolated perfused rat lung compared with control lungs (mean pulmonary artery pressure 32+/-3 versus 21+/-2 mm Hg; P<0.01). Pergolide also caused vasoconstriction in rat pulmonary artery rings. Pergolide inhibited PASMC potassium current density, resulting in membrane depolarization (from -51+/-2 to -44+/-1 mV) and increased cytosolic calcium in both rat and human PASMCs. Pergolide directly inhibited heterologously expressed Kv1.5 and KCa channels. CONCLUSIONS: Pergolide causes Kv channel inhibition and, despite being from a different class of drugs, has pulmonary vascular effects reminiscent of dexfenfluramine. Coupled with their shared proclivity to induce CLHVD, these findings suggest that clinical monitoring for pergolide-induced PAH should be considered.

Animals↗
PubMed1992

Appetite suppressants. A review.

Centrally acting appetite suppressant drugs used in the treatment of obesity fall into 2 broad pharmacological categories; those which act via brain catecholamine pathways and those which act via serotonin pathways. Of the former group, amphetamine and phenmetrazine are no longer recommended because of their stimulant properties and addictive potential. The remaining drugs in this class include amfepramone (diethylpropion), phentermine, mazindol and phenylpropanolamine. All have been shown to reduce appetite and lower food intake, thereby helping obese patients more easily keep to a low-calorie diet and lose weight. They all have some sympathomimetic and stimulant properties. Anorectic drugs which promote serotonin neurotransmission have no such stimulant or sympathomimetic properties. They are fenfluramine, together with its recently introduced dextrorotatory stereoisomer dexfenfluramine, and fluoxetine. They reduce appetite and food intake and are effective in the treatment of obesity. Anorectic drugs should be reserved for those who are clinically at risk from being overweight, and then only as part of a comprehensive weight-reducing programme including regular dietary counselling. Although current licensing regulations only allow their use over a relatively short period (12 to 16 weeks), clinical trials have shown them to be effective over longer periods, particularly in preventing weight regain. Of the compounds currently indicated for use in obesity, dexfenfluramine appears to have the most suitable pharmacological profile, although it should not be given to patients with a history of depression. When used appropriately, appetite suppressants can be of real therapeutic benefit, and pose little risk.

Appetite Depressants↗
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↗
PubMed2000

Diet drug-related cardiac valve disease: the Mayo Clinic echocardiographic laboratory experience.

OBJECTIVE: To describe the prevalence of diet drug-related valvular disease among our referral population and the association of valvular disease with duration of exposure to fenfluramine and phentermine in combination and to dexfenfluramine alone. PATIENTS AND METHODS: In this retrospective review of clinical and echocardiographic data, charts of patients referred for treatment of toxic effects of diet drugs were reviewed, and telephone interviews were conducted. RESULTS: Between June and December 1997, 191 patients (164 women, 27 men; mean age, 47 years) were referred for possible diet drug-related valvular disease. Twenty-eight (28%) of the 99 asymptomatic patients and 40 (43%) of the 92 symptomatic patients had abnormal echocardiographic findings. Valvular lesions among the 68 patients with abnormal echocardiographic findings included mild (or greater) aortic regurgitation in 55 patients (81%), moderate (or greater) mitral regurgitation in 12 (18%), and moderate (or greater) tricuspid regurgitation in 7 (10%). The Food and Drug Administration case definition of diet drug-related valvulopathy was noted in 31 % of this referral population. Of patients with valvulopathy, mean duration of therapy with fenfluramine and phentermine in combination and dexfenfluramine alone was 9 months and 5 months, respectively. Duration of therapy was not associated with presence or absence of disease. Five patients had surgical intervention for severe valvulopathy: 3 had mitral valve repair, 1 had mitral valve replacement, and 1 had aortic valve replacement. Pulmonary hypertension (>40 mm Hg) was found in 24 patients (13%), and 17 (71 %) had pulmonary hypertension in association with valvulopathy. CONCLUSION: This study demonstrated a 31% (60/191) prevalence of valvulopathy in patients with a history of diet drug exposure who were referred for echocardiographic evaluation. The most common finding was mild aortic regurgitation. Twenty-eight percent of asymptomatic patients had abnormal echocardiographic findings. This study emphasizes the spectrum of diet drug-related cardiac disease and the potential for valvulopathy in asymptomatic patients.

Aortic Valve Insufficiency↗
PubMed2005

Anorectics on trial: a half century of federal regulation of prescription appetite suppressants.

Beginning with the passage of the Federal Food, Drug, and Cosmetic Act in 1938 and escalating with the 1962 Kefauver-Harris amendments, increasing pressure has been placed on pharmaceutical manufacturers to demonstrate that a drug's benefits outweigh its risks. Nowhere has the question of risk versus benefit come under greater scrutiny than with anorectics. After the approval in the 1940s and 1950s of a number of amphetamine and amphetamine-like compounds for the treatment of obesity, the U.S. Food and Drug Administration struggled to define the efficacy and safety of these agents. Labeling restrictions on duration of use and warnings about abuse and addiction ultimately contributed to the reduced use of anorectics. That trend continued until the mid-1990s, when the off-label use of fenfluramine plus phentermine (fen-phen) and the approval of dexfenfluramine gave rise to widespread, long-term use of anorectics to treat obesity. The adverse effects that came to be associated with fenfluramine and dexfenfluramine, leading to their eventual withdrawal from the market, gave pause to regulators, physicians, patients, and drug companies alike. Sibutramine, the latest anorectic to enter the market, is now the focus of a landmark trial that is examining, for the first time, whether drug-induced weight loss reduces the risk for fatal and nonfatal cardiovascular disease.

Appetite Depressants↗
PubMed2001

Effects of anorexinogen agents on cloned voltage-gated K(+) channel hKv1.5.

Appetite suppressants have been associated with primary pulmonary hypertension (PPH), inhibition of voltage-gated potassium channels, membrane depolarization, and calcium entry in pulmonary artery smooth muscle cells. In cells taken from pulmonary arteries of primary pulmonary hypertensive patients, voltage-gated potassium channels appear to be dysfunctional and in particular, reduced hKv1.5 gene transcription and hKv1.5 mRNA instability have been shown. We have compared the effects of anorexinogen agents on hKv1.5 channels stably expressed in mammalian cell line. We found that aminorex, phentermine, dexfenfluramine, sibutramine, and fluoxetine cause a dose-dependent inhibition of hKv1.5 current. Aminorex, phentermine, and dexfenfluramine had a K(D) of inhibition greater than to 300 microM and are not potent inhibitors of hKv1.5. Sibutramine and fluoxetine inhibited hKv1.5 current with lower K(D) values of 41 and 21 microM, respectively. Block by both drugs increased rapidly between -20 and +10 mV, coincident with channel opening and suggested an open channel block mechanism. This was confirmed by a slower deactivation time course resulting in a "crossover" phenomenon when tail currents recorded under control conditions and in the presence of either drug were superimposed. Single channel experiments demonstrated that open probability and open duration of hKv1.5 were decreased by fluoxetine and sibutramine. These results indicate that among the anorexinogen agents tested, sibutramine and fluoxetine are the most potent toward hKv1.5 channel, which they preferentially block in the open state. Nevertheless, their inhibitory effects do not correlate with their ability to produce PPH neither with their previously reported therapeutic plasma concentrations.

Algorithms↗
PubMed1989

[Serotonin, food intake and body weight].

Various animal models of hyperphagia and obesity have made possible the study of the effect on food intake of dexfenfluramine, an agent which both inhibits reuptake and stimulates release of 5 HT. These are chronic overfeeding models (hereditary model: Zucker rat, hormonal origin: insulin, ovariectomy, lesions of the VMH, and models including palatable and varied diet: cafétéria diet) and also acute overfeeding models (deprived rats, tail pinch, "dessert" test, metabolic or neuropharmacologic stimuli). Dexfenfluramine administered by osmotic minipump (3 mg/kg/day for up to 4 weeks) reduces food intake and produces weight loss in most of these models.

Animals↗
PubMed1996

[Different therapies in the treatment of obesity in hypertensive patients].

PURPOSE: To evaluate the efficacy and tolerability of different therapies associated with diet in the treatment of hypertensive obese patients. METHODS: In a clinical study we randomly evaluated 39 hypertensive obese patients (body mass index (BMI) > or = 30 kg/m2). After 45 days of diet the patients were again randomly distributed in 3 groups and received in double blind way: group 1-hypocaloric diet+placebo; group 2-hypocaloric diet+dexfenfluramine; group 3-hypocaloric diet+spiruline+fucus+gelatin. We followed their progress during 12 weeks under medication and further 24 weeks without. We evaluated the groups comparing: weight, BMI, blood pressure and side-effects. RESULTS: Twenty seven patients completed the observation. In those patients from groups 1 and 3 no changes in any of parameters were observed. In group 2 we observed a clear loss of weight (-3.8 Kg) and a fall in BMI. Blood Pressure changes were only observed in group 2 (-9.6%). The only patients to maintain weight loss after the termination of use of medicines were those from group 2. We did not observe any side-effects. CONCLUSION: In hypertensive obese patients, when isolated diet is not enough to control weight loss, dexfenfluramine could be useful in association with a controlled diet. The drug assists in weight loss, does not promote side-effects and does not interfere in the treatment of blood pressure.

Adult↗
PubMedDate not supplied

Antiobesity pharmacotherapy in the management of type 2 diabetes.

Obesity is a well-known risk factor for the development of Type 2 diabetes mellitus. The management of the obese diabetic patient remains a challenge for the clinician but, in any case, weight reduction should be considered as a key objective. In this respect, several antiobesity drugs have demonstrated potential. However, while fenfluramine and dexfenfluramine have been shown to promote weight loss and to directly improve insulin sensitivity, being two mechanisms contributing to better blood glucose control in obese Type 2 diabetic patients, they were recently withdrawn due to safety problems. Sibutramine, a new selective norepinephrine and serotonin reuptake inhibitor, promotes weight loss by decreasing food intake, an effect which leads to a mild improvement (significant in patients losing > or =5% of initial body weight) of blood glucose control in obese diabetic patients. Similarly, orlistat, a selective gastrointestinal lipase inhibitor which increases faecal fat losses, enhances diet-induced weight reduction and improves both blood glucose control and vascular risk profile, especially dyslipidaemia, in obese Type 2 diabetic patients. Further studies are required to better identify good responders to pharmacotherapy and specify the role of antiobesity agents in the overall long-term management of obese subjects with Type 2 diabetes. Other novel pharmacological approaches deserve further consideration, for instance beta-3 agonists aiming to increase energy expenditure, drugs interfering with tumor necrosis factor-alpha (TNF-alpha) or free fatty acid release by the adipose tissue or agents that slow gastric emptying. However, until now, results regarding efficacy and/or safety have been disappointing or preliminary in humans.

Appetite Depressants↗