Evidence for the effect of tryptophan on the pattern of food consumption in free feeding and food deprived rats

Latham, Colin J.; Blundell, John

doi:10.1016/0024-3205(79)90307-2

Cited by 73 publications

(19 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our fInding of a lack of effect of L-TRP on carbo hydrate intake in normal controls is contrary to studies in some (Latham and Blundell 1979;Gibbons et al 1981), but not all animal studies (Peters et al 1984). However, following m-CPP, carbohydrate intake was decreased in the total group of subjects and the bulimic patients.…”

Section: Discussioncontrasting

confidence: 82%

“…M-CPP, but not L-TRP, significantly decreased meal size in the combined group, the controls, and to a lesser extent, the bulimics (p � .06). Maximum m-CPP Serotonergic manipulations are known to result in marked changes in feeding behaviors, particularly sati ety responses (Blundell 1977(Blundell , 1984(Blundell , 1986Blundell and Latham, 1978, 1982Latham and Blundell 1979;Samanin et al 1982;Silverstone and Goodall 1986;Garattini et al, 1988Garattini et al, , 1989, which are dysfunctional in bulimic patients (Owen et al 1985;Chiodo and Latimer 1986;Kissileff et al 1986). Pharmacologic en hancement of 5-HT neurotransmission in animals and concentrations were inversely correlated to the number of calories consumed in the total group.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Testmeal Responses Following m-Chlorophenylpiperazine and L-Tryptophan in Bulimics and Controls

Brewerton

Murphy

Jimerson

1994

Neuropsychopharmacol

View full text Add to dashboard Cite

A wealth of data support a role for serotonin (5-HT) function in the mediation of satiety responses, that are impaired in patients with bulimia nervosa. Testmeal results are presented in which 26 bulimic patients and 17 normal controls were given in randomized, double-blind-fashion, placebo, and the 5-HT agents m-chlorophenylpiperazine (m-CPP, 0.5 mglkg p.o.) and L-tryptophan (L-TRP, 100 mglkg I. V.). Three and one-half hours after drug administration, subjects were allowed to eat and lib from a standardized testmeal of 3,500 calories, after which postprandial vomiting was not allowed. M-CPP, but not L-TRP, significantly decreased meal size in the combined group, the controls, and to a lesser extent, the bulimics (p � .06). Maximum m-CPP Serotonergic manipulations are known to result in marked changes in feeding behaviors, particularly sati ety responses (Blundell 1977(Blundell , 1984(Blundell , 1986Blundell and Latham, 1978, 1982Latham and Blundell 1979;Samanin et al. 1982;Silverstone and Goodall 1986;Garattini et al., 1988Garattini et al., , 1989, which are dysfunctional in bulimic patients (Owen et al. 1985;Chiodo and Latimer 1986;Kissileff et al. 1986). Pharmacologic en hancement of 5-HT neurotransmission in animals and concentrations were inversely correlated to the number of calories consumed in the total group. Following m-CPP, there were significant decreases in carbohydrate, protein, and fat intake in the total group of subjects. There were also trends for decreased carbohydrate and protein intake in the bulimics following m-CPP. There were trends for both m-CPP and L-TRP to reduce fat intake in the controls. Differences in the effects between m-CPP and L-TRP are likely due to differential involvement of 5-HT receptor subtypes at presynaptic and postsynaptic sites. These studies in humans confirm reports in animals that m-CPP decreases food intake, including carbohydrates, protein, and fat in a mixed testmeal.

show abstract

Section: Discussioncontrasting

confidence: 82%

mentioning

confidence: 99%

Testmeal Responses Following m-Chlorophenylpiperazine and L-Tryptophan in Bulimics and Controls

Brewerton

Murphy

Jimerson

1994

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…We anticipated that the dosages of fenfluramine or tryptophan would be short-acting (Woolsey et al, 1979; Kyriakides and Silverston, 1979;Blundell et al, 1979). Hence, for calculations of drug effects we used only the snacks consumed during the 4-6 hr after each of the three drug doses.…”

Section: Discussionmentioning

confidence: 99%

“…The low doses of fenfluramine used in this study (45-60 mg/day) are below those generally used to produce anorexia (Weinberger et al, 1978;Blundell et al, 1979;Kyriakides and Silverston, 1979) and did not cause significant weight loss among our subjects studied for 14 treatment days. However, if the chronic use of such doses allows carbohydrate intake to continue to be reduced to the extent observed here (i.e., from 4.2 to 2.4 snackdday, with a net reduction in daily caloric intake of 18%) then such doses may aid in weight reduction among this particular population.…”

Section: Discussionmentioning

confidence: 99%

Carbohydrate craving in obese people: Suppression by treatments affecting serotoninergic transmission

Wurtman

Growdon

et al. 1981

Int. J. Eat. Disord.

159

View full text Add to dashboard Cite

We examined the existence of carbohydrate cravings, and the effects on such cravings of treatments that enhance serotonin release, among 24 obese subjects who claimed to have excessive appetites for carbohydrates. Subjects living in a college dormitory for four weeks were given three fixed meals daily and allowed to choose at will among five protein‐rich or five carbohydrate‐rich isocaloric snack foods, provided via a vending machine. For two weeks, they received no treatment (study 1) or a placebo (study 2); for the next two weeks, they received placebo, d‐1 fenfluramine or 1‐tryptophan. All but one of the subjects exhibited a marked preference for carbohydrate‐rich over protein‐rich snacks during the first two weeks of the study. The average daily intake of carbohydrate‐rich snacks was 4.1 ± 0.4 and of protein‐rich snacks 0.8 ± 0.3. Seventeen of the subjects failed to consume any protein snacks on most days during the baseline or test periods, thus it was not possible for us to examine the effect of test treatments on protein snack intake. Fenfluramine administration significantly reduced carbohydrate snacking in six of nine test subjects, as well as in the group as a whole (2.4 ± 0.6 snacks/day vs 4.2 ± 0.6 during the two‐week baseline period). Tryptophan significantly diminished carbohydrate intake in three of the eight treated subjects, and increased it in one subject; it did not significantly modify snacking patterns in the group as a whole. Placebo administration did not affect carbohydrate intake in any of the seven test subjects. These observations show that some obese people do consume carbohydrate‐rich snacks frequently and preferentially, and that this behavior can sometimes be diminished by treatments thought to enhance serotonin's release (fenfluramine) or synthesis (tryptophan).

show abstract

“…In vivo microdialysis has shown that food intake increases hypothalamic 5-HT release [33][34][35], but a closer investigation into the contribution of 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 5 individual macronutrients to this release revealed that the 5-HT increase is actually due to carbohydrates whereas protein has an opposite effect [36]. Administration of the 5-HT precursor amino acid tryptophan itself also reduces food intake [37]. The first step in 5-HT synthesis is the hydroxylation of tryptophan by tryptophan hydroxylase (Tph) forming 5-hydroxytryptophan (5-HTP).…”

Section: Brain 5-ht and Satietymentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

257

167

View full text Add to dashboard Cite

Serotonin has been implicated in the control of satiety for almost four decades. Historically, the insight that the appetite suppressant effect of fenfluramine is linked to serotonin has stimulated interest in and research into the role of this neurotransmitter in satiety. Various rodent models, including transgenic models, have been developed to identify the involved 5-HT receptor subtypes. This approach also required the availability of receptor ligands of different selectivity, and behavioural techniques had to be developed simultaneously which allow differentiating between unspecific pharmacological effects of these ligands and 'true' 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3 IntroductionWhat are the behavioural and physiological mechanisms that promote satiety? How is satiety defined? Satiety can be seen as a behavioural state which arises from food consumption and suppresses the initiation of eating for a particular period of time [1]. This description alone suggests a high degree of complexity as peripheral post-ingestive and post-absorptive signals need to be relayed to the brain where they are integrated with other signals to produce (or not) the behavioural state called satiety. The state of satiety is brought about a process called satiation, where sensory, cognitive and early post-ingestive mechanisms bring feeding to a halt and thus stopping a meal. Promoting satiation alone must not necessarily lead to reduced total food intake as the frequency of meals could be increased subsequently. Many peripheral and brain mechanisms have been identified that are involved in the expression satiety and it has been suggested that serotonin accelerates satiation and prolongs satiety [2]. In the following, we will review the role of serotonin in satiety in more detail 1 . The reader will see that, despite immense progress made during the last years, the field is still far from being resolved.As serotonin (5-Hydroxytryptamine; 5-HT) is a phylogenetically old neurotransmitter, various functions had time to evolve in different phyla, but maybe also in different species. 5-HT receptors exist in animal cells for millions of years and they are as old as adrenoreceptors ore some peptide receptors, possibly even older [5,6]. Even in invertebrates such as molluscs (Aplysia californica) and annelids (Hirudo medicinalis), 5-HT might functionally be related to food intake [7]. 5-HT is involved in feeding even in the honeybee where it has separate effects in the gut and in the insect brain [8]. In general, however, 5-HT seems rather to be involved in appetitive behaviours in invertebrates whereas it has more of a satiating effect in vertebrates [9]. In general, 5-HT neurons seem to be more extensively distributed throughout the body in lower animals than in higher animals including mammals where 5-HT neurones...

show abstract

Evidence for the effect of tryptophan on the pattern of food consumption in free feeding and food deprived rats

Cited by 73 publications

References 16 publications

Testmeal Responses Following m-Chlorophenylpiperazine and L-Tryptophan in Bulimics and Controls

Testmeal Responses Following m-Chlorophenylpiperazine and L-Tryptophan in Bulimics and Controls

Carbohydrate craving in obese people: Suppression by treatments affecting serotoninergic transmission

Serotonin controlling feeding and satiety

Contact Info

Product

Resources

About