Hypothalamic serotonin in control of eating behavior, meal size, and body weight

Leibowitz, Sarah F.; Alexander, Jesline T.

doi:10.1016/s0006-3223(98)00186-3

Cited by 447 publications

(259 citation statements)

References 128 publications

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“…An important hypothalamic structure in the control of feeding is the PVN where 5-HT and various agonists reduce food intake by decreased meal size and eating rate [4,172]. This pattern is very similar to the effects observed following systemic administration of 5-HT agonists but different from effects as observed after selective stimulation of peripheral receptors [4].…”

Section: Brain Mechanisms Of Serotonergic Satietymentioning

confidence: 64%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

266

167

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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...

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Section: Brain Mechanisms Of Serotonergic Satietymentioning

confidence: 64%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

266

167

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“…It also is possible that our finding of an inverse relationship between cerebral SERT binding and BMI is mediated through genetically and/or environmentally determined interindividual differences in extracellular 5-HT levels. As mentioned above, manipulations that decrease brain 5-HT neurotransmission in animals lead to elevated self-administration of food whereas treatments that increase 5-HT levels induce satiety which subsequently lead to decreased food intake and weight loss (Saller and Stricker, 1976;Waldbillig et al, 1981;Blundell, 1984;Simansky, 1996;Leibowitz and Alexander, 1998). It has been shown that serotonergic acting agents, especially when injected directly into the hypothalamus, suppress carbohydrate consumption while having little or no effect on the ingestion of protein or fat (Leibowitz and Alexander, 1998).…”

Section: Regionmentioning

confidence: 99%

“…As mentioned above, manipulations that decrease brain 5-HT neurotransmission in animals lead to elevated self-administration of food whereas treatments that increase 5-HT levels induce satiety which subsequently lead to decreased food intake and weight loss (Saller and Stricker, 1976;Waldbillig et al, 1981;Blundell, 1984;Simansky, 1996;Leibowitz and Alexander, 1998). It has been shown that serotonergic acting agents, especially when injected directly into the hypothalamus, suppress carbohydrate consumption while having little or no effect on the ingestion of protein or fat (Leibowitz and Alexander, 1998). Likewise, carbohydrate ingestion leads to increased circulating levels of the 5-HT amino acid precursor, tryptophan (Fernstrom et al, 1975;Noach, 1994;Wurtman and Wurtman, 1995), as well as increased hypothalamic and raphe nuclei 5-HT (Leibowitz and Alexander, 1998).…”

Section: Regionmentioning

confidence: 99%

“…It has been shown that serotonergic acting agents, especially when injected directly into the hypothalamus, suppress carbohydrate consumption while having little or no effect on the ingestion of protein or fat (Leibowitz and Alexander, 1998). Likewise, carbohydrate ingestion leads to increased circulating levels of the 5-HT amino acid precursor, tryptophan (Fernstrom et al, 1975;Noach, 1994;Wurtman and Wurtman, 1995), as well as increased hypothalamic and raphe nuclei 5-HT (Leibowitz and Alexander, 1998). Thus, 5-HT as a feedback on eating, serves to terminate the meal and yield a state of satiety.…”

Section: Regionmentioning

confidence: 99%

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Cerebral serotonin transporter binding is inversely related to body mass index

et al. 2010

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“…A negative feedback loop exists between the consumption of carbohydrate and the turnover of 5-HT in the hypothalamus, which involves circulating hormones (insulin, corticosterone, adipose tissue-derived hormone, leptin, and so on) and glucose in the process. 5 This is supported by an evidence of interaction between the 5HT2C and leptin genes in weight gain and circulating leptin level among schizophrenia subjects. 6 Other literature reviews on studies related to antipsychotic-associated weight gain have summarized the importance of genetics in the phenotype of antipsychotic-induced weight gain, and potential candidate genes have been suggested.…”

Section: Introductionmentioning

confidence: 84%

ADRA1A gene is associated with BMI in chronic schizophrenia patients exposed to antipsychotics

et al. 2009

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Noradrenaline and adrenaline are neurotransmitters of the sympathetic nervous system that interact with various adrenergic receptor (ADR) subtypes, and this regulates the basal metabolic rate, thermogenesis and efficiency of energy utilization. We examined a possible role of the gene coding for ADRA1A receptor in weight gain in schizophrenia subjects exposed to antipsychotics. A total of 401 schizophrenia in-patients treated with antipsychotics for 42 years were recruited and a final 394 DNA samples were genotyped. Their body mass indexes (BMIs) were recorded for 12 months and parameterized to be correlated in regression. Among the 58 single-nucleotide polymorphisms (SNPs) genotyped, 44 valid SNPs, which had minor allele frequency X0.03, were analyzed in statistics. Linear regression model with age, gender, diabetes, use of typical antipsychotics and use of atypical antipsychotics as covariates, with or without gender interaction, showed evidence of associations between the ADRA1A gene and BMI. Most of the SNPs associated with BMI are located in the promoter and intron regions, and being female appeared to enhance the gene effect. Our study suggests that the ADRA1A gene is involved in weight gain among schizophrenia patients treated with antipsychotics. Further molecular dissection of the ADRA1A gene warrants better understanding on weight gain mechanisms in schizophrenia.

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Hypothalamic serotonin in control of eating behavior, meal size, and body weight

Cited by 447 publications

References 128 publications

Serotonin controlling feeding and satiety

Serotonin controlling feeding and satiety

Cerebral serotonin transporter binding is inversely related to body mass index

ADRA1A gene is associated with BMI in chronic schizophrenia patients exposed to antipsychotics

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