Combined effect of obesity and aging on feeding-induced monoamine release in the rostromedial hypothalamus of the Zucker rat

Lemierre, Stéphanie; Rouch, Claude; Nicolaı̈dis, Stylianos; Orosco, M.

doi:10.1038/sj.ijo.0800717

Cited by 17 publications

(5 citation statements)

References 31 publications

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“…Indeed, in vivo microdialysis showed a lower basal 5-HT release [314], but a, compared to lean controls, increased serotonergic response to a meal [315]. The latter effect declines with age [316] which would also be in line with ex vivo 5-HT measures [313]. A lower hypothalamic baseline concentration, although not being found in some studies, could be explained with an increased control via raphe somatodendritic 5-HT1A autoreceptors, although the physiological significance of intrinsically hyperexcitable dorsal raphe neurons in Zucker rats needs to be established [282].…”

Section: Changes In the Brain Satiety In Different Nutritional Statesmentioning

confidence: 94%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

257

181

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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: Changes In the Brain Satiety In Different Nutritional Statesmentioning

confidence: 94%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

257

181

View full text Add to dashboard Cite

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“…Several lines of evidence, including data from animal models, genetic association studies, and human neuroimaging studies support the hypothesis of imbalanced dopamine availability and function in obesity. Rodent obesity models, either genetic or environmental, display changes in basal dopamine levels and altered levels of D2 receptor expression compared to lean animals (the direction and magnitude of which are dependent on brain region [138][139][140] ) as well as differential dopamine response to feeding [141][142][143][144][145][146] (e.g., both basal and ingestion-related DA release is increased in the LHA 143 ). Similarly, genetic linkage studies in human populations have found a correlation between BMI categories and/or changes in food intake behaviors with polymorphisms of several dopaminergic genes including DAT (SLC6A4) 147 dopamine receptors D2 and D4, [147][148][149][150][151][152][153][154][155] as well as monoamine oxidase A.…”

Section: Modulation Of Dopaminergic Circuitry By Peripheral Metabolic...mentioning

confidence: 99%

Central dopaminergic circuitry controlling food intake and reward: implications for the regulation of obesity

Vucetic

Reyes

2010

WIREs Mechanisms of Disease

120

108

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Prevalence of obesity in the general population has increased in the past 15 years from 15% to 35%. With increasing obesity, the coincident medical and social consequences are becoming more alarming. Control over food intake is crucial for the maintenance of body weight and represents an important target for the treatment of obesity. Central nervous system mechanisms responsible for control of food intake have evolved to sense the nutrient and energy levels in the organism and to coordinate appropriate responses to adjust energy intake and expenditure. This homeostatic system is crucial for maintenance of stable body weight over long periods of time of uneven energy availability. However, not only the caloric and nutritional value of food but also hedonic and emotional aspects of feeding affect food intake. In modern society, the increased availability of highly palatable and rewarding (fat, sweet) food can significantly affect homeostatic balance, resulting in dysregulated food intake. This review will focus on the role of hypothalamic and mesolimbic/mesocortical dopaminergic (DA) circuitry in coding homeostatic and hedonic signals for the regulation of food intake and maintenance of caloric balance. The interaction of dopamine with peripheral and central indices of nutritional status (e.g., leptin, ghrelin, neuropeptide Y), and the susceptibility of the dopamine system to prenatal insults will be discussed. Additionally, the importance of alterations in dopamine signaling that occur coincidently with obesity will be addressed.

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“…Dopaminergic transmission is altered in obese and insulin resistant animals. Basal and feeding evoked dopamine release is exaggerated in several nuclei of the hypothalamus of obese Zucker rats (18–20), whereas DRD2 expression is reduced in hypothalamic nuclei of obese animal models (21,22). The number of DRD2 binding sites in the striatum of obese humans is reduced and inversely correlated with body mass index (23).…”

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confidence: 99%

Blocking Dopamine D2 Receptors by Haloperidol Curtails the Beneficial Impact of Calorie Restriction on the Metabolic Phenotype of High-Fat Diet Induced Obese Mice

Weenen

Auvinen

Parlevliet

et al. 2011

Journal of Neuroendocrinology

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Calorie restriction is the most effective way of expanding life-span and decreasing morbidity. It improves insulin sensitivity and delays the age-related loss of dopamine receptor D(2) (DRD2) expression in the brain. Conversely, high-fat feeding is associated with obesity, insulin resistance and a reduced number of DRD2 binding sites. We hypothesised that the metabolic benefit of calorie restriction involves the preservation of appropriate DRD2 transmission. The food intake of wild-type C57Bl6 male mice was restricted to 60% of ad lib. intake while they were treated with the DRD2 antagonist haloperidol or vehicle using s.c. implanted pellets. Mice with ad lib. access to food receiving vehicle treatment served as controls. All mice received high-fat food throughout the experiment. After 10 weeks, an i.p. glucose tolerance test was performed and, after 12 weeks, a hyperinsulinaemic euglycaemic clamp. Hypothalamic DRD2 binding was also determined after 12 weeks of treatment. Calorie-restricted (CR) vehicle mice were glucose tolerant and insulin sensitive compared to ad lib. (AL) fed vehicle mice. CR mice treated with haloperidol were slightly heavier than vehicle treated CR mice. Haloperidol completely abolished the beneficial impact of calorie restriction on glucose tolerance and partly reduced the insulin sensitivity observed in CR vehicle mice. The metabolic differences between AL and CR vehicle mice were not accompanied by alterations in hypothalamic DRD2 binding. In conclusion, blocking DRD2 curtails the metabolic effects of calorie restriction. Although this suggests that the dopaminergic system could be involved in the metabolic benefits of calorie restriction, restricting access to high-fat food does not increase (hypothalamic) DRD2 binding capacity, which argues against this inference.

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Combined effect of obesity and aging on feeding-induced monoamine release in the rostromedial hypothalamus of the Zucker rat

Cited by 17 publications

References 31 publications

Serotonin controlling feeding and satiety

Serotonin controlling feeding and satiety

Central dopaminergic circuitry controlling food intake and reward: implications for the regulation of obesity

Blocking Dopamine D2 Receptors by Haloperidol Curtails the Beneficial Impact of Calorie Restriction on the Metabolic Phenotype of High-Fat Diet Induced Obese Mice

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