Meal-induced changes in extracellular 5-HT in medial hypothalamus of lean (Fa/Fa) and obese (fa/fa) Zucker rats

Fanti, Brant A. De; Hamilton, Jock S.; Horwitz, Barbara A

doi:10.1016/s0006-8993(01)02371-x

Cited by 30 publications

(17 citation statements)

References 33 publications

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“…A role for central serotonergic neurons in the regulation of feeding and maintenance of body weight has been well documented, and hypothalamic serotonergic mechanisms have been hypothesized to mediate at least some of these effects (Voigt et al 2000;De Fanti et al 2001;Orosco and Gerozissis 2001). In the present study, the destruction of serotonergic nerve terminals produced a decrease in body weight, which is consistent with the hypothesis of a central serotonergic involvement in feeding.…”

Section: Discussionsupporting

confidence: 89%

Destruction of serotonergic nerve terminals prevents fluoxetine-induced desensitization of hypothalamic 5-HT 1A receptors

et al. 2002

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Section: Discussionsupporting

confidence: 89%

Destruction of serotonergic nerve terminals prevents fluoxetine-induced desensitization of hypothalamic 5-HT 1A receptors

et al. 2002

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“…Interestingly, the 5-HT1A agonist induced hypophagia in obese, but not in lean Zucker rats, where it expectedly stimulated feeding [313]. The aggravated hypothalamic 5-HT release in response to a meal in obese Zucker rats has been interpreted as a reduced postsynaptic sensitivity to satiety signals [315,317].…”

Section: Changes In the Brain Satiety In Different Nutritional Statesmentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

270

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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“…5-HT, which is primarily synthesized by neurons in the dorsal raphe nucleus of the midbrain, also has a role in the central regulation of both food intake and glucose homeostasis 65 , specifically through binding to hypothalamic 5-HT 2C receptors 66 . Fenfluramine, a drug that increases 5-HT bioavailability, suppresses food intake both in humans and rodents 66 , whereas global deletion of the 5-HT 2C receptor in mice results in hyperphagia, obesity and obesity-associated insulin resistance with impaired glucose tolerance 67 .…”

Section: Glucose Regulation By the Arcmentioning

confidence: 99%

Wired on sugar: the role of the CNS in the regulation of glucose homeostasis

2012

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Obesity and type 2 diabetes mellitus (T2DM) — disorders of energy homeostasis and glucose homeostasis, respectively — are tightly linked and the incidences of both conditions are increasing in parallel. The CNS integrates information regarding peripheral nutrient and hormonal changes and processes this information to regulate energy homeostasis. Recent findings indicate that some of the neural circuits and mechanisms underlying energy balance are also essential for the regulation of glucose homeostasis. We propose that disruption of these overlapping pathways links the metabolic disturbances associated with obesity and T2DM. A better understanding of these converging mechanisms may lead to therapeutic strategies that target both T2DM and obesity.

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Meal-induced changes in extracellular 5-HT in medial hypothalamus of lean (Fa/Fa) and obese (fa/fa) Zucker rats

Cited by 30 publications

References 33 publications

Destruction of serotonergic nerve terminals prevents fluoxetine-induced desensitization of hypothalamic 5-HT 1A receptors

Destruction of serotonergic nerve terminals prevents fluoxetine-induced desensitization of hypothalamic 5-HT 1A receptors

Serotonin controlling feeding and satiety

Wired on sugar: the role of the CNS in the regulation of glucose homeostasis

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