Impairment of the serotonergic control of feeding in adult female rats exposed to intra-uterine malnutrition

Porto, Laura Cristina Jardim; Sardinha, Fátima Lúcia de Carvalho; Telles, Mônica Marques; Guimarães, Regina B.; Albuquerque, Kelse Tibau de; Andrade, Iracema Senna de; Oyama, Lila Missae; Nascimento, Cláudia Maria Oller do; Santos, Oscar Fernando Pavão dos; Ribeiro, Eliane B.

doi:10.1017/s0007114508061503

Cited by 26 publications

(28 citation statements)

References 33 publications

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“…On the other hand, obese Zucker rats had an exacerbated serotonergic response to food, probably due to resistance to the released neurotransmitter. A similar profile was found in female adult rats undernourished in utero, which were obese, had impairment of serotonin hypophagia and enhanced release of serotonin in response to a meal 1,5,6,18 .…”

Section: Estimating Neurotransmitter Release: Brain Microdialysissupporting

confidence: 69%

“…Gender differences were detected, as only the restricted females developed increased body fatness and leptinemia. Although both genders had impairment of insulin-and serotonin-induced hypophagia, the females were more affected 17,18 .…”

Section: Intrauterine Undernutrition and Obesitymentioning

confidence: 92%

“…In our hands, the combination of in vivo microdialysis, to sample brain intracellular fluid, and HPLC with electrochemical detection (EC), to measure serotonin levels in the microdialysate samples, has yielded numerous data on the participation of the serotonergic system in the physiology and pathophysiology of feeding control 1,5,6,10,18,[20][21][22] .…”

Section: Estimating Neurotransmitter Release: Brain Microdialysismentioning

confidence: 99%

“…This method has been used to determine the levels of serotonin and its main metabolite (5-HIAA) in MD samples collected from the hypothalamus. Because it is present in very low amounts in the hypothalamic microdialysates (in the order of fentomols), serotonin requires a high sensitivity method to be detected and HPLC-EC conditions able to maximize the capacity to measure this amine have been adopted 5,6,10,18,[20][21][22] .…”

Section: Estimating Neurotransmitter Release: Brain Microdialysismentioning

confidence: 99%

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Studying the central control of food intake and obesity in rats

Ribeiro

2009

Rev. Nutr.

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A B S T R A C TThe central nervous system regulates energy intake and expenditure through a complex network of neurotransmitters and neuromodulators. It is of great interest to understand the relevance of these systems to the physiological control of energy balance and to the disturbances of obesity. The present paper discusses some of the methods to address this field used at the laboratory of Endocrine Physiology of Universidade Federal de São Paulo. Initially, different experimental models of rat obesity are presented, namely the hypothalamic induced monosodium glutamate model, the Zucker genetic model, and the dietary model. The principles of brain microdialysis are also presented, the technique applied to obtain representative samples of the extracellular fluid of brain sites involved in feeding control. The microdialysate levels of serotonin, an important anorexigenic neurotransmitter, are determined by HPLC with electrochemical detection. The immunoblot technique (Western blot) is used to determine hypothalamic levels of proteins relevant to the anorexigenic effect of serotonin and to analyze the acute activation of the insulin signaling cascade in the hypothalamus. The final section addresses the potential applications of proteomics in the study of the central control of feeding.Indexing terms: Brain microdialysis. Experimental Studies. Food intake. Hypothalamus. Obesity. Rats. R E S U M O

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Section: Estimating Neurotransmitter Release: Brain Microdialysissupporting

confidence: 69%

Section: Intrauterine Undernutrition and Obesitymentioning

confidence: 92%

Section: Estimating Neurotransmitter Release: Brain Microdialysismentioning

confidence: 99%

Section: Estimating Neurotransmitter Release: Brain Microdialysismentioning

confidence: 99%

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Studying the central control of food intake and obesity in rats

Ribeiro

2009

Rev. Nutr.

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“…Intrauterine undernutrition leads to resistance to the hypophagic effect of intracerebroventricular 5-HT and dysregulations of hypothalamic 5-HT1B receptor, 5-HT2C receptor and 5-HTT protein expression. Adult offspring of such undernourished rats developed obesity despite normal habitual food intake suggesting the involvement of further satiety and metabolic mechanisms [375]. Nutritional programming by overnutrition has also been demonstrated after feeding a Western-style diet to lactating dams.…”

Section: Serotonin and The Pharmacotherapy Of Obesitymentioning

confidence: 98%

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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A proteomics–metabolomics approach indicates changes in hypothalamic glutamate–GABA metabolism of adult female rats submitted to intrauterine growth restriction

et al. 2018

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PurposeIntrauterine growth restriction (IUGR) has been shown to induce the programming of metabolic disturbances and obesity, associated with hypothalamic derangements. The present study aimed at investigating the effects of IUGR on the protein and metabolite profiles of the hypothalamus of adult female rats.MethodsWistar rats were mated and either had ad libitum access to food (control group) or received only 50% of the control intake (restricted group) during the whole pregnancy. Both groups ate ad libitum throughout lactation. At 4 months of age, the control and restricted female offspring was euthanized for blood and tissues collection. The hypothalami were processed for data independent acquisition mass spectrometry-based proteomics or targeted mass spectrometry-based metabolomics.ResultsThe adult females submitted to IUGR showed increased glycemia and body adiposity, with normal body weight and food intake. IUGR modulated significantly 28 hypothalamic proteins and 7 hypothalamic metabolites. The effects of IUGR on hypothalamic proteins and metabolites included downregulation of glutamine synthetase, glutamate decarboxylase, glutamate dehydrogenase, isocitrate dehydrogenase, α-ketoglutarate, and up-regulation of NADH dehydrogenase and phosphoenolpyruvate. Integrated pathway analysis indicated that IUGR affected GABAergic synapse, glutamate metabolism, and TCA cycle, highly interconnected pathways whose derangement has potentially multiple consequences.ConclusionThe present findings suggested that the effects of IUGR on GABA/glutamate–glutamine cycle may be involved in the programming of obesity and hyperglycemia in female rats.Electronic supplementary materialThe online version of this article (10.1007/s00394-018-1851-6) contains supplementary material, which is available to authorized users.

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Impairment of the serotonergic control of feeding in adult female rats exposed to intra-uterine malnutrition

Cited by 26 publications

References 33 publications

Studying the central control of food intake and obesity in rats

Studying the central control of food intake and obesity in rats

Serotonin controlling feeding and satiety

A proteomics–metabolomics approach indicates changes in hypothalamic glutamate–GABA metabolism of adult female rats submitted to intrauterine growth restriction

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