Paraventricular hypothalamic α-melanocyte-stimulating hormone and MTII reduce feeding without causing aversive effects

Wirth, Mary J.; Olszewski, Pawel K.; Yu, Carolyn; Levine, Allen S.; Giraudo, Silvia Q.

doi:10.1016/s0196-9781(00)00367-3

Cited by 105 publications

(69 citation statements)

References 17 publications

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“…BDNF has also been suggested as an important downstream effector of melanocortin-4 receptor signaling, and one study showed that melanocortin administration stimulates BDNF expression in the VMH (89). However, like leptin, the time course of melanocortin-induced anorexia (19,88) does not match that of BDNF. Although these data do not exclude BDNF interaction with either leptin or melanocortins, the timing differences in behavioral responses suggest that BDNF likely does not mediate leptin-and melanocortin-induced feeding inhibition.…”

Section: Discussionmentioning

confidence: 99%

Brain-derived neurotrophic factor in the ventromedial nucleus of the hypothalamus reduces energy intake

Wang

Bomberg²,

Levine³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Recent studies show that brainderived neurotrophic factor (BDNF) decreases feeding and body weight after peripheral and ventricular administration. BDNF mRNA and protein, and its receptor TrkB, are widely distributed in the hypothalamus and other brain regions. However, there are few reports on specific brain sites of actions for BDNF. We evaluated the effect of BDNF, given into the ventromedial nucleus of the hypothalamus (VMH), on normal and deprivation-and neuropeptide Y (NPY)-induced feeding behavior and body weight. BDNF injected unilaterally or bilaterally into the VMH of food-deprived and nondeprived rats significantly decreased feeding and body weight gain within the 0-to 24-h and the 24-to 48-h postinjection intervals. Doses effectively producing inhibition of feeding behavior did not establish a conditioned taste aversion. BDNF-induced feeding inhibition was attenuated by pretreatment of the TrkB-Fc fusion protein that blocks binding between BDNF and its receptor TrkB. VMH-injected BDNF significantly decreased VMH NPY-induced feeding at 1, 2, and 4 h after injection. In summary, BDNF in the VMH significantly decreases food intake and body weight gain, by TrkB receptor-mediated actions. Furthermore, the anorectic effects of BDNF in this site appear to be mediated by NPY. These data suggest that the VMH is an important site of action for BDNF in its effects on energy metabolism. food intake; body weight THE VENTROMEDIAL NUCLEUS OF THE HYPOTHALAMUS (VMH) is a brain area important to the regulation of energy metabolism. Early studies indicated that VMH lesions resulted in hyperphagia and obesity (28,38,66), whereas electrical stimulation of the VMH immediately suppressed feeding and induced lipolysis (65). Glucose-sensing neurons (7,27,55,74,75) and receptors for neuropeptides important to energy metabolism have been identified in the VMH, including leptin (13,17,20,22,51), melanocortin (26), neuropeptide Y (NPY) (43), corticotrophin-releasing hormone (49), CCK (12), insulin (33), and orexin (44) receptors. Many biological agents given into the VMH have been demonstrated to affect feeding. Food intake is inhibited by administration of histamine (4, 47), glucagon-like peptide 1 (70), serotonin agonists (25), urocortin (58), CCK (79), leptin (51), and insulin (78), whereas thyroid hormone (3,5,3Ј-triiodothyronine) (40), GABA or GABA agonists (32,34,35), norepinephrine (73), orexin (74), and NPY induce feeding after administration into the VMH (5,9,24,31,43,56,76).Anatomically, the VMH receives inputs from regions important to the regulation of energy metabolism, including the hypothalamic arcuate nucleus (ARC) (2, 14, 23), lateral hypothalamus (18, 67, 80), amygdala (45, 50), and lateral septum. The VMH also projects to ARC (77), paraventricular nucleus (PVN) (42, 52), lateral hypothalamus (72, 80), dorsomedial nucleus of the hypothalamus (46, 80), amygdala (6, 68), lateral septum (68), ventral tegmental area (68), nucleus accumbens (6), and nucleus of the solitary tract (6). These behavioral and neuroanatom...

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Section: Discussionmentioning

confidence: 99%

Brain-derived neurotrophic factor in the ventromedial nucleus of the hypothalamus reduces energy intake

Wang

Bomberg²,

Levine³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The PVN receives input from the arcuate nucleus [173,174] and also accommodates MC receptors [175][176][177]. Local administration of MC3/MC4 agonists into the PVN reduces food intake whereas antagonists administered into the PVN increase food intake [178][179][180]. Although injections of 5-HT1B agonists into the PVN reduce food intake, blockade of the PVN 5-HT1B receptors or lesions of this region did not inhibit the satiating effects of systemic d-fenfluramine [181,182].…”

Section: Brain Mechanisms Of Serotonergic Satietymentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

259

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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“…cholecystokinin (CCK) (Hamamura et al 1991), NPY (Lambert et al 1995), ghrelin (Lawrence et al 2002), orexin-A (Edwards et al 1999, Shirasaka et al 2001), leptin (Van Dijk et al 1996, Elmquist et al 1997 and glucagon-like peptide 1 (GLP-1) (Van Dijk et al 1996). Administration of a melanocortin agonist directly into the PVN results in potent inhibition of food intake (Giraudo et al 1998, Kim et al 2000a, and inhibits the orexigenic effect of NPY administration (Wirth et al 2001), whereas, the administration of a melanocortin antagonist to the PVN results in a potent increase in food intake (Giraudo et al 1998). Electrophysiological studies in the PVN have shown that neurons expressing NPY/AgRP attenuate inhibitory GABA-ergic signalling, whereas POMC neurons potentiate GABAergic signalling (Cowley et al 1999).…”

Section: Pvnmentioning

confidence: 99%

Appetite control

Wynne¹,

Stanley²,

McGowan³

et al. 2005

Journal of Endocrinology

474

403

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Our understanding of the physiological systems that regulate food intake and body weight has increased immensely over the past decade. Brain centres, including the hypothalamus, brainstem and reward centres, signal via neuropeptides which regulate energy homeostasis. Insulin and hormones synthesized by adipose tissue reflect the long-term nutritional status of the body and are able to influence these circuits. Circulating gut hormones modulate these pathways acutely and result in appetite stimulation or satiety effects. This review discusses central neuronal networks and peripheral signals which contribute energy homeostasis, and how a loss of the homeostatic process may result in obesity. It also considers future therapeutic targets for the treatment of obesity.

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Paraventricular hypothalamic α-melanocyte-stimulating hormone and MTII reduce feeding without causing aversive effects

Cited by 105 publications

References 17 publications

Brain-derived neurotrophic factor in the ventromedial nucleus of the hypothalamus reduces energy intake

Brain-derived neurotrophic factor in the ventromedial nucleus of the hypothalamus reduces energy intake

Serotonin controlling feeding and satiety

Appetite control

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