Feeding signals and brain circuitry. Eur J Neurosci

Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
European Journal of Neuroscience (Impact Factor: 3.18). 10/2009; 30(9):1688-96. DOI: 10.1111/j.1460-9568.2009.06963.x
Source: PubMed


Food intake is a major physiological function in animals and must be entrained to the circadian oscillations in food availability. In the last two decades a growing number of reports have shed light on the hormonal, cellular and molecular mechanisms involved in the regulation of food intake. Brain areas located in the hypothalamus have been shown to play a pivotal role in the regulation of energy metabolism, controlling energy balance. In these areas, neuronal plasticity has been reported that is dependent upon key hormones, such as leptin and ghrelin, that are produced by peripheral organs. This review will provide an overview of recent discoveries relevant to understanding these issues.

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Available from: Marcelo O Dietrich, Jul 23, 2015
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    • "The hypothalamus is traditionally recognized as the main brain region regulating food intake. It regulates feeding as a function of caloric and nutritional requirements, by sensing macronutrients and through the action of circulating regulatory hormones, neuropeptides and neuromodulators such as leptin, cholecystokinin (CCK), ghrelin, orexin/hypocretin, insulin, neuropeptide Y (NPY) and endocannabinoids (Coll et al., 2007; Dietrich and Horvath, 2009; Blouet and Schwartz, 2010; Volkow et al., 2011). In particular, homeostatic food intake is tightly regulated by communication among hypothalamic nuclei including the arcuate nucleus (ARC), the paraventricular nucleus of the hypothalamus (PVH), the ventromedial and dorsomedial hypothalamus, as well as the lateral hypothalamic area (LHA). "
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    ABSTRACT: Hunger, mostly initiated by a deficiency in energy, induces food seeking and intake. However, the drive toward food is not only regulated by physiological needs, but is motivated by the pleasure derived from ingestion of food, in particular palatable foods. Therefore, feeding is viewed as an adaptive motivated behavior that involves integrated communication between homeostatic feeding circuits and reward circuits. The initiation and termination of a feeding episode are instructed by a variety of neuronal signals, and maladaptive plasticity in almost any component of the network may lead to the development of pathological eating disorders. In this review we will summarize the latest understanding of how the feeding circuits and reward circuits in the brain interact. We will emphasize communication between the hypothalamus and the mesolimbic dopamine system and highlight complexities, discrepancies, open questions and future directions for the field.
    04/2015; 10(2). DOI:10.1007/s11515-015-1348-0
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    • "Consequently, the brain needs to be informed about the amount of energy available, so that it can adjust its feeding and metabolic activities and accurately distribute the available energy over essential life processes including adaptation. For this purpose the organism employs various neurochemical brain messengers, such as neuropeptide Y (NPY), insulin, cholecystokinin (CCK), urocortin1 (Ucn1), and nesfatin-1 (e.g., Kalra et al., 1999; Dietrich and Horvath, 2009; Kozicz et al., 2011; Williams and Elmquist, 2012) and ghrelin/leptin-based signaling systems that inform the brain about the amount of peripheral energy information (Zhang et al., 1994; Meier and Gressner, 2004; Roubos et al., 2012). Evidently, prevention and therapy of disorders such as obesity and depression would enormously benefit from a better insight into the ways stress and feeding stimuli are integrated by this complex neuroendocrine signaling system. "
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    ABSTRACT: Leptin targets the brain to regulate feeding, neuroendocrine function and metabolism. The leptin receptor is present in hypothalamic centers controlling energy metabolism as well as in the centrally projecting Edinger-Westphal nucleus (EWcp), a region implicated in the stress response and in various aspects of stress-related behaviors. We hypothesized that the stress response by cocaine- and amphetamine-regulated transcript (CART)-producing EWcp-neurons would depend on the animal's energy state. To test this hypothesis, we investigated the effects of changes in energy state (mimicked by low, normal and high leptin levels, which were achieved by 24 h fasting, normal chow and leptin injection, respectively) on the response of CART neurons in the EWcp of rats subjected or not to acute restraint stress. Our data show that leptin treatment alone significantly increases CART mRNA expression in the rat EWcp and that in leptin receptor deficient (db/db) mice, the number of CART producing neurons in this nucleus is reduced. This suggests that leptin has a stimulatory effect on the production of CART in the EWcp under non-stressed condition. Under stressed condition, however, leptin blunts stress-induced activation of EWcp neurons and decreases their CART mRNA expression. Interestingly, fasting, does not influence the stress-induced activation of EWcp-neurons, and specifically EWcp-CART neurons are not activated. These results suggest that the stress response by the EWcp depends to some degree on the animal's energy state, a mechanism that may contribute to a better understanding of the complex interplay between obesity and stress.
    Frontiers in Neuroanatomy 03/2014; 8:8. DOI:10.3389/fnana.2014.00008 · 3.54 Impact Factor
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    • "Complex organisms must also coordinate whole-body energy balance with that of cellular energetics. In mammals, the hypothalamus located in the basal part of the brain plays a critical role in orchestrating whole-body energy homeostasis (Dietrich and Horvath, 2009). More specifically, a subset of neurons located in the arcuate nucleus of the hypothalamus that produces agouti-related peptide (Agrp) and neuropeptide-Y (NPY) (Broberger et al., 1998; Horvath et al., 1997; Ollmann et al., 1997) exerts a fundamental role in the promotion of feeding (Chen et al., 2004; Clark et al., 1984; Zarjevski et al., 1993). "
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    ABSTRACT: Mitochondria are key organelles in the maintenance of cellular energy metabolism and integrity. Here, we show that mitochondria number decrease but their size increase in orexigenic agouti-related protein (Agrp) neurons during the transition from fasted to fed to overfed state. These fusion-like dynamic changes were cell-type specific, as they occurred in the opposite direction in anorexigenic pro-opiomelanocortin (POMC) neurons. Interfering with mitochondrial fusion mechanisms in Agrp neurons by cell-selectively knocking down mitofusin 1 (Mfn1) or mitofusin 2 (Mfn2) resulted in altered mitochondria size and density in these cells. Deficiency in mitofusins impaired the electric activity of Agrp neurons during high-fat diet (HFD), an event reversed by cell-selective administration of ATP. Agrp-specific Mfn1 or Mfn2 knockout mice gained less weight when fed a HFD due to decreased fat mass. Overall, our data unmask an important role for mitochondrial dynamics governed by Mfn1 and Mfn2 in Agrp neurons in central regulation of whole-body energy metabolism.
    Cell 09/2013; 155(1):188-99. DOI:10.1016/j.cell.2013.09.004 · 32.24 Impact Factor
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