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Central Control of Food intake

Central Control of Food intake

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An essay for the 2011 Undergraduate Awards Competition by Sarah Wrafter. Originally submitted for Applied Nutrition at Trinity College, Dublin, with lecturer Dr Daniel McCartney in the category of Medical Sciences
An essay for the 2011 Undergraduate Awards Competition by Sarah Wrafter. Originally submitted for Applied Nutrition at Trinity College, Dublin, with lecturer Dr Daniel McCartney in the category of Medical Sciences

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Published by: Undergraduate Awards on Aug 29, 2012
Copyright:Attribution Non-commercial

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10/27/2013

 
 123
CentralControl of food intake
 
2
 Abstract 
4
The cross sectional National Adult Nutrition Survey has just been published. Results show
5
obesity rates in Ireland have risen significantly. Almost 26% of men and 21% of women are
6
now obese. Weight gain is as a result of excessive energy intake over energy expenditure.
7
This article aims to provide a clear understanding of the complex role central control has on
8
food intake. Central control encompasses the role of the hypothalamus, the brainstem, and
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various hormones. This article examines these aforementioned roles in depth. In conclusion,
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central control of food intake is maintained by complex pathways and neuronal circuits
11
within the hypothalamus and brain stem which receive peripheral signals such as gut
12
hormones.
13
Introduction
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The hypothalamus is segmented into interconnecting nuclei, the lateral hypothalamic area
15
(LHA), arcuate nucleus (ARC), paraventricular nucleus (PVN), dorsomedial nucleus (DMN)
16
and ventromedial nucleus (VMN) (Bloom
et al.,
2009). These nuclei play a critical role in
17
merging signals from central and peripheral pathways (Martini
et al.,
2007). Neuronal
18
connections between these nuclei combine to form a complex network in which orexigenic
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and anorexigenic circuits influence intake, with the main central messages conveyed by
20
neuropeptides, monoamines and endocannabinoids (Bloom
et al.,
2009). Gut hormones also
21
affect food intake. Acting as neurotransmitters they influence the central nervous system in
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the control of energy intake. Glucagon-like peptide-1, oxyntomodulin, pancreatic
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polypeptide and peptide YY quell appetite, whilst ghrelin augments appetite, through
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afferent vagal fibres to the caudal brainstem or directly through the hypothalamus (Bloom
25
et al.,
2010).
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327
 Arcuate nucleus
 
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The brain provides central control of food intake, with ARC an essential hypothalamic
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nucleus in the regulation of appetite. Within the ARC there are two major neuronal
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populations implicated in the regulation of energy intake. Neurons releasing neuropeptide Y
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(NPY) and agouti-related peptide (AGRP) stimulate food intake (Kyrkouli
et al.,
1986)
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whereas neurons co-expressing pro-opiomelanocortin (POMC) and cocaine- and
33
amphetamine-regulated transcript (CART) suppress intake (Kristensen
et al.,
1998).
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Neuronal projections from these two populations then connect with other hypothalamic
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areas associated with appetite control including the LHA, DMN and PVN (Bouret
et al.,
 
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2004).
37
NPY/AgRP neurons
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NPY plays a key role in regulation of consumption through its effects on energy intake and
39
expenditure (Bloom
et al.
, 2009).NPY/AgRP neurons have vast extensions within the
40
hypothalamus compassing the PVN, DMN and LHA, which appear to be the main targets for
41
the orexigenic effects of NPY (Baker
et al.,
1995). NPY acts on five receptors (Y1-Y5),
42
although its appetite stimulating properties are mediated through incitement of 
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hypothalamic Y1R and Y5R in addition to local inhibition of POMC neurons in the ARC (Cai
et 
44
al.
, 2004). Bewick et al carried out further research on the effect of NPY/AGRP neurons on
45
energy intake. A reduction in the number of arcuate AGRP/NPY neurons after
46
embryogenesis in mice leads to a lean, hypophagic phenotype and suggests that AGRP/NPY
47
neurons have a critical role in regulating food intake (2005).
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