Altered Cerebrospinal Fluid Neuropeptide Y and Peptide YY Immunoreactivity in Anorexia and Bulimia Nervosa

Kaye, Walter H.; Berrettini, Wade H.; Gwirtsman, Harry E.; George, David T.

doi:10.1001/archpsyc.1990.01810180048008

Cited by 171 publications

(60 citation statements)

References 61 publications

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“…Since the structure of NPY is highly conserved in vertebrates (2, 26) and it induces similar robust feeding in other species (1, 4), a universal physiological role of NPY within the neural network that regulates ingestive behavior in vertebrates is possible. Furthermore, experimental hyperphagia in diabetic rats is also associated with a general activation of hypothalamic NPYergic neurons (27)(28)(29), and concentrations ofNPY are significantly altered in the CSF of patients with eating disorders (30). It is, therefore, possible that abnormal shifts in either secretion or expression of NPY action selectively at discrete anatomical substrates in the brain, which include the PVN, underlie the etiology of clinical eating disorders-namely, anorexia nervosa, bulimia, and obesity.…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y secretion increases in the paraventricular nucleus in association with increased appetite for food.

Kalra

Dube

Sahu

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

585

232

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Feeding in mammals is a periodic behavior; however, knowledge of how the brain signals an intermittent eating pattern is scanty. Recent indirect evidence indicates that one of the signals encoded in the structure of neuropeptide Y (NPY) is to stimulate robust feeding. Therefore, two series of experiments were undertaken to characterize NPY secretion within the paraventricular nucleus (PVN) in association with eating behavior in the rat. Dynamic changes in NPY concentration in several hypothalamic sites and release in the PVN were assessed before and during the course of food consumption in rats trained to eat daily only for 4 h. Only in the PVN were NPY concentrations elevated before the introduction of food and, thereafter, levels decreased significantly during the course ofeating. A similar temporal pattern in NPY release into the PVN interstitium was evident in samples collected by push-pull cannula perfusion in unrestrained rats. In addition, in food-deprived rats displaying a robust drive for feeding, NPY release in the PVN was also markedly enhanced in the shape of high-amplitude secretory episodes as compared to a lower release rate in rats receiving food ad libitum. The higher rate of NPY release in fasted rats returned to the control range after 24 h of ad libitum food supply. These rmdings of intense and dynamic NPY neurosecretory activity within a discrete hypothalamic site in association with an increased drive for food consumption demonstrate that NPY release in the PVN is an important orexigenic signal for periodic eating behavior. These results have important global implications for elucidating the underlying causes of the pathophysiology of eating disorders-anorexia nervosa, bulimia, and obesity-as well as constituting a specific contextual model for the formulation and testing of suitable NPY receptor agonists and antagonists for therapeutic intervention.Neural circuits that integrate metabolic, neural, and hormonal signals leading to intermittent motivation to eat reside in the hypothalamus. There is now a consensus that stimulation of hunger or appetite for food is encoded in a few specific signals in the hypothalamus. Among peptides and amines that stimulate feeding, neuropeptide Y (NPY) is found to be the most potent enhancer of consummatory behavior in a large number of species (1-4). NPY is produced in the arcuate nucleus (ARC) ofthe hypothalamus and other regions of the brain, including discrete cell groups in the brainstem. The fiber systems from the ARC and brainstem project into various hypothalamic sites previously implicated in regulation of feeding behavior (5-8). In fact, not only administration into the cerebroventricular system (3, 9, 10) but microinjection of NPY into various hypothalamic sites (11-13) rapidly elicited robust feeding responses in rats. Continuous NPY infusion into the third cerebroventricle evoked continuous episodic feeding during the infusion and postinfusion intervals (14). Multiple daily injections of NPY into the paraventricular nucleus (PVN) of the...

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Section: Discussionmentioning

confidence: 99%

Neuropeptide Y secretion increases in the paraventricular nucleus in association with increased appetite for food.

Kalra

Dube

Sahu

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

585

232

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“…For instance, people with anorexia nervosa who are underweight and malnourished have been found to have significantly increased concentrations of NPY in the cerebrospinal fluid compared to normal weight controls, and this change is significantly correlated with the decrease in serum and cerebrospinal fluid leptin concentrations (Kaye et al, 1990, Martinez et al, 1993, Hebebrand et al, 1995, Grinspoon et al, 1996, Baranowska et al, 1997, Ferron et al, 1997and Mantzoros et al, 1997. Moreover, the elevated cerebrospinal fluid NPY levels in people with anorexia nervosa are normalized when their eating behavior and body weight are restored to normal, suggesting that increases in central NPY levels may be a biological adaptation to energy deficit in humans (Kaye et al, 1990 andGendall et al, 1999) as well as in rodents. In keeping with this, a polymorphism in human preproNPY, a p.L7P substitution, has been shown to cause altered NPY secretion, and association studies suggest that this functional substitution may be a strong independent risk factor for various metabolic and cardiovascular diseases (Pesonen, 2008).…”

Section: Insights From Humansmentioning

confidence: 99%

Role of the arcuate nucleus of the hypothalamus in regulation of body weight during energy deficit

Sainsbury

Zhang

2010

Molecular and Cellular Endocrinology

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Acute or long-term energy deficit in lean or obese rodents or humans stimulates food intake or appetite and reduces metabolic rate or energy expenditure. These changes contribute to weight regain in post-obese animals and humans. Some studies show that the reduction in metabolic rate with energy deficit in overweight people is transient. Energy restriction has been shown in some but not all studies to reduce physical activity, and this may represent an additional energy-conserving adaptation. Energy restriction up-regulates expression of the orexigenic neuropeptide Y, agouti related peptide and opioids and down-regulates that of the anorexigenic alpha-melanocyte stimulating hormone or its precursor pro-opioomelanocortin and the co-expressed cocaine and amphetamine-regulated transcript in the arcuate nucleus of the hypothalamus. Recapitulating these hypothalamic changes in sated animals mimics the effects of energy deficit, namely increased food intake, reduced physical activity and reduced metabolic rate, suggesting that these energy-conserving adaptations are at least partially mediated by the hypothalamus.

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“…Ancak reseptörlerdeki aşağı ayarlama (down-regülasyon) nedeniyle etkisiz kalmaktadır. [63] NPY1R ve NPY5R iştah uyarımı ile sıkı ilişkilidir. Oysa NPY2R ve NPY4R iştahın baskılanmasına yol açar.…”

Section: Yeme Davranışıunclassified

“…Oysa NPY2R ve NPY4R iştahın baskılanmasına yol açar. [63] Stres ve obezite arasında ilişkiye işaret eden çok sayıda araştırma olmakla birlikte doğrudan bir ilişki bulmak zordur. Strese yanıt olarak, bazı insanlar kilo alırken bazıları da kilo kaybederler.…”

Section: Yeme Davranışıunclassified

Neuropeptide Y and Stress

Gülsün¹,

Tamam²

2012

Psikiyatride Guncel Yaklasimlar - Current Approaches in Psychia

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ÖZETStres ve bireysel baş etme yetilerinin nörobiyolojik yönü birçok araştırmacının ilgi odağı olmuştur. Bir dizi çalışmada genetik değişkenler ile strese tepki düzeyleri ve yaşam olayları arasında bir ilişki olduğu gösterilmiştir. Nöropeptid Y stres esnekliğini düzenleyen sistemlerden biridir. Uzun süreli ya da tekrarlayan stres durumlarında nöropeptid Y beynin anahtar bölgelerinden salınır. Bu sistem stresle ilgili bozukluklara yatkınlığı farklı kişilerde farklı esneklikte işleyiş gösterir. Gen-çevre etkileşimleri için özellikle ilgi çekici olan strese duyarlı sinyal moleküllerini kodlayan genlerin değişimidir. Bu durum strese yatkınlığa ya da esnekliğe katkıda bulunabilir. Nöropeptid Y sistemi de strese davranışsal uyumda anahtar rol oynamaktadır. Nöropeptid Y düzeyinin azalmış olması tedaviye dirençli depresyonda ve travma sonrası stres bozukluğunda da gözlenmiştir. Düşük nöropeptid Y ekspresyonunun ya da strese yanıt olarak nöropeptid Y sisteminin yeterince işlevsel olmaması ve sonucunda ortaya çıkan stres esnekliğinin az olması stresle ilişkili bozukluklara yatkınlığı arttırabilmektedir. Anahtar Sözcükler: Nöropeptid Y, stres, stres esnekliği ABSTRACTThe neurobiological aspects of stress and coping skills has been the focus of interest for many researchers. Some of the studies has shown that there is a significant relationship among genetically variables, stress response and life events. Neuropeptide Y is one of the systems regulating the stress response. Under the prolonged or repeated trauma neuropeptide Y is released from the brain's key areas. This system shows different levels of functioning in individuals with different levels of resilience. There is particular interest in the variations of genes that encode stress-sensitive signaling molecules during geneenvironment interaction. This condition may contribute to susceptibility of stress or stress resilience. Neuropeptide Y system plays a key role in the adaptation to behavioral stress. The reduced levels of neuropeptide Y have also been observed in treatment-resistant depression and posttraumatic stress disorder. Lower level of neuropeptide Y expression and dysfunctional neuro-

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Altered Cerebrospinal Fluid Neuropeptide Y and Peptide YY Immunoreactivity in Anorexia and Bulimia Nervosa

Cited by 171 publications

References 61 publications

Neuropeptide Y secretion increases in the paraventricular nucleus in association with increased appetite for food.

Neuropeptide Y secretion increases in the paraventricular nucleus in association with increased appetite for food.

Role of the arcuate nucleus of the hypothalamus in regulation of body weight during energy deficit

Neuropeptide Y and Stress

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