The effect of dexamethasone on neuropeptide y concentrations in specific hypothalamic regions

McKibbin, P.E.; Cotton, Stephen J.; McCarthy, H. D.; Williams, Gareth

doi:10.1016/0024-3205(92)90020-p

Cited by 35 publications

(20 citation statements)

References 31 publications

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“…All of these changes were reversed by GC replacement (Gyengesi et al, 2010). In addition, GCs produce an increase of NPY mRNA and protein in the ARC (Wilding et al, 1993) and in PVN (Krysiak et al, 1999;McKibbin et al, 1992) in rats. Different stressors such as brief session of inescapable foot shocks and 1-h restraint increase NPY mRNA levels in the ARC of rats (Conrad and McEwen, 2000;Kas et al, 2005).…”

Section: Central Orexigenic Effectsmentioning

confidence: 93%

“…(Dagogo-Jack et al, 1997;Miell et al, 1996;Newcomer et al, 1998;Slieker et al, 1996;York, 1996) CRH and Ucn 3 (Bernier, 2006;Ohata and Shibasaki, 2011;Smagin et al, 1998) CART (Kask et al, 2000;Xu et al, 2010) Nesfatin-1 (Goebel et al, 2009;Stengel et al, 2011) NPW (Beck et al, 2010) Melanocortins (Liu et al, 2007;Yamano et al, 2004) central monoaminergic systems (Gibson, 2006) autonomous nervous system (Seematter et al, 2004) Stress induces hyperphagia due to reduction of: sensor specific satiety (Ahn and Phillips, 2012;Ortolani et al, 2011) stressor aversiveness (Piazza and Le Moal, 1997) CRH signaling? (Foster et al, 2009;la Fleur et al, 2005;Pecoraro et al, 2004) due to activation of central reward pathways (Piazza and Le Moal, 1997), due to alterations in gut microbiota (Tehrani et al, 2012) Glucocorticoids induce hyperphagia (Dallman, 1993;Drapeau et al, 2003;Epel et al, 2000;Tataranni et al, 1996) due to increased signaling of: NPY (Gyengesi et al, 2010;Krysiak et al, 1999;McKibbin et al, 1992;White et al, 1994;Wilding et al, 1993), AgRP (Coll et al, 2005;Savontaus et al, 2002), Nociceptin (Green and Devine, 2009;Nativio et al, 2011;…”

Section: Q4mentioning

confidence: 99%

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Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis

Бажан¹,

Zelena²

2013

Brain Research Bulletin

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a b s t r a c tThe prevalence of obesity is increasing worldwide with serious consequences such as diabetes mellitus type 2 and cardiovascular diseases. Emotional stress is considered to be one of the main reasons of obesity development in humans. However, there are some contradictory results, which should be addressed. First of all stress induces anorexia, but not overeating in laboratory animals. Glucocorticoids, the effector molecules of the hypothalamo-pituitary-adrenocortical (HPA) axis stimulate and stress inhibits food intake. It is also not clear if stress is diabetogenic or an antidiabetogenic factor. The review will discusses these issues and the involvement of the whole HPA axis and its separate molecules (glucocorticoids, adrenocorticotropin, corticotropin-releasing hormone) in food intake regulation under stress.

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Section: Central Orexigenic Effectsmentioning

confidence: 93%

Section: Q4mentioning

confidence: 99%

Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis

Бажан¹,

Zelena²

2013

Brain Research Bulletin

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“…Therefore, the relationship between NPY synthesis and release was tested in another state of combined insulin and leptin deficiency, severe streptozotocininduced diabetes in a rat model [74]. Diabetes in the rat increases NPY mRNA and NPY peptide [197,198], and it can be suppressed in the insulin-deficient animal by peripheral administration of insulin to lower glycaemia [197,198], or into the CNS without any effect on glycaemia [75]. Similarly NPY is spontaneously overexpressed in the hypothalamus of leptin-deficient ob/ob mice [199], and this response attenuated by the administration of leptin [200±202].…”

Section: Brain Neurotransmitters In the Regulation Of Body Adipositymentioning

confidence: 99%

Obesity, diabetes and the central nervous system

et al. 1998

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Nearly 25 years ago, one of us wrote a collaborative review entitled ªObesity and Diabetes, the Odd Coupleº [1]. At that time we pointed out that obesity was a risk factor for diabetes mellitus, despite the fact that most obese people do not have and never will develop diabetes. We also pointed out that obesity is associated with insulin resistance and hyperinsulinaemia, whereas in the non-obese, diabetes is characterized by hypoinsulinaemia and hyperglycaemia. We asked, how is it that such different syndromes interact so closely? We concluded that while these two syndromes are likely to have independent risk factors and mechanisms, their known interactions made it likely that shared metabolic defects are involved in their pathogenesis. We concluded that further studies into the pathophysiology of these syndromes were needed to explain this apparently paradoxical association.In the intervening years, considerable advance has been made into the pathophysiology of both syndromes. First, it is now clear that hyperglycaemia in Type II (non-insulin-dependent) diabetes is not the result of a regulatory failure, but is an adaptive response to impaired beta-cell function and insulin resistance, and we have reviewed this extensively [2]. More recently, obesity has similarly been shown to result from a dysregulation of food intake and energy expenditure rather than a loss of control over food intake [3±5]. In either case the critical variable (blood glucose or body adiposity) is defended at an abnormal level due to a regulatory defect, and both hyperglycaemia and obesity have undesirable long-term metabolic and vascular complications. What is now apparent is that there is overlap among the hormones, neuropeptides, and receptors involved in these two disorders, and it is our belief that it is this sharing which plays a prominent role in their association.In this article, we review our present understanding of the major elements of the feedback loops for body weight regulation in order to provide a comprehensive framework within which to place a torrent of new studies. We focus primarily on recent data implicating insulin, leptin, and hypothalamic neuropeptides as major elements. In this process we point out where the energy balance and glucose regulating systems intersect and indicate where common signalling mechanisms participate in their association. We conclude by synthesizing this information into a model that can explain how a single underlying set of pathophysiological factors can lead first to obesity and subsequently to Type II diabetes. Diabetologia (1998) 41: 863±881

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“…Not all studies have found that adrenalectomy significantly reduces NPY synthesis [ 1291 and the changes induced by the synthetic glucocorticoid dexamethasone are not entirely consistent with increased NPY synthesis, perhaps because it has powerful catabolic effects in addition to replacing glucocorticoids [130]. High doses of RU-486 did not decrease hypothalamic NPY mRNA levels infulfa Zucker rats [ 13 11 or diminish either hyperphagia or increased regional hypothalamic NPY levels in diabetic rats (Burns, Dryden & Williams, in preparation).…”

Section: Glucocorticoidsmentioning

confidence: 99%

Neuropeptide Y and energy balance: one way ahead for the treatment of obesity?

Dryden

Frankish

Wang

et al. 1994

Eur J Clin Investigation

123

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Abstract. Obesity is a vast and ever-expanding problem in affluent societies, which we have so far failed to confront. Over 20% of Western European and North American adults are overweight to a degree which may potentially shorten their life expectancy. Obesity has well-known associations with non-insulin-dependent diabetes (NIDDM), hypertension, dyslipidaemia and coronary heart disease, as well as less obvious links with diseases such as osteoarthrosis and various malignancies; it also causes considerable problems through reduced mobility and decreased quality of life. The overall financial burden of obesity is impossible to calculate precisely, but may account for 6-8% of total health-care expenditure in North America [ 13 (similar estimates probably apply to Western Europe).Obesity is difficult to treat and many patients remain obstinately overweight despite our best efforts. The available options range from behavioural therapy to gastrointestinal surgery and include numerous drugs designed to suppress appetite or increase energy expenditure. As in many other areas of medicine, the length and diversity of this list are reliable signs that effective treatment is still beyond our reach.This article argues that new anti-obesity drugs may emerge from recent advances in understanding the control of energy balance in rodents. The discussion is structured around neuropeptide Y (NPY), a major brain peptide which at present appears to be important in regulating energy balance and seems a promising candidate for therapeutic exploitation.

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The effect of dexamethasone on neuropeptide y concentrations in specific hypothalamic regions

Cited by 35 publications

References 31 publications

Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis

Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis

Obesity, diabetes and the central nervous system

Neuropeptide Y and energy balance: one way ahead for the treatment of obesity?

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