Hypothalamic gene expression following ghrelin therapy to gastrectomized rodents

Egecioglu, Emil; Stenström, Björn; Pinnock, Scarlett B.; Tung, L. Y. C.; Cour, Charlotta Dornonville de la; Lindqvist, Andreas; Håkanson, R.; Syversen, Unni; Chen, Duan; Dickson, Suzanne L.

doi:10.1016/j.regpep.2007.09.006

Cited by 17 publications

(11 citation statements)

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“…A c c e p t e d M a n u s c r i p t 3 GHS-R1a, promoting production and secretion of their orexigenic neuropeptides to suppress pro-POMC neuronal activity while promoting food intake (Cowley et al, 2003;Egecioglu et al, 2008). Interplay between ghrelin and orexin (Toshinai et al, 2003) suggests that arousal and wakefulness may be required for ghrelin's orexigenic effect (Olszewski et al, 2008).…”

Section: Page 3 Of 44mentioning

confidence: 99%

Ghrelin in obesity and endocrine diseases

Scerif

Goldstone

Korbonits

2011

Molecular and Cellular Endocrinology

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Section: Page 3 Of 44mentioning

confidence: 99%

Ghrelin in obesity and endocrine diseases

Scerif

Goldstone

Korbonits

2011

Molecular and Cellular Endocrinology

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“…Ghrelin not only stimulates appetite but also affects peripheral glucose and lipid metabolism as well as energy expenditure, in a way that leads to the accumulation and preservation of energy stores (Tschöp et al 2000, Theander-Carrillo et al 2006. Ghrelin is thought to modulate the expression of hypothalamic neuropeptides such as neuropeptide Y (NPY) and agouti-related peptide (AgRP) within the arcuate nucleus (ARC) and melaninconcentrating hormone in the lateral hypothalamus (Seoane et al 2003, Smith et al 2005, Egecioglu et al 2008). The GHSR is mainly expressed in the ARC, the ventromedial (VMN) and the paraventricular nuclei (PVN) in the hypothalamus, as well as in the area postrema, the nucleus of the solitary tract (NTS), the dorsal motor nucleus of the vagus and the parasympathetic preganglionic neurons (Bennett et al 1997, Guan et al 1997, Zigman et al 2005.…”

Section: Introductionmentioning

confidence: 99%

Shedding light on the intricate puzzle of ghrelin's effects on appetite regulation

Kola¹,

Korbonits²

2009

Journal of Endocrinology

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Ghrelin, a hormone primarily produced by the stomach, has a wide range of metabolic and non-metabolic effects. It also stimulates food intake through activation of various hypothalamic and brain stem neurons. A series of recent studies have explored the intracellular mechanisms of the appetite-inducing effect of ghrelin in the hypothalamus, shedding light on the intricate mechanisms of appetite regulation. AMP-activated protein kinase (AMPK) is a key metabolic enzyme involved in appetite regulation.Calmodulin kinase kinase 2 (CaMKK2) has been identified as an upstream kinase of AMPK and a key mediator in the effect of ghrelin on AMPK activity. The fatty acid pathway, hypothalamic mitochondrial respiration, and uncoupling protein 2 have been outlined as downstream targets of AMPK and mediators of ghrelin's appetite stimulating effect. This short overview summarises the present data in this field.

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“…Studies using various rat models have shown that mechanical factors and changes in gastrointestinal and adipose hormones, as well as hypothalamic neuropeptides may contribute to GB-induced weight loss by promoting catabolic processes [7][8][9][10][11]. As the rats are nocturnal animals, their characteristic pattern of consuming food during the day or night provides a useful model for human ad libitum eating.…”

Section: Introductionmentioning

confidence: 99%