The mechanism underlying the central glucagon-induced hyperglycemia and anorexia in chicks

Honda, Kazuhisa; Kamisoyama, Hiroshi; Uemura, Taku; Yanagi, Takashi; Sakai, Noboru; Kurose, Yohei; Sugahara, Kunio; Katoh, K.; Hasegawa, Shin

doi:10.1016/j.cbpa.2012.08.005

Cited by 21 publications

(23 citation statements)

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“…Central administration of glucagon significantly increased hypothlamic CRF expression and plasma corticosterone concentraton in layer chicks, suggesting that CRF is a downstream mediator of the glucagon-induced anorexigenic pathway (Honda et al, 2012a). Also, central administration of NMU significantly increased hypothlamic CRF expression in layer chicks, suggesting that CRF might be a downstream mediator of the NMU-induced anorexigenic pathway .…”

Section: Discussionmentioning

confidence: 79%

“…Central administration of glucagon suppresses feeding behavior in mammals and chickens (Honda et al, , 2012aInokuchi et al, 1984). However, any other behavioral changes were not reported when glucagon was administered centrally in mammals and birds.…”

Section: Discussionmentioning

confidence: 92%

“…We previously showed that the central administration of several anorexigenic peptides significantly decreased food intake and plasma glucose concentration in chicks (Honda et al, 2012a(Honda et al, , 2014a(Honda et al, , b, 2015a. The anorexigenic peptidedecreased plasma glucose would be the result of suppressed food intake because fasting decreases plasma glucose concentration in general.…”

Section: Discussionmentioning

confidence: 99%

“…We previously showed that the central administration of glucagon suppresses food intake in layer chicks and suggested that corticotropin-releasing factor (CRF) -and/or hyperglycemia-mediated pathways are involved in the anorexigenic action of glucagon in layer chicks (Honda et al, , 2012a. We also showed that the central administration of neuromedin U (NMU) suppresses food intake and induces wing-flapping behavior in layer chicks .…”

Section: Introductionmentioning

confidence: 99%

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Glucagon and Neuromedin U Suppress Food Intake in Broiler Chicks

et al. 2015

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Several peptides show different effects on food intake between broiler and layer chicks. For example, the central administration of β-melanocyte-stimulating hormone decreased food intake in layer chicks but not in broiler chicks. The central administration of agouti-related protein increased food intake in layer chicks but not in broiler chicks. We previously reported that glucagon and neuromedin U (NMU) suppress food intake in layer chicks when administered centrally. However, the effects of these peptides on food intake in broiler chicks have not been examined. In the present study, we thus examined whether these peptides also show anorexigenic effects in broiler chicks. The intracerebroventricular administration of glucagon significantly suppressed food intake and increased plasma glucose concentration in broiler chicks. The hyperglycemic effect of glucagon had been shown in layer chicks in our previous studies. Intracerebroventricular administration of NMU significantly suppressed food intake and induced wingflapping behavior in broiler chicks as well as in layer chicks. All our findings demonstrate that glucagon and NMU function as anorxigenic peptides in both broiler and layer chicks.

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Section: Discussionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Glucagon and Neuromedin U Suppress Food Intake in Broiler Chicks

et al. 2015

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“…glucagon administration to modulate peripheral glucose levels in different species of animals [5][6][7]. Most intriguing, however, is the earliest study in dogs where a high dose i.c.v.…”

Section: Introductionmentioning

confidence: 99%

Glucagon action in the brain

Abraham

Lam

2016

Diabetologia

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In recent years, novel discoveries have reshaped our understanding of the biology of brain glucagon in the regulation of peripheral homeostasis. Here we compare and contrast brain glucagon action in feeding vs glucose regulation and depict the physiological relevance of brain glucagon by reviewing their actions in two key regions of the central nervous system: the mediobasal hypothalamus and the dorsal vagal complex. These novel findings pave the way to future therapeutic strategies aimed at enhancing brain glucagon action for the treatment of diabetes and obesity. This review summarises

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Glucagon and lipid signaling in the hypothalamus

et al. 2014

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Hyperglycemia, caused in part by elevated hepatic glucose production (GP), is a hallmark feature of diabetes and obesity. The hypothalamus responds to hormones and nutrients to regulate hepatic GP and glucose homeostasis. This invited perspective focuses on the molecular signaling and biochemical pathways involved in the gluco-regulatory action of hypothalamic glucagon signaling and lipid sensing in health and disease. Recent evidence generated via genetic, molecular and chemical experimental approaches indicates that glucagon and lipid signaling independently trigger complementary hypothalamic mechanisms to lower GP. Thus, targeting hypothalamic glucagon or lipid signaling may have therapeutic potential in diabetes and obesity.

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The mechanism underlying the central glucagon-induced hyperglycemia and anorexia in chicks

Cited by 21 publications

References 34 publications

Glucagon and Neuromedin U Suppress Food Intake in Broiler Chicks

Glucagon and Neuromedin U Suppress Food Intake in Broiler Chicks

Glucagon action in the brain

Glucagon and lipid signaling in the hypothalamus

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