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Kazunari Nohara, Suhuan Liu, Matthew S Meyers, Aurélie Waget, Mathieu Ferron, Gérard Karsenty, Rémy Burcelin and Franck Mauvais-Jarvis

precocial species that give birth to mature young. In both groups, synaptogenesis of hypothalamic centers that control energy homeostasis and adipose tissue development occurs during the second trimester of pregnancy ( Ailhaud et al . 1992 , Koutcherov et

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Patricia Joseph-Bravo, Lorraine Jaimes-Hoy and Jean-Louis Charli

important player in energy homeostasis ( Hollenberg 2008 , Fliers et al . 2014 , McAninch & Bianco 2014 , Mullur et al . 2014 ). The activity of the HPT axis is stringently regulated by neuronal stimuli impinging on TRH neurons and by the negative

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J D Bailey, J G Berardinelli, T E Rocke and R A Bessen

energy homeostasis, in general, is subject to prion-induced alteration. We hypothesized, as have others ( Ye et al . 1994 a , b , 1997 ), that there are two potential explanations for prion-induced alteration in energy homeostasis: one that involves

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Karla J Suchacki, Fiona Roberts, Andrea Lovdel, Colin Farquharson, Nik M Morton, Vicky E MacRae and William P Cawthorn

organ with possible roles in the hormonal modulation of systemic energy homeostasis. Osteocalcin Also known as BGP (bone Gla protein), osteocalcin (OCN) is the most abundant osteoblast-specific non-collagenous protein. OCN is initially synthesised

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Michael Rosenbaum and Rudolph L Leibel

of their effects in the hypothalamus, thus energizing speculation as to the nature of these metabolic markers of energy stores. Mayer (1955) proposed that energy homeostasis and body energy stores were largely regulated by the interactions of

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V Ott, M Fasshauer, A Dalski, HH Klein and J Klein

Ciliary neurotrophic factor (CNTF) plays an important role in regulating neuronal growth. Recently, central anorexigenic effects of this cytokine have been characterized. However, peripheral effects on tissues that actively contribute to the regulation of energy homeostasis have not been described. Here, we report direct potent and selective effects of CNTF on growth factor and metabolic signalling intermediates in mouse brown adipocytes. CNTF stimulates STAT3, MAP kinase, Akt, and p70 S6 kinase. We find that, next to mediating Akt and p70 S6 kinase activation, both phosphatidylinositol 3-kinase and protein kinase C are separately acting, main intermediates for inducing mitogen-activated protein (MAP) kinase activation. On a functional level, CNTF enhances beta3-adrenergic induction of uncoupling protein-1. Thus, these results demonstrate direct effects of CNTF on adipose tissue signalling and metabolism and suggest a novel role for this cytokine in the peripheral regulation of energy homeostasis.

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Filipe de Vadder and Gilles Mithieux

Introduction The worldwide increase in obesity and associated illnesses such as type 2 diabetes has urged the scientific community to improve our understanding of the mechanisms underlying energy homeostasis. A well-documented area relates to

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Patricia Joseph-Bravo, Lorraine Jaimes-Hoy and Jean-Louis Charli

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CR Barb, AS Robertson, JB Barrett, RR Kraeling and KL Houseknecht

A recently discovered class of receptors, melanocortin-3 and -4 receptor (MC3/4-R), are located within the brain and modulate feed intake in rodents. Stimulation of the receptor (agonist) inhibits feed intake whereas blockade (antagonist) of the receptor increases intake. Our knowledge of factors regulating voluntary feed intake in humans and domestic animals is very limited. i.c.v. administration of an MC3/4-R agonist, NDP-MSH, suppressed (P<0.05) feed intake compared with controls at 12, 24, 48 and 72 h after treatment in growing pigs. Fed pigs were more responsive to the MC3/4-R agonist then fasted animals. However, i.c.v. treatment with MC3/4-R antagonist, SHU9119, failed to stimulate intake. The failure of MC3/4-R antagonist to stimulate feed intake suggests involvement of other brain hormone(s) which antagonize the action of SHU9119 at the MC3/4-R, blocking its stimulatory effect on intake. Treatment with NDP-MSH or SHU9119, across a wide dose range, failed to affect LH and GH secretion, except for the 10 micro g dose of NDP-MSH, which exhibited both a stimulatory and an inhibitory effect on GH secretion in fasted animals. Treatment with agouti-related peptide, a natural brain hormone that blocks the MC3/4R, failed to stimulate feed intake. These results do not support the idea that endogenous melanocortin pays a critical role in regulating feed intake and pituitary hormone secretion in the pig. SHU9119 blocked the NDP-MSH-induced increase in cAMP in HEK293 cells expressing the porcine MC4-R sequence without the missense mutation. The EC(50) and IC(50) values were similar to the human MC4-R, confirming that SHU9119 is a pig MC4-R antagonist. However, pigs were heterozygous for an MC4-R gene missense mutation. It is possible that the MC4-R mutation alters function and this may explain the failure to demonstrate MC3/4-R involvement in modulating feeding behavior and LH and GH secretion in the pig.

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Hiroyuki Shimizu, Kinji Inoue and Masatomo Mori

activity and locomotion. There are complex but integrated interconnections among the hypothalamic nuclei that coordinate the maintenance of energy homeostasis through regulating food intake and energy expenditure ( Schwartz et al. 2000 , Flier 2004