TY - JOUR
T1 - Melanocortin neurons
T2 - Multiple routes to regulation of metabolism
AU - Shen, Wen jie
AU - Yao, Ting
AU - Kong, Xingxing
AU - Williams, Kevin W.
AU - Liu, Tiemin
N1 - Funding Information:
This work was supported by grants to T.Y. (China Scholarship Council 201406280111), X.K. (US National Institutes of Health Grant 5K99DK106550), K.W.W. (R01 DK100699) and T.L. (AHA 14SDG20370016).
Funding Information:
This work was supported by grants to T.Y. ( China Scholarship Council 201406280111 ), X.K. ( US National Institutes of Health Grant 5K99DK106550 ), K.W.W. ( R01 DK100699 ) and T.L. ( AHA 14SDG20370016 ).
Publisher Copyright:
© 2017
PY - 2017/10
Y1 - 2017/10
N2 - The burden of disability, premature death, escalating health care costs and lost economic productivity due to obesity and its associated complications including hypertension, stroke, cardiovascular disease and type 2 diabetes is staggering [1,2]. A better understanding of metabolic homeostatic pathways will provide us with insights into the biological mechanisms of obesity and how to fundamentally address this epidemic [3–6]. In mammals, energy balance is maintained via a homeostatic system involving both peripheral and central melanocortin systems; changes in body weight reflect an unbalance of the energetic state [7–9]. Although the primary cause of obesity is unknown, there is significant effort to understand the role of the central melanocortin pathway in the brain as it has been shown that deficiency of proopiomelanocortin (POMC) [10,11] and melanocortin 4 receptors (MC4R) [12–15] in both rodents and humans results in severe hyperphagia and obesity [16–23]. In this review, we will summarize how the central melanocortin pathway helps regulate body mass and adiposity within a ‘healthy’ range through the ‘nutrient sensing’ network [24–28]. This article is part of a Special Issue entitled: Melanocortin Receptors - edited by Ya-Xiong Tao.
AB - The burden of disability, premature death, escalating health care costs and lost economic productivity due to obesity and its associated complications including hypertension, stroke, cardiovascular disease and type 2 diabetes is staggering [1,2]. A better understanding of metabolic homeostatic pathways will provide us with insights into the biological mechanisms of obesity and how to fundamentally address this epidemic [3–6]. In mammals, energy balance is maintained via a homeostatic system involving both peripheral and central melanocortin systems; changes in body weight reflect an unbalance of the energetic state [7–9]. Although the primary cause of obesity is unknown, there is significant effort to understand the role of the central melanocortin pathway in the brain as it has been shown that deficiency of proopiomelanocortin (POMC) [10,11] and melanocortin 4 receptors (MC4R) [12–15] in both rodents and humans results in severe hyperphagia and obesity [16–23]. In this review, we will summarize how the central melanocortin pathway helps regulate body mass and adiposity within a ‘healthy’ range through the ‘nutrient sensing’ network [24–28]. This article is part of a Special Issue entitled: Melanocortin Receptors - edited by Ya-Xiong Tao.
KW - Agouti related peptide neurons
KW - Central melanocortin pathway
KW - Melanocortin 4 receptors
KW - Metabolism
KW - Proopiomelanocortin neurons
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U2 - 10.1016/j.bbadis.2017.05.007
DO - 10.1016/j.bbadis.2017.05.007
M3 - Review article
C2 - 28499988
AN - SCOPUS:85019845465
SN - 0925-4439
VL - 1863
SP - 2477
EP - 2485
JO - Biochimica et Biophysica Acta - Molecular Basis of Disease
JF - Biochimica et Biophysica Acta - Molecular Basis of Disease
IS - 10
ER -