基本信息
浏览量:44
职业迁徙
个人简介
My primary professional activity is basic science and my major research areas are the following:
Leptin signaling and action in the central nervous system
Leptin is an adipocyte-derived hormone that acts in the brain to regulate a variety of processes and behaviors including food intake, energy expenditure and neuroendocrine function. Leptin is structurally related to cytokines and acts on receptors that belong to the cytokine-receptor superfamily. Leptin activates cytokine-like signal transduction by stimulating the JAK-STAT3 pathway. Using immunohistochemical approaches, my laboratory have demonstrated presence of leptin-responsive neurons in several regions of the hypothalamus and in extra-hypothalamic regions of the CNS, including the brainstem. Leptin action on these cells regulates the activity of various neuropeptides and neuronal circuits that combined controls energy homeostasis. A central long-term goal of my research is to chemically characterize leptin-responsive cells and to determine the role of these in leptin's action energy intake and body weight. I also have initiated a new research program aimed at understanding leptin signaling in the brainstem where leptin may modulate meal-signals from the stomach and gut.
Leptin and the central melanocortin system
Lack of leptin, leptin receptors, pro-opiomelanocortin (POMC) or its receptors, produce severe obesity in mice and humans, thus demonstrating a critical role of this leptin-melanocortin pathway in regulation of bodyweight. A major effort in my laboratory is to investigate how leptin influences POMC neurons to produce the appetite-reducing peptide, MSH. Furthermore, in a new line of research I plan to elucidate how leptin regulates post-translational modification of MSH. This process has strong effects on the biological activity of this peptide to inhibit appetite and is likely an important component of leptin action to regulate bodyweight.
Mechanisms of leptin resistance in the CNS and causes of obesity
Most humans with obesity and many rodent models of obesity are characterized by a resistance to the weight-reducing effects of leptin that has yet to be explained. Potential mechanisms for leptin resistance include defects in transport of leptin into the brain, defects in leptin signal transduction in target cells in the brain, and antagonism of leptin action at steps beyond the initial leptin-responsive neurons. Using detailed anatomic analyses I have recently discovered that only some parts of the brain are resistant to leptin while other regions remain leptin sensitive in diet-induced obese mice. A significant goal of my research is therefore to elucidate mechanisms causing leptin-resistant signaling and to determine the role of leptin-resistant cells in development of obesity. Furthermore, a key aim of my future scientific program is to understand the mechanism by which regional differences in leptin sensitivity develop. Knowledge of these issues is critical for the field and will likely lead to the identification of novel pathways and proteins that are useful as anti-obesity drug targets.
Leptin signaling and action in the central nervous system
Leptin is an adipocyte-derived hormone that acts in the brain to regulate a variety of processes and behaviors including food intake, energy expenditure and neuroendocrine function. Leptin is structurally related to cytokines and acts on receptors that belong to the cytokine-receptor superfamily. Leptin activates cytokine-like signal transduction by stimulating the JAK-STAT3 pathway. Using immunohistochemical approaches, my laboratory have demonstrated presence of leptin-responsive neurons in several regions of the hypothalamus and in extra-hypothalamic regions of the CNS, including the brainstem. Leptin action on these cells regulates the activity of various neuropeptides and neuronal circuits that combined controls energy homeostasis. A central long-term goal of my research is to chemically characterize leptin-responsive cells and to determine the role of these in leptin's action energy intake and body weight. I also have initiated a new research program aimed at understanding leptin signaling in the brainstem where leptin may modulate meal-signals from the stomach and gut.
Leptin and the central melanocortin system
Lack of leptin, leptin receptors, pro-opiomelanocortin (POMC) or its receptors, produce severe obesity in mice and humans, thus demonstrating a critical role of this leptin-melanocortin pathway in regulation of bodyweight. A major effort in my laboratory is to investigate how leptin influences POMC neurons to produce the appetite-reducing peptide, MSH. Furthermore, in a new line of research I plan to elucidate how leptin regulates post-translational modification of MSH. This process has strong effects on the biological activity of this peptide to inhibit appetite and is likely an important component of leptin action to regulate bodyweight.
Mechanisms of leptin resistance in the CNS and causes of obesity
Most humans with obesity and many rodent models of obesity are characterized by a resistance to the weight-reducing effects of leptin that has yet to be explained. Potential mechanisms for leptin resistance include defects in transport of leptin into the brain, defects in leptin signal transduction in target cells in the brain, and antagonism of leptin action at steps beyond the initial leptin-responsive neurons. Using detailed anatomic analyses I have recently discovered that only some parts of the brain are resistant to leptin while other regions remain leptin sensitive in diet-induced obese mice. A significant goal of my research is therefore to elucidate mechanisms causing leptin-resistant signaling and to determine the role of leptin-resistant cells in development of obesity. Furthermore, a key aim of my future scientific program is to understand the mechanism by which regional differences in leptin sensitivity develop. Knowledge of these issues is critical for the field and will likely lead to the identification of novel pathways and proteins that are useful as anti-obesity drug targets.
研究兴趣
论文共 48 篇作者统计合作学者相似作者
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mag(2015)
引用22浏览0引用
22
0
Aykut Üner,Gabriel H M Gonçalves, Wenjing Li, Matheus Porceban, Nicole Caron,Milena Schönke,Eric Delpire,Kenji Sakimura,Christian Bjørbæk
Proopiomelanocortin Gene, Expression Leptin,Heike Munzberg,Lihong Huo,Eduardo A Nillni,Anthony N Hollenberg,Christian Bjorbaek
mag(2013)
引用23浏览0引用
23
0
ENDOCRINOLOGY (2013)
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作者统计
#Papers: 48
#Citation: 7517
H-Index: 34
G-Index: 48
Sociability: 5
Diversity: 0
Activity: 0
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