Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance

Leptin, the long-sought satiety factor of adipocytes origin, has emerged as one of the major signals that relay the status of fat stores to the hypothalamus and plays a significant role in energy homeostasis. Understanding the mechanisms of leptin signaling in the hypothalamus during normal and path...

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Bibliographic Details
Published inFrontiers in neuroendocrinology Vol. 24; no. 4; pp. 225 - 253
Main Author Sahu, Abhiram
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.12.2003
Subjects
3',5'-Cyclic-AMP Phosphodiesterases - metabolism
Animals
Cyclic AMP - metabolism
Cyclic Nucleotide Phosphodiesterases, Type 3
DNA-Binding Proteins - metabolism
Energy Metabolism - physiology
Homeostasis
Humans
Hypothalamus - cytology
Hypothalamus - metabolism
Janus Kinase 2
Leptin - metabolism
Neurons - metabolism
Obesity - physiopathology
Phosphatidylinositol 3-Kinases - metabolism
Protein-Tyrosine Kinases - metabolism
Proto-Oncogene Proteins
Second Messenger Systems - physiology
Signal Transduction - physiology
STAT3 Transcription Factor
Trans-Activators - metabolism
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Abstract Leptin, the long-sought satiety factor of adipocytes origin, has emerged as one of the major signals that relay the status of fat stores to the hypothalamus and plays a significant role in energy homeostasis. Understanding the mechanisms of leptin signaling in the hypothalamus during normal and pathological conditions, such as obesity, has been the subject of intensive research during the last decade. It is now established that leptin action in the hypothalamus in regulation of food intake and body weight is mediated by a neural circuitry comprising of orexigenic and anorectic signals, including NPY, MCH, galanin, orexin, GALP, α-MSH, NT, and CRH. In addition to the conventional JAK2–STAT3 pathway, it has become evident that PI3K–PDE3B–cAMP pathway plays a critical role in leptin signaling in the hypothalamus. It is now established that central leptin resistance contributes to the development of diet-induced obesity and ageing associated obesity. Central leptin resistance also occurs due to hyperleptinimia produced by exogenous leptin infusion. A defective nutritional regulation of leptin receptor gene expression and reduced STAT3 signaling may be involved in the development of leptin resistance in DIO. However, leptin resistance in the hypothalamic neurons may occur despite an intact JAK2–STAT3 pathway of leptin signaling. Thus, in addition to defective JAK2–STAT3 pathway, defects in other leptin signaling pathways may be involved in leptin resistance. We hypothesize that defective regulation of PI3K–PDE3B–cAMP pathway may be one of the mechanisms behind the development of central leptin resistance seen in obesity.
AbstractList Leptin, the long-sought satiety factor of adipocytes origin, has emerged as one of the major signals that relay the status of fat stores to the hypothalamus and plays a significant role in energy homeostasis. Understanding the mechanisms of leptin signaling in the hypothalamus during normal and pathological conditions, such as obesity, has been the subject of intensive research during the last decade. It is now established that leptin action in the hypothalamus in regulation of food intake and body weight is mediated by a neural circuitry comprising of orexigenic and anorectic signals, including NPY, MCH, galanin, orexin, GALP, alpha-MSH, NT, and CRH. In addition to the conventional JAK2-STAT3 pathway, it has become evident that PI3K-PDE3B-cAMP pathway plays a critical role in leptin signaling in the hypothalamus. It is now established that central leptin resistance contributes to the development of diet-induced obesity and ageing associated obesity. Central leptin resistance also occurs due to hyperleptinimia produced by exogenous leptin infusion. A defective nutritional regulation of leptin receptor gene expression and reduced STAT3 signaling may be involved in the development of leptin resistance in DIO. However, leptin resistance in the hypothalamic neurons may occur despite an intact JAK2-STAT3 pathway of leptin signaling. Thus, in addition to defective JAK2-STAT3 pathway, defects in other leptin signaling pathways may be involved in leptin resistance. We hypothesize that defective regulation of PI3K-PDE3B-cAMP pathway may be one of the mechanisms behind the development of central leptin resistance seen in obesity.Leptin, the long-sought satiety factor of adipocytes origin, has emerged as one of the major signals that relay the status of fat stores to the hypothalamus and plays a significant role in energy homeostasis. Understanding the mechanisms of leptin signaling in the hypothalamus during normal and pathological conditions, such as obesity, has been the subject of intensive research during the last decade. It is now established that leptin action in the hypothalamus in regulation of food intake and body weight is mediated by a neural circuitry comprising of orexigenic and anorectic signals, including NPY, MCH, galanin, orexin, GALP, alpha-MSH, NT, and CRH. In addition to the conventional JAK2-STAT3 pathway, it has become evident that PI3K-PDE3B-cAMP pathway plays a critical role in leptin signaling in the hypothalamus. It is now established that central leptin resistance contributes to the development of diet-induced obesity and ageing associated obesity. Central leptin resistance also occurs due to hyperleptinimia produced by exogenous leptin infusion. A defective nutritional regulation of leptin receptor gene expression and reduced STAT3 signaling may be involved in the development of leptin resistance in DIO. However, leptin resistance in the hypothalamic neurons may occur despite an intact JAK2-STAT3 pathway of leptin signaling. Thus, in addition to defective JAK2-STAT3 pathway, defects in other leptin signaling pathways may be involved in leptin resistance. We hypothesize that defective regulation of PI3K-PDE3B-cAMP pathway may be one of the mechanisms behind the development of central leptin resistance seen in obesity.
Leptin, the long-sought satiety factor of adipocytes origin, has emerged as one of the major signals that relay the status of fat stores to the hypothalamus and plays a significant role in energy homeostasis. Understanding the mechanisms of leptin signaling in the hypothalamus during normal and pathological conditions, such as obesity, has been the subject of intensive research during the last decade. It is now established that leptin action in the hypothalamus in regulation of food intake and body weight is mediated by a neural circuitry comprising of orexigenic and anorectic signals, including NPY, MCH, galanin, orexin, GALP, α-MSH, NT, and CRH. In addition to the conventional JAK2–STAT3 pathway, it has become evident that PI3K–PDE3B–cAMP pathway plays a critical role in leptin signaling in the hypothalamus. It is now established that central leptin resistance contributes to the development of diet-induced obesity and ageing associated obesity. Central leptin resistance also occurs due to hyperleptinimia produced by exogenous leptin infusion. A defective nutritional regulation of leptin receptor gene expression and reduced STAT3 signaling may be involved in the development of leptin resistance in DIO. However, leptin resistance in the hypothalamic neurons may occur despite an intact JAK2–STAT3 pathway of leptin signaling. Thus, in addition to defective JAK2–STAT3 pathway, defects in other leptin signaling pathways may be involved in leptin resistance. We hypothesize that defective regulation of PI3K–PDE3B–cAMP pathway may be one of the mechanisms behind the development of central leptin resistance seen in obesity.
Leptin, the long-sought satiety factor of adipocytes origin, has emerged as one of the major signals that relay the status of fat stores to the hypothalamus and plays a significant role in energy homeostasis. Understanding the mechanisms of leptin signaling in the hypothalamus during normal and pathological conditions, such as obesity, has been the subject of intensive research during the last decade. It is now established that leptin action in the hypothalamus in regulation of food intake and body weight is mediated by a neural circuitry comprising of orexigenic and anorectic signals, including NPY, MCH, galanin, orexin, GALP, alpha-MSH, NT, and CRH. In addition to the conventional JAK2-STAT3 pathway, it has become evident that PI3K-PDE3B-cAMP pathway plays a critical role in leptin signaling in the hypothalamus. It is now established that central leptin resistance contributes to the development of diet-induced obesity and ageing associated obesity. Central leptin resistance also occurs due to hyperleptinimia produced by exogenous leptin infusion. A defective nutritional regulation of leptin receptor gene expression and reduced STAT3 signaling may be involved in the development of leptin resistance in DIO. However, leptin resistance in the hypothalamic neurons may occur despite an intact JAK2-STAT3 pathway of leptin signaling. Thus, in addition to defective JAK2-STAT3 pathway, defects in other leptin signaling pathways may be involved in leptin resistance. We hypothesize that defective regulation of PI3K-PDE3B-cAMP pathway may be one of the mechanisms behind the development of central leptin resistance seen in obesity.
Author Sahu, Abhiram
Author_xml – sequence: 1
  givenname: Abhiram
  surname: Sahu
  fullname: Sahu, Abhiram
  email: asahu@pitt.edu
  organization: Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, S829 Scaife Hall, 3550 Terrace Street, Pittsburgh, PA 15261, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/14726256$$D View this record in MEDLINE/PubMed
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Snippet Leptin, the long-sought satiety factor of adipocytes origin, has emerged as one of the major signals that relay the status of fat stores to the hypothalamus...
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SubjectTerms 3',5'-Cyclic-AMP Phosphodiesterases - metabolism
Animals
Cyclic AMP - metabolism
Cyclic Nucleotide Phosphodiesterases, Type 3
DNA-Binding Proteins - metabolism
Energy Metabolism - physiology
Homeostasis
Humans
Hypothalamus - cytology
Hypothalamus - metabolism
Janus Kinase 2
Leptin - metabolism
Neurons - metabolism
Obesity - physiopathology
Phosphatidylinositol 3-Kinases - metabolism
Protein-Tyrosine Kinases - metabolism
Proto-Oncogene Proteins
Second Messenger Systems - physiology
Signal Transduction - physiology
STAT3 Transcription Factor
Trans-Activators - metabolism
Title Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0091302203000475
https://dx.doi.org/10.1016/j.yfrne.2003.10.001
https://www.ncbi.nlm.nih.gov/pubmed/14726256
https://www.proquest.com/docview/71503529
Volume 24
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