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  • Male  (2)
  • 2020-2022
  • 2005-2009  (2)
  • 1945-1949
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  • 1
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    Regulation of pancreatic beta cell mass by neuronal signals from the liver (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-22
    Description: Metabolic regulation in mammals requires communication between multiple organs and tissues. The rise in the incidence of obesity and associated metabolic disorders, including type 2 diabetes, has renewed interest in interorgan communication. We used mouse models to explore the mechanism whereby obesity enhances pancreatic beta cell mass, pathophysiological compensation for insulin resistance. We found that hepatic activation of extracellular regulated kinase (ERK) signaling induced pancreatic beta cell proliferation through a neuronal-mediated relay of metabolic signals. This metabolic relay from the liver to the pancreas is involved in obesity-induced islet expansion. In mouse models of insulin-deficient diabetes, liver-selective activation of ERK signaling increased beta cell mass and normalized serum glucose levels. Thus, interorgan metabolic relay systems may serve as valuable targets in regenerative treatments for diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Imai, Junta -- Katagiri, Hideki -- Yamada, Tetsuya -- Ishigaki, Yasushi -- Suzuki, Toshinobu -- Kudo, Hirohito -- Uno, Kenji -- Hasegawa, Yutaka -- Gao, Junhong -- Kaneko, Keizo -- Ishihara, Hisamitsu -- Niijima, Akira -- Nakazato, Masamitsu -- Asano, Tomoichiro -- Minokoshi, Yasuhiko -- Oka, Yoshitomo -- New York, N.Y. -- Science. 2008 Nov 21;322(5905):1250-4. doi: 10.1126/science.1163971.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19023081" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Central Nervous System/metabolism ; Diabetes Mellitus, Experimental/metabolism ; Hyperplasia ; Insulin/metabolism ; Insulin Resistance ; Insulin-Secreting Cells/*metabolism/pathology ; Liver/*metabolism ; MAP Kinase Kinase 1/*metabolism ; *MAP Kinase Signaling System ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/*metabolism ; Obesity/*metabolism ; Pancreas/innervation ; Recombinant Proteins/metabolism ; Vagus Nerve/cytology/metabolism ; Xenopus
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Neuronal pathway from the liver modulates energy expenditure and systemic insulin sensitivity (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: Coordinated control of energy metabolism and glucose homeostasis requires communication between organs and tissues. We identified a neuronal pathway that participates in the cross talk between the liver and adipose tissue. By studying a mouse model, we showed that adenovirus-mediated expression of peroxisome proliferator-activated receptor (PPAR)-g2 in the liver induces acute hepatic steatosis while markedly decreasing peripheral adiposity. These changes were accompanied by increased energy expenditure and improved systemic insulin sensitivity. Hepatic vagotomy and selective afferent blockage of the hepatic vagus revealed that the effects on peripheral tissues involve the afferent vagal nerve. Furthermore, an antidiabetic thiazolidinedione, a PPARg agonist, enhanced this pathway. This neuronal pathway from the liver may function to protect against metabolic perturbation induced by excessive energy storage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uno, Kenji -- Katagiri, Hideki -- Yamada, Tetsuya -- Ishigaki, Yasushi -- Ogihara, Takehide -- Imai, Junta -- Hasegawa, Yutaka -- Gao, Junhong -- Kaneko, Keizo -- Iwasaki, Hiroko -- Ishihara, Hisamitsu -- Sasano, Hironobu -- Inukai, Kouichi -- Mizuguchi, Hiroyuki -- Asano, Tomoichiro -- Shiota, Masakazu -- Nakazato, Masamitsu -- Oka, Yoshitomo -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1656-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778057" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/innervation/*metabolism ; Afferent Pathways/physiology ; Animals ; Blood Glucose/analysis ; Dietary Fats/administration & dosage ; Efferent Pathways/physiology ; *Energy Metabolism ; Fatty Liver/pathology ; Glucose/metabolism ; Glucose Tolerance Test ; Hypoglycemic Agents/pharmacology ; Insulin/blood/*physiology ; Insulin Resistance ; Lipolysis ; Liver/*innervation/*metabolism/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/metabolism ; Oxygen Consumption ; PPAR gamma/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Sympathetic Nervous System/physiology ; Vagotomy ; Vagus Nerve/*physiology ; Weight Gain
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
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