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  • Male  (2)
  • Adrenal Cortex/metabolism  (1)
  • Action Potentials
  • American Association for the Advancement of Science (AAAS)  (3)
  • 1
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    Independent and additive effects of central POMC and leptin pathways on murine obesity (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: The lethal yellow (AY/a) mouse has a defect in proopiomelanocortin (POMC) signaling in the brain that leads to obesity, and is resistant to the anorexigenic effects of the hormone leptin. It has been proposed that the weight-reducing effects of leptin are thus transmitted primarily by way of POMC neurons. However, the central effects of defective POMC signaling, and the absence of leptin, on weight gain in double-mutant lethal yellow (AY/a) leptin-deficient (lepob/lepob) mice were shown to be independent and additive. Furthermore, deletion of the leptin gene restored leptin sensitivity to AY/a mice. This result implies that in the AY/a mouse, obesity is independent of leptin action, and resistance to leptin results from desensitization of leptin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boston, B A -- Blaydon, K M -- Varnerin, J -- Cone, R D -- DK/AR517330/DK/NIDDK NIH HHS/ -- DK02404/DK/NIDDK NIH HHS/ -- HD33703/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1641-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Oregon Health Sciences University, Portland, OR 97201, USA. Laboratories, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374468" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Agouti Signaling Protein ; Alleles ; Animals ; Arcuate Nucleus of Hypothalamus/*metabolism ; Blood Glucose/analysis ; Corticosterone/blood ; Crosses, Genetic ; Eating/drug effects ; Energy Metabolism ; Female ; Homeostasis ; Insulin/blood ; *Intercellular Signaling Peptides and Proteins ; Leptin ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Neurons/metabolism ; Obesity/genetics/*metabolism ; Pro-Opiomelanocortin/*metabolism ; Proteins/genetics/*metabolism/pharmacology ; Signal Transduction ; 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)
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  • 2
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    Activation of central melanocortin pathways by fenfluramine (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-27
    Description: D-fenfluramine (d-FEN) was once widely prescribed and was among the most effective weight loss drugs, but was withdrawn from clinical use because of reports of cardiac complications in a subset of patients. Discerning the neurobiology underlying the anorexic action of d-FEN may facilitate the development of new drugs to prevent and treat obesity. Through a combination of functional neuroanatomy, feeding, and electrophysiology studies in rodents, we show that d-FEN-induced anorexia requires activation of central nervous system melanocortin pathways. These results provide a mechanistic explanation of d-FEN's anorexic actions and indicate that drugs targeting these downstream melanocortin pathways may prove to be effective and more selective anti-obesity treatments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heisler, Lora K -- Cowley, Michael A -- Tecott, Laurence H -- Fan, Wei -- Low, Malcolm J -- Smart, James L -- Rubinstein, Marcelo -- Tatro, Jeffrey B -- Marcus, Jacob N -- Holstege, Henne -- Lee, Charlotte E -- Cone, Roger D -- Elmquist, Joel K -- F31HG00201/HG/NHGRI NIH HHS/ -- P01DK056116/DK/NIDDK NIH HHS/ -- P01DK55819/DK/NIDDK NIH HHS/ -- R01MH061583/MH/NIMH NIH HHS/ -- R01MH44694/MH/NIMH NIH HHS/ -- R01MH61624/MH/NIMH NIH HHS/ -- R03TW01233/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 2002 Jul 26;297(5581):609-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12142539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Appetite Depressants/*pharmacology ; Arcuate Nucleus of Hypothalamus/*drug effects/metabolism ; Feeding Behavior/*drug effects ; Fenfluramine/*pharmacology ; Male ; Melanocyte-Stimulating Hormones/pharmacology ; Mice ; Mice, Obese ; Mice, Transgenic ; Neurons/drug effects/metabolism ; Paraventricular Hypothalamic Nucleus/drug effects/metabolism ; Patch-Clamp Techniques ; Pro-Opiomelanocortin/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor, Melanocortin, Type 3 ; Receptor, Melanocortin, Type 4 ; Receptor, Serotonin, 5-HT2C ; Receptors, Corticotropin/metabolism ; Receptors, Serotonin/metabolism ; Serotonin/metabolism ; Serotonin Agents/pharmacology ; alpha-MSH/*metabolism
    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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  • 3
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    The cloning of a family of genes that encode the melanocortin receptors (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-28
    Description: Melanocyte-stimulating hormone (MSH) and adrenocorticotropic hormone (ACTH) regulate pigmentation and adrenal cortical function, respectively. These peptides also have a variety of biological activities in other areas, including the brain, the pituitary, and the immune system. A complete understanding of the biological activities of these hormones requires the isolation and characterization of their corresponding receptors. The murine and human MSH receptors (MSH-Rs) and a human ACTH receptor (ACTH-R) were cloned. These receptors define a subfamily of receptors coupled to guanine nucleotide-binding proteins that may include the cannabinoid receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mountjoy, K G -- Robbins, L S -- Mortrud, M T -- Cone, R D -- R01 DK43859-02/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1248-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute for Advanced Biomedical Research, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1325670" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex/metabolism ; Amino Acid Sequence ; Animals ; Blotting, Northern ; Cloning, Molecular ; Dose-Response Relationship, Drug ; GTP-Binding Proteins/metabolism ; Humans ; Melanocyte-Stimulating Hormones/physiology ; Melanocytes/metabolism ; Mice ; Molecular Sequence Data ; Polymerase Chain Reaction ; RNA, Messenger/biosynthesis ; Receptors, Corticotropin ; Receptors, Pituitary Hormone/biosynthesis/*genetics ; Sequence Homology, Nucleic Acid
    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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