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Islet Studies

Uncoupling Protein 2: A Possible Link Between Fatty Acid Excess and Impaired Glucose-Induced Insulin Secretion?

  1. Nathalie Lameloise1,
  2. Patrick Muzzin1,
  3. Marc Prentki23 and
  4. Françoise Assimacopoulos-Jeannet1
  1. 1Department of Medical Biochemistry, Centre Médical Universitaire, Medical Faculty, University of Geneva, Geneva, Switzerland
  2. 2Molecular Nutrition Unit, Department of Nutrition, University of Montreal
  3. 3CHUM, Centre de Recherche and Institut du Cancer, Montreal, Quebec, Canada
    Diabetes 2001 Apr; 50(4): 803-809. https://doi.org/10.2337/diabetes.50.4.803
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    Article Information

    vol. 50 no. 4 803-809
    DOI 
    https://doi.org/10.2337/diabetes.50.4.803
    PubMed 
    11289045

    Published By 
    American Diabetes Association
    Print ISSN 
    0012-1797
    Online ISSN 
    1939-327X
    History 
    • Published in print April 1, 2001.

    Copyright & Usage 
    © 2001

    Author Information

    1. Nathalie Lameloise1,
    2. Patrick Muzzin1,
    3. Marc Prentki23 and
    4. Françoise Assimacopoulos-Jeannet1
    1. 1Department of Medical Biochemistry, Centre Médical Universitaire, Medical Faculty, University of Geneva, Geneva, Switzerland
    2. 2Molecular Nutrition Unit, Department of Nutrition, University of Montreal
    3. 3CHUM, Centre de Recherche and Institut du Cancer, Montreal, Quebec, Canada
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      Uncoupling Protein 2: A Possible Link Between Fatty Acid Excess and Impaired Glucose-Induced Insulin Secretion?
      Nathalie Lameloise, Patrick Muzzin, Marc Prentki, Françoise Assimacopoulos-Jeannet
      Diabetes Apr 2001, 50 (4) 803-809; DOI: 10.2337/diabetes.50.4.803

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      Uncoupling Protein 2: A Possible Link Between Fatty Acid Excess and Impaired Glucose-Induced Insulin Secretion?
      Nathalie Lameloise, Patrick Muzzin, Marc Prentki, Françoise Assimacopoulos-Jeannet
      Diabetes Apr 2001, 50 (4) 803-809; DOI: 10.2337/diabetes.50.4.803
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      • Acyl-Ghrelin Influences Pancreatic β-Cell Function by Interference with KATP Channels
      • Pancreatic β-Cell–Specific Deletion of VPS41 Causes Diabetes Due to Defects in Insulin Secretion
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