Circulating triacylglycerols but not pancreatic fat associate with insulin secretion in healthy humans.

Journal: Metabolism: clinical and experimental
PMID: 29273469

Abstract

BACKGROUND: Loss of adequate insulin secretion for the prevailing insulin resistance is critical for the development of type 2 diabetes and has been suggested to result from circulating lipids (triacylglycerols [TG] or free fatty acids) and/or adipocytokines or from ectopic lipid storage in the pancreas. This study aimed to address whether circulating lipids, adipocytokines or pancreatic fat primarily associates with lower insulin secretion.

Authors

  • Bettina Nowotny
    Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany; Division of Endocrinology and Diabetology, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research, München-Neuherberg, Germany.
  • Sabine Kahl
    Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany; Division of Endocrinology and Diabetology, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research, München-Neuherberg, Germany.
  • Birgit Klüppelholz
    German Center for Diabetes Research, München-Neuherberg, Germany; Institute for Biometrics and Epidemiology, German Diabetes Center, Leibniz Institute for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany.
  • Barbara Hoffmann
    IUF - Leibniz Research Institute for Environmental Medicine, Institute for Occupational, Social and Environmental Medicine, Heinrich-Heine University, Düsseldorf, Germany.
  • Guido Giani
    German Center for Diabetes Research, München-Neuherberg, Germany; Institute for Biometrics and Epidemiology, German Diabetes Center, Leibniz Institute for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany.
  • Roshan Livingstone
    Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany; German Center for Diabetes Research, München-Neuherberg, Germany.
  • Peter J Nowotny
    Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany; German Center for Diabetes Research, München-Neuherberg, Germany.
  • Valerie Stamm
    Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany; German Center for Diabetes Research, München-Neuherberg, Germany.
  • Christian Herder
    Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany; German Center for Diabetes Research, München-Neuherberg, Germany.
  • Andrea Tura
    Metabolic Unit, Institute of Neuroscience, CNR, Padova, Italy.
  • Giovanni Pacini
    Metabolic Unit, Institute of Neuroscience, CNR, Padova, Italy.
  • Jong-Hee Hwang
    Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany; German Center for Diabetes Research, München-Neuherberg, Germany.
  • Michael Roden
    Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany; Division of Endocrinology and Diabetology, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research, München-Neuherberg, Germany. Electronic address: michael.roden@ddz.uni-duesseldorf.de.

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