Dietary lipids and sweeteners regulate glucagon-like peptide-2 secretion

  • Shingo Sato
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Ryota Hokari
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Chie Kurihara
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Hirokazu Sato
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Kazuyuki Narimatsu
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Hideaki Hozumi
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Toshihide Ueda
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Masaaki Higashiyama
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Yoshikiyo Okada
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Chikako Watanabe
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Shunsuke Komoto
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Kengo Tomita
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Atsushi Kawaguchi
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Shigeaki Nagao
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan
  • Soichiro Miura
    Department of Internal Medicine, National Defense Medical College, Saitama, Japan

抄録

<jats:p> Glucagon-like peptide-2 (GLP-2) is a potent intestinal growth factor derived from enteroendocrine L cells. Although food intake is known to increase GLP-2 secretion, its regulatory mechanisms are largely unknown as a result of its very short half-life in venules. The aims of this study were to compare the effects of luminal nutrients on the stimulation of GLP-2 secretion in vivo using lymph samples and to clarify the involvement of the sweet taste receptor in this process in vitro. Lymph samples were collected from the thoracic duct after bolus administration of dietary lipids or sweetening agents into the duodenum of rats. Human enteroendocrine NCI-H716 cells were also used to compare the effects of various nutrients on GLP-2 secretion. GLP-2 concentrations were measured by ELISA in vivo and in vitro. GLP-2 secretion was enhanced by polyunsaturated fatty acid- and monounsaturated fatty acid-rich dietary oils, dietary carbohydrates, and some kinds of sweeteners in rats; this effect was reproduced in NCI-H716 cells using α-linolenic acid (αLA), glucose, and sweeteners. GLP-2 secretion induced by sweetening agents was inhibited by lactisole, a sweetness-antagonizing inhibitor of T1R3. In contrast, lactisole was unable to inhibit GLP-2 secretion induced by αLA alone. Our results suggested that fatty acid- and sweetener-induced GLP-2 secretion may be mediated by two different pathways, with the sweet taste receptor involved in the regulation of the latter. </jats:p>

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