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Free fatty acids regulate insulin secretion from pancreatic β cells through GPR40

Author

Listed:
  • Yasuaki Itoh

    (Takeda Chemical Industries, Ltd)

  • Yuji Kawamata

    (Takeda Chemical Industries, Ltd)

  • Masataka Harada

    (Takeda Chemical Industries, Ltd)

  • Makoto Kobayashi

    (Takeda Chemical Industries, Ltd)

  • Ryo Fujii

    (Takeda Chemical Industries, Ltd)

  • Shoji Fukusumi

    (Takeda Chemical Industries, Ltd)

  • Kazuhiro Ogi

    (Takeda Chemical Industries, Ltd)

  • Masaki Hosoya

    (Takeda Chemical Industries, Ltd)

  • Yasuhiro Tanaka

    (Takeda Chemical Industries, Ltd)

  • Hiroshi Uejima

    (Takeda Chemical Industries, Ltd)

  • Hideyuki Tanaka

    (Takeda Chemical Industries, Ltd)

  • Minoru Maruyama

    (Takeda Chemical Industries, Ltd)

  • Rie Satoh

    (Takeda Chemical Industries, Ltd)

  • Shoichi Okubo

    (Takeda Chemical Industries, Ltd)

  • Hideki Kizawa

    (Takeda Chemical Industries, Ltd)

  • Hidetoshi Komatsu

    (Takeda Chemical Industries, Ltd)

  • Fumika Matsumura

    (Takeda Chemical Industries, Ltd)

  • Yuko Noguchi

    (Takeda Chemical Industries, Ltd)

  • Tokuyuki Shinohara

    (Takeda Chemical Industries, Ltd)

  • Shuji Hinuma

    (Takeda Chemical Industries, Ltd)

  • Yukio Fujisawa

    (Takeda Chemical Industries, Ltd)

  • Masahiko Fujino

    (Takeda Chemical Industries, Ltd)

Abstract

Diabetes, a disease in which carbohydrate and lipid metabolism are regulated improperly by insulin, is a serious worldwide health issue1,2. Insulin is secreted from pancreatic β cells in response to elevated plasma glucose, with various factors modifying its secretion3. Free fatty acids (FFAs) provide an important energy source as nutrients, and they also act as signalling molecules in various cellular processes, including insulin secretion4,5. Although FFAs are thought to promote insulin secretion in an acute phase, this mechanism is not clearly understood6. Here we show that a G-protein-coupled receptor, GPR40, which is abundantly expressed in the pancreas, functions as a receptor for long-chain FFAs. Furthermore, we show that long-chain FFAs amplify glucose-stimulated insulin secretion from pancreatic β cells by activating GPR40. Our results indicate that GPR40 agonists and/or antagonists show potential for the development of new anti-diabetic drugs.

Suggested Citation

  • Yasuaki Itoh & Yuji Kawamata & Masataka Harada & Makoto Kobayashi & Ryo Fujii & Shoji Fukusumi & Kazuhiro Ogi & Masaki Hosoya & Yasuhiro Tanaka & Hiroshi Uejima & Hideyuki Tanaka & Minoru Maruyama & R, 2003. "Free fatty acids regulate insulin secretion from pancreatic β cells through GPR40," Nature, Nature, vol. 422(6928), pages 173-176, March.
  • Handle: RePEc:nat:nature:v:422:y:2003:i:6928:d:10.1038_nature01478
    DOI: 10.1038/nature01478
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    Cited by:

    1. Maria Thürmer & André Gollowitzer & Helmut Pein & Konstantin Neukirch & Elif Gelmez & Lorenz Waltl & Natalie Wielsch & René Winkler & Konstantin Löser & Julia Grander & Madlen Hotze & Sönke Harder & A, 2022. "PI(18:1/18:1) is a SCD1-derived lipokine that limits stress signaling," Nature Communications, Nature, vol. 13(1), pages 1-21, December.
    2. Alka Singh & Kandahalli Venkataranganayaka Abhilasha & Kathya R. Acharya & Haibo Liu & Niraj K. Nirala & Velayoudame Parthibane & Govind Kunduri & Thiruvaimozhi Abimannan & Jacob Tantalla & Lihua Juli, 2024. "A nutrient responsive lipase mediates gut-brain communication to regulate insulin secretion in Drosophila," Nature Communications, Nature, vol. 15(1), pages 1-19, December.
    3. Ah Lee & Myoung Lee & Sanghyun Lee & Eun Cho, 2015. "Comparative Study on Antioxidant Activity of Vegetable Oils under in vitro and Cellular System," Journal of Agricultural Science, Canadian Center of Science and Education, vol. 7(3), pages 1-58, February.

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