Palmitic acid-rich diet suppresses glucose-stimulated insulin secretion (GSIS) and induces endoplasmic reticulum (ER) stress in pancreatic islets in mice

Takumi Hirata, Toshihide Kawai, Hiroshi Hirose, Kumiko Tanaka, Hideaki Kurosawa, Chikako Fujii, Haruhisa Fujita, Yoshiko Seto, Hideo Matsumoto, Hiroshi Itoh

Research output: Contribution to journalArticle

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Abstract

The objective was to clarify whether dietary palmitic acid supplementation affects glucose-stimulated insulin secretion (GSIS) and the endoplasmic reticulum (ER) stress pathway in pancreatic islets in mice. Eight-week-old male C57BL/6J mice were randomly divided into three treatment diet groups: control diet, palmitic acid-supplemented diet (PAL) and oleic acid-supplemented diet (OLE). After 2 weeks of treatment, intraperitoneal glucose tolerance test and intraperitoneal insulin tolerance test were performed. GSIS was assessed by pancreatic perfusion in situ with basal (100 mg/dL) glucose followed by a high (300 mg/dL) glucose concentration. We measured mRNA levels of ER stress markers such as C/EBP homologous protein (CHOP), immunoglobulin heavy-chain binding protein (BIP) and X-box binding protein (XBP)-1 using real-time polymerase chain reaction (PCR) analyses in isolated islets. Immunohistochemical staining was also performed. Mice fed PAL showed significantly decreased glucose tolerance (p < 0.05). In the perfusion study, GSIS was significantly suppressed in the PAL group (p < 0.05). Semi-quantitative RT-PCR revealed that islet CHOP, BIP, and XBP-1 mRNA expression were significantly increased in the PAL group (p < 0.05). TUNEL-positive β-cells were not detected in all groups. Dietary palmitic acid-supplementation for 2 weeks might suppress GSIS and induce ER stress in pancreatic islets in mice, in the early stage of lipotoxicity.

Original languageEnglish
JournalEndocrine Research
DOIs
Publication statusAccepted/In press - 2015 Jul 10

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Endoplasmic Reticulum Stress
Palmitic Acid
Islets of Langerhans
Insulin
Diet
Glucose
Transcription Factor CHOP
Perfusion
Messenger RNA
In Situ Nick-End Labeling
Oleic Acid
Glucose Tolerance Test
Inbred C57BL Mouse
Protein Binding
Real-Time Polymerase Chain Reaction
Carrier Proteins
Staining and Labeling
Polymerase Chain Reaction
Control Groups

Keywords

  • Dietary palmitic acid
  • ER stress
  • lipotoxicity
  • β-cell

ASJC Scopus subject areas

  • Endocrinology

Cite this

Palmitic acid-rich diet suppresses glucose-stimulated insulin secretion (GSIS) and induces endoplasmic reticulum (ER) stress in pancreatic islets in mice. / Hirata, Takumi; Kawai, Toshihide; Hirose, Hiroshi; Tanaka, Kumiko; Kurosawa, Hideaki; Fujii, Chikako; Fujita, Haruhisa; Seto, Yoshiko; Matsumoto, Hideo; Itoh, Hiroshi.

In: Endocrine Research, 10.07.2015.

Research output: Contribution to journalArticle

Hirata, Takumi ; Kawai, Toshihide ; Hirose, Hiroshi ; Tanaka, Kumiko ; Kurosawa, Hideaki ; Fujii, Chikako ; Fujita, Haruhisa ; Seto, Yoshiko ; Matsumoto, Hideo ; Itoh, Hiroshi. / Palmitic acid-rich diet suppresses glucose-stimulated insulin secretion (GSIS) and induces endoplasmic reticulum (ER) stress in pancreatic islets in mice. In: Endocrine Research. 2015.
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AU - Kawai, Toshihide

AU - Hirose, Hiroshi

AU - Tanaka, Kumiko

AU - Kurosawa, Hideaki

AU - Fujii, Chikako

AU - Fujita, Haruhisa

AU - Seto, Yoshiko

AU - Matsumoto, Hideo

AU - Itoh, Hiroshi

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AB - The objective was to clarify whether dietary palmitic acid supplementation affects glucose-stimulated insulin secretion (GSIS) and the endoplasmic reticulum (ER) stress pathway in pancreatic islets in mice. Eight-week-old male C57BL/6J mice were randomly divided into three treatment diet groups: control diet, palmitic acid-supplemented diet (PAL) and oleic acid-supplemented diet (OLE). After 2 weeks of treatment, intraperitoneal glucose tolerance test and intraperitoneal insulin tolerance test were performed. GSIS was assessed by pancreatic perfusion in situ with basal (100 mg/dL) glucose followed by a high (300 mg/dL) glucose concentration. We measured mRNA levels of ER stress markers such as C/EBP homologous protein (CHOP), immunoglobulin heavy-chain binding protein (BIP) and X-box binding protein (XBP)-1 using real-time polymerase chain reaction (PCR) analyses in isolated islets. Immunohistochemical staining was also performed. Mice fed PAL showed significantly decreased glucose tolerance (p < 0.05). In the perfusion study, GSIS was significantly suppressed in the PAL group (p < 0.05). Semi-quantitative RT-PCR revealed that islet CHOP, BIP, and XBP-1 mRNA expression were significantly increased in the PAL group (p < 0.05). TUNEL-positive β-cells were not detected in all groups. Dietary palmitic acid-supplementation for 2 weeks might suppress GSIS and induce ER stress in pancreatic islets in mice, in the early stage of lipotoxicity.

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