Sensory and motor physiological functions are impaired in gastric inhibitory polypeptide receptor‐deficient mice

Journal of Diabetes Investigation

Tetsuji Okawa⁶  Hideki Kamiya⁷  Tatsuhito Himeno⁶  Yusuke Seino⁴  Shin Tsunekawa⁶  Yoshitaka Hayashi¹  Norio Harada⁵  Yuichiro Yamada²  Nobuya Inagaki⁵  Yutaka Seino³  Yutaka Oiso⁶ 

[1] Department of Genetics, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan;Department of Endocrinology, Diabetes and Geriatric Medicine, Akita University Graduate School of Medicine, Akita, Japan;Kansai Electric Power Hospital, Osaka, Japan;Department of Metabolic Medicine, Nagoya University School of Medicine, Nagoya, Japan;Department of Diabetes and Clinical Nutrition, Kyoto University Graduate School of Medicine, Kyoto, Japan;Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Nagoya, Japan;Department of Chronic Kidney Disease Initiatives, Nagoya University Graduate School of Medicine, Nagoya, Japan

关键词: Gastric inhibitory polypeptide;    Incretins;    Peripheral nervous system;   

DOI  :  10.1111/jdi.12129

来源: Wiley

【 摘 要 】

Abstract

Aims/Introduction

Gastric inhibitory polypeptide (GIP) is an incretin secreted from the gastrointestinal tract after an ingestion of nutrients, and stimulates an insulin secretion from the pancreatic islets. Additionally, GIP has important roles in extrapancreatic tissues: fat accumulation in adipose tissue, neuroprotective effects in the central nervous system and an inhibition of bone resorption. In the current study, we investigated the effects of GIP signaling on the peripheral nervous system (PNS).

Materials and Methods

First, the presence of the GIP receptor (GIPR) in mouse dorsal root ganglion (DRG) was evaluated utilizing immunohistochemical analysis, western blotting and reverse transcription polymerase chain reaction. DRG neurons of male wild-type mice (WT) were cultured with or without GIP, and their neurite lengths were quantified. Functions of the PNS were evaluated in GIPR-deficient mice (gipr−/−) and WT by using current perception thresholds (CPTs), Thermal Plantar Test (TPT), and motor (MNCV) and sensory nerve conduction velocity (SNCV, respectively). Sciatic nerve blood flow (SNBF) and plantar skin blood flow (PSBF) were also evaluated.

Results

We confirmed the expression of GIPR in DRG neurons. The neurite outgrowths of DRG neurons were promoted by the GIP administrations. The gipr−/− showed impaired perception functions in the examination of CPTs and TPT. Both MNCV and SNCV were delayed in gipr−/− compared with these in WT. There was no difference in SNBF and PSBF between WT and gipr−/−.

Conclusions

Our findings show that the GIP signal could exert direct physiological roles in the PNS, which might be directly exerted on the PNS.

【 授权许可】

CC BY-NC   
© 2013 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and Wiley Publishing Asia Pty Ltd

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