Sensory and motor physiological functions are impaired in gastric inhibitory polypeptide receptor‐deficient mice. Issue 1 (16th October 2013)

• Record Type: Journal Article
• Authors: Okawa, Tetsuji; Kamiya, Hideki; Himeno, Tatsuhito; Seino, Yusuke; Tsunekawa, Shin; Hayashi, Yoshitaka; Harada, Norio; Yamada, Yuichiro; Inagaki, Nobuya; Seino, Yutaka; Oiso, Yutaka; Nakamura, Jiro
• Is Part Of: Journal of diabetes investigation. Volume 5:Issue 1(2014:Feb.)
• Page Start: 31
• Page End: 47
• Publication Date: 2013-10-16
• Subjects: Diabetes -- Periodicals; Diabetes -- Research -- Periodicals; Diabetes Mellitus -- Periodicals; 616.462005
• DOI: 10.1111/jdi.12129
• Languages: English
• ISSNs: 2040-1116

Abstract

<abstract abstract-type="main" id="jdi12129-abs-0001"> <title>Abstract</title> <sec id="jdi12129-sec-0001" sec-type="section"> <title>Aims/Introduction</title> <p>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).</p> </sec> <sec id="jdi12129-sec-0002" sec-type="section"> <title>Materials and Methods</title> <p>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 (<italic>gipr</italic>−/−) 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.</p> </sec> <sec id="jdi12129-sec-0003" sec-type="section"> <title>Results</title> <p>We confirmed the expression of GIPR in DRG neurons. The neurite outgrowths of DRG neurons were promoted by the GIP administrations. The <italic>gipr</italic>−/− showed impaired perception functions in the examination of CPTs and TPT. Both MNCV and SNCV were delayed in <italic>gipr</italic>−/− compared with these in WT. There was no difference in SNBF and PSBF between WT and <italic>gipr</italic>−/−.</p> </sec> <sec id="jdi12129-sec-0004" sec-type="section"> <title>Conclusions</title> <p>Our findings show that the GIP signal could exert direct physiological roles in the PNS, which might be directly exerted on the PNS.</p> </sec> </abstract>