Format

Send to

Choose Destination
Biochem Biophys Res Commun. 2015 Oct 30;466(4):717-22. doi: 10.1016/j.bbrc.2015.09.006. Epub 2015 Sep 5.

Arginine-induced insulin secretion in endoplasmic reticulum.

Author information

1
National Center for Geriatrics and Gerontology, Obu, Aichi 474-8511, Japan.
2
National Center for Geriatrics and Gerontology, Obu, Aichi 474-8511, Japan; Tokyo Medical University, Shinjyuku, Tokyo 160-8402, Japan.
3
National Center for Geriatrics and Gerontology, Obu, Aichi 474-8511, Japan. Electronic address: dai.ncgg@gmail.com.

Abstract

Arginine, a semi-essential amino acid, is known as one of the most strongest insulin secretagogues in a glucose-dependent manner, but major mechanism is unknown. Arginine induced insulin secretion in mice as well as β cell line, NIT-1, in which more than 90% of intracellular insulin is prionsulin without arginine cultivation. Arginine administration reduced prionsulin amount in 30 s, then insulin is secreted from NIT1 cells. These data indicated that the target factor(s) for arginine-induced insulin secretion located in endoplasmic reticulum (ER). We established the screening system for identifying the arginine mimetics. Brazilian propolis, not Chinese propolis, induced insulin secretion. To identify target factor(s) of arginine induced insulin secretion, our previous study was that nanobeads technology facilitated us to purify chemical-target factors. This time we chose the other way, proinsulin associating factor purification and arginine-immobilized agarose. Three proinsulin associating factors and 5 arginine interacting factors were identified. Among theses factors, Calnexin (CNX) was the only one factor, which belonged to both groups, suggesting that CNX might play a key role in arginine-induced insulin secretion in ER.

KEYWORDS:

Arginine; Brazilian propolis; Diabetes mellitus; Endoplasmic reticulum; Glucose; Insulin

PMID:
26348775
DOI:
10.1016/j.bbrc.2015.09.006
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center