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Non-traditional roles of complement in type 2 diabetes : Metabolism, insulin secretion and homeostasis

King, Ben C. LU and Blom, Anna M. LU (2017) In Molecular Immunology 84. p.34-42
Abstract

Type 2 Diabetes (T2D) is a disease of increasing importance and represents a growing burden on global healthcare and human health. In T2D, loss of effectiveness of insulin signaling in peripheral tissues cannot be compensated for by adequate insulin secretion, leading to hyperglycemia and resultant complications. In recent years, inflammation has been identified as a central component of T2D, both in inducing peripheral insulin resistance as well as in the pancreatic islet, where it contributes to loss of insulin secretion and death of insulin-secreting beta cells. In this review we will focus on non-traditional roles of complement proteins which have been identified in T2D-associated inflammation, beta cell secretory function, and in... (More)

Type 2 Diabetes (T2D) is a disease of increasing importance and represents a growing burden on global healthcare and human health. In T2D, loss of effectiveness of insulin signaling in peripheral tissues cannot be compensated for by adequate insulin secretion, leading to hyperglycemia and resultant complications. In recent years, inflammation has been identified as a central component of T2D, both in inducing peripheral insulin resistance as well as in the pancreatic islet, where it contributes to loss of insulin secretion and death of insulin-secreting beta cells. In this review we will focus on non-traditional roles of complement proteins which have been identified in T2D-associated inflammation, beta cell secretory function, and in maintaining homeostasis of the pancreatic islet. Improved understanding of both traditional and novel roles of complement proteins in T2D may lead to new therapeutic approaches for this global disease.

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Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
C4BP, CD59, Complement, Diabetes, Inflammasome, Insulin secretion
in
Molecular Immunology
volume
84
pages
9 pages
publisher
Pergamon
external identifiers
  • scopus:85008162305
  • wos:000400201600006
ISSN
0161-5890
DOI
10.1016/j.molimm.2016.12.009
language
English
LU publication?
yes
id
026963fe-96b6-443e-8384-e8ae0738e500
date added to LUP
2017-01-23 13:50:58
date last changed
2018-05-29 11:31:16
@article{026963fe-96b6-443e-8384-e8ae0738e500,
  abstract     = {<p>Type 2 Diabetes (T2D) is a disease of increasing importance and represents a growing burden on global healthcare and human health. In T2D, loss of effectiveness of insulin signaling in peripheral tissues cannot be compensated for by adequate insulin secretion, leading to hyperglycemia and resultant complications. In recent years, inflammation has been identified as a central component of T2D, both in inducing peripheral insulin resistance as well as in the pancreatic islet, where it contributes to loss of insulin secretion and death of insulin-secreting beta cells. In this review we will focus on non-traditional roles of complement proteins which have been identified in T2D-associated inflammation, beta cell secretory function, and in maintaining homeostasis of the pancreatic islet. Improved understanding of both traditional and novel roles of complement proteins in T2D may lead to new therapeutic approaches for this global disease.</p>},
  author       = {King, Ben C. and Blom, Anna M.},
  issn         = {0161-5890},
  keyword      = {C4BP,CD59,Complement,Diabetes,Inflammasome,Insulin secretion},
  language     = {eng},
  pages        = {34--42},
  publisher    = {Pergamon},
  series       = {Molecular Immunology},
  title        = {Non-traditional roles of complement in type 2 diabetes : Metabolism, insulin secretion and homeostasis},
  url          = {http://dx.doi.org/10.1016/j.molimm.2016.12.009},
  volume       = {84},
  year         = {2017},
}