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From association to function : MTNR1B

Bonnefond, Amélie and Lyssenko, Valeriya LU (2016) In The Genetics of Type 2 Diabetes and Related Traits: Biology, Physiology and Translation p.403-421
Abstract

The discovery that variants in the melatonin receptor 2 (MTNR1B) gene were associated with glucose levels, insulin secretion, and risk for type 2 diabetes (T2D) in genome-wide association studies (GWAS) reinforced the previously suggested link between glucose homeostasis and circadian rhythmicity. Diurnal secretion of melatonin has reported to be altered in people with diabetes and rodent models of T2D. The proposed underlying mechanisms by which altered melatonin signaling could predispose to progression to T2D and gestational diabetes mellitus (GDM) involve altered expression of MTNR1B in pancreatic beta cells, leading to impaired insulin secretion, consequent increased fasting glucose concentrations, and eventually overt T2D. Thus... (More)

The discovery that variants in the melatonin receptor 2 (MTNR1B) gene were associated with glucose levels, insulin secretion, and risk for type 2 diabetes (T2D) in genome-wide association studies (GWAS) reinforced the previously suggested link between glucose homeostasis and circadian rhythmicity. Diurnal secretion of melatonin has reported to be altered in people with diabetes and rodent models of T2D. The proposed underlying mechanisms by which altered melatonin signaling could predispose to progression to T2D and gestational diabetes mellitus (GDM) involve altered expression of MTNR1B in pancreatic beta cells, leading to impaired insulin secretion, consequent increased fasting glucose concentrations, and eventually overt T2D. Thus blocking the inhibition of insulin secretion may have potential clinical implications, and these effects could be more pronounced in individuals carrying risk genotypes. Finally, given that melatonin could emerge as an attractive treatment for a variety of conditions including pregnancies associated with GDM, preeclampsia, and intrauterine growth retardation, pharmacogenetic studies are warranted to determine treatment response and side effects according to genotype.

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author
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
in
The Genetics of Type 2 Diabetes and Related Traits: Biology, Physiology and Translation
pages
19 pages
publisher
Springer International Publishing
external identifiers
  • Scopus:84978208909
ISBN
9783319015743
9783319015736
DOI
10.1007/978-3-319-01574-3_19
language
English
LU publication?
yes
id
a24ab48b-4726-449c-aa64-ea1933782372
date added to LUP
2016-07-25 14:37:10
date last changed
2017-01-01 08:31:06
@inbook{a24ab48b-4726-449c-aa64-ea1933782372,
  abstract     = {<p>The discovery that variants in the melatonin receptor 2 (MTNR1B) gene were associated with glucose levels, insulin secretion, and risk for type 2 diabetes (T2D) in genome-wide association studies (GWAS) reinforced the previously suggested link between glucose homeostasis and circadian rhythmicity. Diurnal secretion of melatonin has reported to be altered in people with diabetes and rodent models of T2D. The proposed underlying mechanisms by which altered melatonin signaling could predispose to progression to T2D and gestational diabetes mellitus (GDM) involve altered expression of MTNR1B in pancreatic beta cells, leading to impaired insulin secretion, consequent increased fasting glucose concentrations, and eventually overt T2D. Thus blocking the inhibition of insulin secretion may have potential clinical implications, and these effects could be more pronounced in individuals carrying risk genotypes. Finally, given that melatonin could emerge as an attractive treatment for a variety of conditions including pregnancies associated with GDM, preeclampsia, and intrauterine growth retardation, pharmacogenetic studies are warranted to determine treatment response and side effects according to genotype.</p>},
  author       = {Bonnefond, Amélie and Lyssenko, Valeriya},
  isbn         = {9783319015743},
  language     = {eng},
  month        = {01},
  pages        = {403--421},
  publisher    = {Springer International Publishing},
  series       = {The Genetics of Type 2 Diabetes and Related Traits: Biology, Physiology and Translation},
  title        = {From association to function : MTNR1B},
  url          = {http://dx.doi.org/10.1007/978-3-319-01574-3_19},
  year         = {2016},
}