Linkage study of embryopathy-Polygenic inheritance of diabetes-induced skeletal malformations in the rat
(2012) In Reproductive Toxicology 33(3). p.297-307- Abstract
- We developed an inbred rat model of diabetic embryopathy, in which the offspring displays skeletal malformations (agnathia or micrognathia) when the mother is diabetic, and no malformations when she is not diabetic. Our aim was to find genes controlling the embryonic maldevelopment in a diabetic environment. We contrasted the fetal outcome in inbred Sprague-Dawley L rats (20% skeletal malformations in diabetic pregnancy) with that of inbred Wistar Furth rats (denoted W, no skeletal malformations in diabetic pregnancy). We used offspring from the backcross F-1 x L to probe for the genetic basis for malformation of the mandible in diabetic pregnancy. A set of 186 fetuses (93 affected, 93 unaffected) was subjected to a whole genome scan with... (More)
- We developed an inbred rat model of diabetic embryopathy, in which the offspring displays skeletal malformations (agnathia or micrognathia) when the mother is diabetic, and no malformations when she is not diabetic. Our aim was to find genes controlling the embryonic maldevelopment in a diabetic environment. We contrasted the fetal outcome in inbred Sprague-Dawley L rats (20% skeletal malformations in diabetic pregnancy) with that of inbred Wistar Furth rats (denoted W, no skeletal malformations in diabetic pregnancy). We used offspring from the backcross F-1 x L to probe for the genetic basis for malformation of the mandible in diabetic pregnancy. A set of 186 fetuses (93 affected, 93 unaffected) was subjected to a whole genome scan with 160 micro satellites. Analysis of genotype distribution indicated 7 loci on chromosome 4, 10 (3 loci), 14, 18, and 19 in the teratogenic process (and 14 other loci on 12 chromosomes with less strong association to the malformations), several of which contained genes implicated in other experimental studies of diabetic embryopathy. These candidate genes will be scrutinized in further experimentation. We conclude that the genetic involvement in rodent diabetic embryopathy is polygenic and predisposing for congenital malformations. (C) 2011 Elsevier Inc. All rights reserved. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2562974
- author
- Nordquist, Niklas ; Luthman, Holger LU ; Pettersson, Ulf and Eriksson, Ulf J.
- organization
- publishing date
- 2012
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Rat, Diabetes-in-pregnancy, Streptozotocin, Congenital anomalies, Mandible, Whole genome scan, Micro satellites, Genetic predisposition
- in
- Reproductive Toxicology
- volume
- 33
- issue
- 3
- pages
- 297 - 307
- publisher
- Elsevier
- external identifiers
-
- wos:000303361200005
- scopus:84859739848
- pmid:22227068
- ISSN
- 1873-1708
- DOI
- 10.1016/j.reprotox.2011.12.009
- language
- English
- LU publication?
- yes
- id
- 7d256812-1536-47ec-8a5b-4cafef64cc56 (old id 2562974)
- date added to LUP
- 2016-04-01 14:25:50
- date last changed
- 2022-01-28 00:35:19
@article{7d256812-1536-47ec-8a5b-4cafef64cc56,
abstract = {{We developed an inbred rat model of diabetic embryopathy, in which the offspring displays skeletal malformations (agnathia or micrognathia) when the mother is diabetic, and no malformations when she is not diabetic. Our aim was to find genes controlling the embryonic maldevelopment in a diabetic environment. We contrasted the fetal outcome in inbred Sprague-Dawley L rats (20% skeletal malformations in diabetic pregnancy) with that of inbred Wistar Furth rats (denoted W, no skeletal malformations in diabetic pregnancy). We used offspring from the backcross F-1 x L to probe for the genetic basis for malformation of the mandible in diabetic pregnancy. A set of 186 fetuses (93 affected, 93 unaffected) was subjected to a whole genome scan with 160 micro satellites. Analysis of genotype distribution indicated 7 loci on chromosome 4, 10 (3 loci), 14, 18, and 19 in the teratogenic process (and 14 other loci on 12 chromosomes with less strong association to the malformations), several of which contained genes implicated in other experimental studies of diabetic embryopathy. These candidate genes will be scrutinized in further experimentation. We conclude that the genetic involvement in rodent diabetic embryopathy is polygenic and predisposing for congenital malformations. (C) 2011 Elsevier Inc. All rights reserved.}},
author = {{Nordquist, Niklas and Luthman, Holger and Pettersson, Ulf and Eriksson, Ulf J.}},
issn = {{1873-1708}},
keywords = {{Rat; Diabetes-in-pregnancy; Streptozotocin; Congenital anomalies; Mandible; Whole genome scan; Micro satellites; Genetic predisposition}},
language = {{eng}},
number = {{3}},
pages = {{297--307}},
publisher = {{Elsevier}},
series = {{Reproductive Toxicology}},
title = {{Linkage study of embryopathy-Polygenic inheritance of diabetes-induced skeletal malformations in the rat}},
url = {{http://dx.doi.org/10.1016/j.reprotox.2011.12.009}},
doi = {{10.1016/j.reprotox.2011.12.009}},
volume = {{33}},
year = {{2012}},
}