2012 Fiscal Year Final Research Report
Epigenetic study of effects of obese pregnancy on her offspring in terms of inflammation
| Project/Area Number |
22591821
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Obstetrics and gynecology
|
|---|
| Research Institution | Tohoku University (2012)
Mie University (2010-2011) |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
UMEKAWA Takashi 三重大学, 医学部附属病院, 助教 (80422864)
MURABAYASHI Nao 三重大学, 医学部附属病院, 助教 (10378416)
SAGAWA Norimasa 三重大学, 医学系研究科, リサーチアソシ エイト (00162321)
SUGAWARA Junichi 東北大学, 東北メディカル・メガバンク機 構, 教授 (60280880)
|
|---|
| Project Period (FY) |
2010 – 2012
|
| Keywords | 妊娠 / インスリン抵抗性 / マウス / 肥満 / 高脂肪食 / 炎症 |
|---|
| Research Abstract |
We investigated the effect of a maternal high-fat diet (HFD) on fetal growth and carbohydrate metabolism using a diet-induced obesity mouse model.
As a result, at 10-week-old, the weight was not different between the normal diet(ND) and high fat diet (HFD) offspring. However, systolic blood pressure was significantly higher in the HFD offspring than in the ND offspring. Although glucose tolerance was significantly lower in the HFD offspring than in the ND offspring, insulin tolerant test did not show significant difference among two groups.The hematoxylin-eosin staining showed islet loss in the HFD offspring.
The present study demonstrated that maternal obesity causes increase of blood pressure and glucose intolerance through beta cell dysfunction in her offspring. Also,we suggest that this obese mice model is a useful tool to assess mechanisms of metabolic syndrome in the offspring.
|
