Grant: Travel Awards - Institute Community Support
Direct Payment
$1,500.00
Hematopoietic AMPK reduces adipose tissue inflammation and hepatic insulin resistance in obesity
EF 2011-12
Résumé
Canadian society is experiencing an epidemic of obesity, brought on by diets with a surplus of calorie dense foods and inactivity. Obesity can cause insulin resistance which overtime leads to type 2 diabetes. At the cellular front line of the fight against these disorders are macrophages. These specialized immune cells play a critical role in regulating our immune system by sensing foreign invaders and mounting an attack. Recent evidence has shown that during obesity, the macrophages that are meant to protect us have been reprogrammed and can contribute to a state of "chronic inflammation", which then leads to insulin resistance. Exciting new findings from our lab have shown that mice lacking a protein called AMP-activated protein kinase (AMPK) specifically in their macrophages, have increased inflammation and insulin resistance. AMPK is a master regulator of metabolism and can turn on fat burning and increase energy in the cell by making more mitochondria (the power house of the cell). The objective of this study was to determine the specific mechanisms by which AMPK regulates this inflammatory switch in macrophages during obesity. We determined that intermediates of fat metabolism, which can be regulated by AMPK, are the critical components that switch the macrophages to an inflammatory state and lead to insulin resistance. These results may shed light on the connection between obesity, inflammation and metabolism and help to identify new ways to prevent type 2 diabetes.
Programme
Travel Awards - Institute Community Support
Bénéficiaire
Emplacement
Ontario, Canada
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
240869
Name
Fullerton Morgan D
Region
Ontario
Country
Canada
Orgtype
Research Institution
Instname2
Nutrition, Metabolism and Diabetes
Theme2
Biomedical
Prcname2
Institute of Nutrition, Metabolism and Diabetes
Projecttitle
Hematopoietic AMPK reduces adipose tissue inflammation and hepatic insulin resistance in obesity
Programtype2
Undefined
Orgnameinp2
Direct Payment
Cihramount2
$1,500
Cihrequipment2
$0
Programname2
Travel Awards - Institute Community Support
Keyworddelim
Fatty Acids; Immunometabolism; Inflammation; Insulin Sensitivity
Abstract
Canadian society is experiencing an epidemic of obesity, brought on by diets with a surplus of calorie dense foods and inactivity. Obesity can cause insulin resistance which overtime leads to type 2 diabetes. At the cellular front line of the fight against these disorders are macrophages. These specialized immune cells play a critical role in regulating our immune system by sensing foreign invaders and mounting an attack. Recent evidence has shown that during obesity, the macrophages that are meant to protect us have been reprogrammed and can contribute to a state of "chronic inflammation", which then leads to insulin resistance. Exciting new findings from our lab have shown that mice lacking a protein called AMP-activated protein kinase (AMPK) specifically in their macrophages, have increased inflammation and insulin resistance. AMPK is a master regulator of metabolism and can turn on fat burning and increase energy in the cell by making more mitochondria (the power house of the cell). The objective of this study was to determine the specific mechanisms by which AMPK regulates this inflammatory switch in macrophages during obesity. We determined that intermediates of fat metabolism, which can be regulated by AMPK, are the critical components that switch the macrophages to an inflammatory state and lead to insulin resistance. These results may shed light on the connection between obesity, inflammation and metabolism and help to identify new ways to prevent type 2 diabetes.
Competitiondate
201109
Approvedterm2
0 yr 1 mth
Pinamesdelim
Fullerton, Morgan D
Approvedterm
0 an 1 mois
Cihrcontribution2
Inst of Nutr Metabolism &Diab~ $1,500~ $0~