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Grant: Operating Grant

University of Calgary

$898,240.00

Feeding Behaviour & Satiety: Cellular & Molecular Physiology of the K-Dependent Na/Ca-Exchanger, NCKX4

FY 2008-09

Summary
Obesity and eating disorders represent an enormous problem in western society, with obvious cost to both individual health and the health care system. Despite intensive investigation and steady advances in our knowledge about the ways in which appetite and eating work, we still do not have a complete picture of how the brain controls these behaviours. Further new insights are necessary to combat this escalating health problem. We have recently discovered that mice lacking the gene for the specialized calcium transport protein known as the K+-dependent Na+/Ca2+-exchanger type 4 or NCKX4 for short, are healthy but weigh 30% less than normal mice because they eat about 30% less food. Although various hormones and brain circuits have previously been suggested to control feeding behavour, this is the first time that a membrane calcium transport protein has been shown to have an effect on eating behaviour. Our discovery creates a whole new opportunity both to understand the way eating is normally controlled, and to study an unexpected target for the development of new treatments for eating disorders and obesity. The experiments proposed here will lead to an in depth understanding of where and how the NCKX4 protein works in brain nerve pathways that control feeding behaviour and satiety. This information will be critical in understanding normal feeding behaviour and the events that underlie its dys-regulation, possibly leading toward the development of novel therapeutic agents for eating disorders.
Program
Operating Grant
Location
Alberta, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
179795
Name
Lytton Jonathan
Region
Alberta
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Neurosciences, Mental Health and Addiction
Theme2
Biomedical
Prcname2
Metabolism
Projecttitle
Feeding Behaviour & Satiety: Cellular & Molecular Physiology of the K-Dependent Na/Ca-Exchanger, NCKX4
Programtype2
Operating Grants
Orgnameinp2
University of Calgary
Cihramount2
$898,240
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Calcium Homeostasis; Membrane Transport; Molecular Biology; Neuronal Function; Obesity; Sodium-Calcium Exchange
Abstract
Obesity and eating disorders represent an enormous problem in western society, with obvious cost to both individual health and the health care system. Despite intensive investigation and steady advances in our knowledge about the ways in which appetite and eating work, we still do not have a complete picture of how the brain controls these behaviours. Further new insights are necessary to combat this escalating health problem. We have recently discovered that mice lacking the gene for the specialized calcium transport protein known as the K+-dependent Na+/Ca2+-exchanger type 4 or NCKX4 for short, are healthy but weigh 30% less than normal mice because they eat about 30% less food. Although various hormones and brain circuits have previously been suggested to control feeding behavour, this is the first time that a membrane calcium transport protein has been shown to have an effect on eating behaviour. Our discovery creates a whole new opportunity both to understand the way eating is normally controlled, and to study an unexpected target for the development of new treatments for eating disorders and obesity. The experiments proposed here will lead to an in depth understanding of where and how the NCKX4 protein works in brain nerve pathways that control feeding behaviour and satiety. This information will be critical in understanding normal feeding behaviour and the events that underlie its dys-regulation, possibly leading toward the development of novel therapeutic agents for eating disorders.
Competitiondate
200903
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Lytton, Jonathan
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $898,240~ $0~