Abstract
Dysfunction of the endocannabinoid system (ECS) has been identified in metabolic disease. Cannabinoid receptor 1 (CB1) is abundantly expressed in the brain but also expressed in the periphery. Cannabinoid receptor 2 (CB2) is more abundant in the periphery, including the immune cells. In obesity, global antagonism of overexpressed CB1 reduces bodyweight but leads to centrally mediated adverse psychological outcomes. Emerging research in isolated cultured cells or tissues has demonstrated that targeting the endocannabinoid system in the periphery alleviates the pathologies associated with metabolic disease. Further, peripheral specific cannabinoid ligands can reverse aspects of the metabolic phenotype. This Keynote review will focus on current research on the functionality of peripheral modulation of the ECS for the treatment of obesity. This Keynote review discusses the peripheral modulation of the ECS in liver, adipose tissue, heart, skeletal muscle, gastrointestinal tract, pancreas, kidney and the immuno-inflammatory system.
| Original language | English |
|---|---|
| Pages (from-to) | 592-604 |
| Number of pages | 13 |
| Journal | Drug Discovery Today |
| Volume | 23 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 1 Mar 2018 |
Cite this
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Peripheral modulation of the endocannabinoid system in metabolic disease. / Shrestha, Nirajan; Cuffe, James S.M.; Hutchinson, Dana S.; Headrick, John P.; Perkins, Anthony V.; McAinch, Andrew J.; Hryciw, Deanne H.
In: Drug Discovery Today, Vol. 23, No. 3, 01.03.2018, p. 592-604.Research output: Contribution to journal › Review Article › Research › peer-review
TY - JOUR
T1 - Peripheral modulation of the endocannabinoid system in metabolic disease
AU - Shrestha, Nirajan
AU - Cuffe, James S.M.
AU - Hutchinson, Dana S.
AU - Headrick, John P.
AU - Perkins, Anthony V.
AU - McAinch, Andrew J.
AU - Hryciw, Deanne H.
PY - 2018/3/1
Y1 - 2018/3/1
N2 - Dysfunction of the endocannabinoid system (ECS) has been identified in metabolic disease. Cannabinoid receptor 1 (CB1) is abundantly expressed in the brain but also expressed in the periphery. Cannabinoid receptor 2 (CB2) is more abundant in the periphery, including the immune cells. In obesity, global antagonism of overexpressed CB1 reduces bodyweight but leads to centrally mediated adverse psychological outcomes. Emerging research in isolated cultured cells or tissues has demonstrated that targeting the endocannabinoid system in the periphery alleviates the pathologies associated with metabolic disease. Further, peripheral specific cannabinoid ligands can reverse aspects of the metabolic phenotype. This Keynote review will focus on current research on the functionality of peripheral modulation of the ECS for the treatment of obesity. This Keynote review discusses the peripheral modulation of the ECS in liver, adipose tissue, heart, skeletal muscle, gastrointestinal tract, pancreas, kidney and the immuno-inflammatory system.
AB - Dysfunction of the endocannabinoid system (ECS) has been identified in metabolic disease. Cannabinoid receptor 1 (CB1) is abundantly expressed in the brain but also expressed in the periphery. Cannabinoid receptor 2 (CB2) is more abundant in the periphery, including the immune cells. In obesity, global antagonism of overexpressed CB1 reduces bodyweight but leads to centrally mediated adverse psychological outcomes. Emerging research in isolated cultured cells or tissues has demonstrated that targeting the endocannabinoid system in the periphery alleviates the pathologies associated with metabolic disease. Further, peripheral specific cannabinoid ligands can reverse aspects of the metabolic phenotype. This Keynote review will focus on current research on the functionality of peripheral modulation of the ECS for the treatment of obesity. This Keynote review discusses the peripheral modulation of the ECS in liver, adipose tissue, heart, skeletal muscle, gastrointestinal tract, pancreas, kidney and the immuno-inflammatory system.
UR - http://www.scopus.com/inward/record.url?scp=85040602029&partnerID=8YFLogxK
U2 - 10.1016/j.drudis.2018.01.029
DO - 10.1016/j.drudis.2018.01.029
M3 - Review Article
VL - 23
SP - 592
EP - 604
JO - Drug Discovery Today
JF - Drug Discovery Today
SN - 1359-6446
IS - 3
ER -