Role and regulation of acylethanolamides in energy balance: focus on adipocytes and β‐cells

The endocannabinoid, arachidonoylethanolamide (AEA), and the peroxisome proliferator‐activated receptor (PPAR)‐α ligand, oleylethanolamide (OEA) produce opposite effects on lipogenesis. The regulation of OEA and its anti‐inflammatory congener, palmitoylethanolamide (PEA), in adipocytes and pancreati...

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Veröffentlicht in:British journal of pharmacology 2007-11, Vol.152 (5), p.676-690
Hauptverfasser: Matias, I, Gonthier, M‐P, Petrosino, S, Docimo, L, Capasso, R, Hoareau, L, Monteleone, P, Roche, R, Izzo, A A, Di Marzo, V
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container_title British journal of pharmacology
container_volume 152
creator Matias, I
Gonthier, M‐P
Petrosino, S
Docimo, L
Capasso, R
Hoareau, L
Monteleone, P
Roche, R
Izzo, A A
Di Marzo, V
description The endocannabinoid, arachidonoylethanolamide (AEA), and the peroxisome proliferator‐activated receptor (PPAR)‐α ligand, oleylethanolamide (OEA) produce opposite effects on lipogenesis. The regulation of OEA and its anti‐inflammatory congener, palmitoylethanolamide (PEA), in adipocytes and pancreatic β‐cells has not been investigated. We report here the results of studies on acylethanolamide regulation in these cells during obesity and hyperglycaemia, and provide an overview of acylethanolamide role in metabolic control. We analysed by liquid chromatography‐mass spectrometry OEA and PEA levels in: 1) mouse 3T3F442A adipocytes during insulin‐induced differentiation, 2) rat insulinoma RIN m5F β‐cells kept in ‘low’ or ‘high’ glucose, 3) adipose tissue and pancreas of mice with high fat diet‐induced obesity (DIO), and 4) in visceral fat or blood of obese or type 2 diabetes (T2D) patients. In adipocytes, OEA levels remain unchanged during differentiation, whereas those of PEA decrease significantly, and are under the negative control of both leptin and PPAR‐γ. PEA is significantly downregulated in subcutaneous adipose tissue of DIO mice. In RIN m5F insulinoma β‐cells, OEA and PEA levels are inhibited by ‘very high’ glucose, this effect being enhanced by insulin, whereas in cells kept for 24 h in ‘high’ glucose, they are stimulated by both glucose and insulin. Elevated OEA and PEA levels are found in the blood of T2D patients. Reduced PEA levels in hypertrophic adipocytes might play a role in obesity‐related pro‐inflammatory states. In β‐cells and human blood, OEA and PEA are down‐ or up‐regulated under conditions of transient or chronic hyperglycaemia, respectively. British Journal of Pharmacology (2007) 152, 676–690; doi:10.1038/sj.bjp.0707424; published online 20 August 2007
doi_str_mv 10.1038/sj.bjp.0707424
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In RIN m5F insulinoma β‐cells, OEA and PEA levels are inhibited by ‘very high’ glucose, this effect being enhanced by insulin, whereas in cells kept for 24 h in ‘high’ glucose, they are stimulated by both glucose and insulin. Elevated OEA and PEA levels are found in the blood of T2D patients. Reduced PEA levels in hypertrophic adipocytes might play a role in obesity‐related pro‐inflammatory states. In β‐cells and human blood, OEA and PEA are down‐ or up‐regulated under conditions of transient or chronic hyperglycaemia, respectively. 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The regulation of OEA and its anti‐inflammatory congener, palmitoylethanolamide (PEA), in adipocytes and pancreatic β‐cells has not been investigated. We report here the results of studies on acylethanolamide regulation in these cells during obesity and hyperglycaemia, and provide an overview of acylethanolamide role in metabolic control. We analysed by liquid chromatography‐mass spectrometry OEA and PEA levels in: 1) mouse 3T3F442A adipocytes during insulin‐induced differentiation, 2) rat insulinoma RIN m5F β‐cells kept in ‘low’ or ‘high’ glucose, 3) adipose tissue and pancreas of mice with high fat diet‐induced obesity (DIO), and 4) in visceral fat or blood of obese or type 2 diabetes (T2D) patients. In adipocytes, OEA levels remain unchanged during differentiation, whereas those of PEA decrease significantly, and are under the negative control of both leptin and PPAR‐γ. PEA is significantly downregulated in subcutaneous adipose tissue of DIO mice. In RIN m5F insulinoma β‐cells, OEA and PEA levels are inhibited by ‘very high’ glucose, this effect being enhanced by insulin, whereas in cells kept for 24 h in ‘high’ glucose, they are stimulated by both glucose and insulin. Elevated OEA and PEA levels are found in the blood of T2D patients. Reduced PEA levels in hypertrophic adipocytes might play a role in obesity‐related pro‐inflammatory states. In β‐cells and human blood, OEA and PEA are down‐ or up‐regulated under conditions of transient or chronic hyperglycaemia, respectively. 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subjects 3T3 Cells
Adipocytes - cytology
Adipocytes - drug effects
Adipocytes - metabolism
Adult
Aged
Amides - blood
Amides - metabolism
anandamide
Animals
Arachidonic Acids - blood
Arachidonic Acids - metabolism
Diabetes Mellitus, Type 2 - blood
Endocannabinoids
Energy Metabolism - physiology
Ethanolamines
fat
Female
Humans
Insulin-Secreting Cells - cytology
Insulin-Secreting Cells - drug effects
Insulin-Secreting Cells - metabolism
Leptin - pharmacology
lipolysis
Male
Mice
Mice, Inbred C57BL
Middle Aged
Models, Biological
Obesity - blood
Oleic Acids - blood
Oleic Acids - metabolism
oleylethanolamide
Palmitic Acids - blood
Palmitic Acids - metabolism
palmitoylethanolamide
pancreas
Polyunsaturated Alkamides - blood
Polyunsaturated Alkamides - metabolism
PPAR gamma - agonists
PPAR gamma - genetics
PPAR gamma - metabolism
Review Literature as Topic
Reviews
Structure-Activity Relationship
title Role and regulation of acylethanolamides in energy balance: focus on adipocytes and β‐cells
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