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Role of the endocannabinoid system in obesity induced by neuropeptide Y overexpression in noradrenergic neurons

Title: Role of the endocannabinoid system in obesity induced by neuropeptide Y overexpression in noradrenergic neurons
Authors: Vähätalo LH; Ruohonen ST; Mäkelä S; Ailanen L; Penttinen AM; Stormi T; Kauko T; Piscitelli F; Silvestri C; Savontaus E; Di Marzo V
Contributors: biolääketieteen laitos, Institute of Biomedicine; biostatistiikka, Biostatistics; farmakologia lääkekehitys ja lääkehoito, Pharmacology, Drug Development and Therapeutics; tyks, vsshp, tyks, varha; 1.2.246.10.2458963.20.76761397710; 1.2.246.10.2458963.20.77952289591; 2607102; 2607302
Publication Year: 2022
Collection: University of Turku: UTUPub / Turun yliopisto
Description: Objective: Endocannabinoids and neuropeptide Y (NPY) promote energy storage via central and peripheral mechanisms. In the hypothalamus, the two systems were suggested to interact. To investigate such interplay also in non-hypothalamic tissues, we evaluated endocannabinoid levels in obese OE-NPY DβH mice, which overexpress NPY in the noradrenergic neurons in the sympathetic nervous system and the brain. Methods: The levels of the endocannabinoids anandamide and 2-arachidonoylglycerol were measured in key regulatory tissues, i.e. hypothalamus, pancreas, epididymal white adipose tissue, liver and soleus muscle, over the development of metabolic dysfunctions in OE-NPY DβH mice. The effects of a 5-week treatment with the CB1 receptor inverse agonist AM251 on adiposity and glucose metabolism were studied. Results: 2-arachidonoylglycerol levels were increased in the hypothalamus and epididymal white adipose tissue of pre-obese and obese OE-NPY DβH mice. Anandamide levels in adipose tissue and pancreas were increased at 4 months concomitantly with higher fat mass and impaired glucose tolerance. CB1 receptor blockage reduced body weight gain and glucose intolerance in OE-NPY DβH to the level of vehicle-treated wildtype mice. Conclusions: Altered endocannabinoid tone may underlie some of the metabolic dysfunctions in OE-NPY DβH mice, which can be attenuated with CB1 inverse agonism suggesting interactions between endocannabinoids and NPY also in the periphery. CB1 receptors may offer a target for the pharmacological treatment of the metabolic syndrome with altered NPY levels.
Document Type: other/unknown material
Language: English
Relation: e151; Nutrition and Diabetes; https://www.utupub.fi/handle/10024/168462
Availability: https://www.utupub.fi/handle/10024/168462
Accession Number: edsbas.7CEAB216
Database: BASE