Cannabis exposure associated with weight reduction and β-cell protection in an obese rat model

被引:36
作者
Levendal, R-A. [1 ]
Schumann, D. [2 ]
Donath, M. [2 ]
Frost, C. L. [1 ]
机构
[1] Nelson Mandela Metropolitan Univ, Dept Biochem & Microbiol, ZA-6031 Port Elizabeth, South Africa
[2] Univ Basel Hosp, Div Endocrinol Diabet & Metab, CH-4031 Basel, Switzerland
基金
新加坡国家研究基金会;
关键词
Cafeteria diet; Cannabis; THC; Obesity; Cannabinoias; C-MYC EXPRESSION; ENDOCANNABINOID SYSTEM; INSULIN-SECRETION; HIGH-FAT; RECEPTORS; INTERLEUKIN-6; PHARMACOLOGY; BINDING;
D O I
10.1016/j.phymed.2012.02.001
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
The aim of this study was to investigate the effect of an organic cannabis extract on beta-cell secretory function in an in vivo diet-induced obese rat model and determine the associated molecular changes within pancreatic tissue. Diet-induced obese Wistar rats and rats fed on standard pellets were subcutaneously injected with an organic cannabis extract or the vehicle over a 28-day period. The effect of diet and treatment was evaluated using the intraperitoneal glucose tolerance tests (IPGTTs) and qPCR analysis on rat pancreata harvested upon termination of the experiment. The cafeteria diet induced an average weight difference of 32 g and an overall increase in body weight in the experimental groups occurred at a significantly slower rate than the control groups, irrespective of diet. Area under the curve for glucose (AUC(g)) in the obese group was significantly lower compared to the lean group (p < 0.001), with cannabis treatment significantly reducing the AUC(g) in the lean group (p < 0.05), and remained unchanged in the obese group, relative to the obese control group. qPCR analysis showed that the cafeteria diet induced down-regulation of the following genes in the obese control group, relative to lean controls: UCP2, c-MYC and FLIP. Cannabis treatment in the obese group resulted in up-regulation of CB( GLUT2, UCP2 and PKB, relative to the obese control group, while c-MYC levels were down-regulated, relative to the lean control group. Treatment did not significantly change gene expression in the lean group. These results suggest that the cannabis extract protects pancreatic islets against the negative effects of obesity. (C) 2012 Elsevier GmbH. All rights reserved.
引用
收藏
页码:575 / 582
页数:8
相关论文
共 42 条
[1]  
[Anonymous], 2008, OB OV
[2]   The role of the pancreatic endocannabinoid system in glucose metabolism [J].
Bermudez-Silva, Francisco J. ;
Perez, Juan Suarez ;
Nadal, Angel ;
Rodriguez de Fonseca, Fernando .
BEST PRACTICE & RESEARCH CLINICAL ENDOCRINOLOGY & METABOLISM, 2009, 23 (01) :87-102
[3]   Role of cannabinoid CB2 receptors in glucose homeostasis in rats [J].
Bermudez-Silva, Francisco Javier ;
Sanchez-Vera, Irene ;
Suarez, Juan ;
Serrano, Antonia ;
Fuentes, Esther ;
Juan-Pico, Pablo ;
Nadal, Angel ;
Rodriguez de Fonseca, Fernando .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2007, 565 (1-3) :207-211
[4]   Combined interleukin-6 and interleukin-1 deficiency causes obesity in young mice [J].
Chida, D ;
Osaka, T ;
Hashimoto, O ;
Iwakura, Y .
DIABETES, 2006, 55 (04) :971-977
[5]  
Chiou W.C., 1978, J PHARMACOKINETICS B, V6, P1
[6]   Anticoagulant effects of a Cannabis extract in an obese rat model [J].
Coetzee, C. ;
Levendal, R.-A. ;
van de Venter, M. ;
Frost, C. L. .
PHYTOMEDICINE, 2007, 14 (05) :333-337
[7]   Endogenous cannabinoid system as a modulator of food intake [J].
Cota, D ;
Marsicano, G ;
Lutz, B ;
Vicennati, V ;
Stalla, GK ;
Pasquali, R ;
Pagotto, U .
INTERNATIONAL JOURNAL OF OBESITY, 2003, 27 (03) :289-301
[8]   Levels, metabolism, and pharmacological activity of anandamide in CB1 cannabinoid receptor knockout mice:: Evidence for non-CB1, non-CB2 receptor-mediated actions of anandamide in mouse brain [J].
Di Marzo, V ;
Breivogel, CS ;
Tao, Q ;
Bridgen, DT ;
Razdan, RK ;
Zimmer, AM ;
Zimmer, A ;
Martin, BR .
JOURNAL OF NEUROCHEMISTRY, 2000, 75 (06) :2434-2444
[9]   The endocannabinoid system in obesity and type 2 diabetes [J].
Di Marzo, V. .
DIABETOLOGIA, 2008, 51 (08) :1356-1367
[10]  
Di Marzo V, 2011, HANDB EXP PHARMACOL, V203, P75, DOI 10.1007/978-3-642-17214-4_4