Food Nutr Res. 2016 Feb 17;60:28373. doi: 10.3402/fnr.v60.28373. eCollection 2016.
Chronic treatment with epigallocatechin gallate reduces motor hyperactivity and affects in vitro tested intestinal motility of spontaneously hypertensive rats.
Food & nutrition research
Maria Assunta Potenza, Monica Montagnani, Carmela Nacci, Maria Antonietta De Salvia
Affiliations
Affiliations
- Department of Biomedical Sciences and Human Oncology, University of Bari 'Aldo Moro', Bari, Italy.
- Department of Biomedical Sciences and Human Oncology, University of Bari 'Aldo Moro', Bari, Italy; [email protected].
PMID: 26899572
PMCID: PMC4761688 DOI: 10.3402/fnr.v60.28373
Abstract
BACKGROUND: Green tea catechins seem to contribute toward reducing body weight and fat.
OBJECTIVE: We aimed to investigate whether chronic administration of (-)-epigallocatechin-3-gallate (EGCG), the most abundant catechin of green tea, reduces weight gain in spontaneously hypertensive rats (SHR), an animal model of metabolic syndrome, by increasing motor activity and/or by altering gastrointestinal motility.
DESIGN: Nine-week-old SHR were randomly assigned to two groups and treated by gavage for 3 weeks with vehicle dimethyl sulfoxide or EGCG (200 mg/kg/day). Age-matched Wistar-Kyoto (WKY) control rats were treated with vehicle alone. The effect of chronic administration of EGCG was evaluated on open-field motor activity and on ex vivo colonic and duodenal motility. Moreover, in vitro acute effect of 20-min incubation with EGCG (100 µM) or vehicle was evaluated in colonic and duodenal specimens from untreated WKY rats and SHR.
RESULTS: Vehicle-treated SHR were normoglycemic and hyperinsulinemic, and showed a reduction of plasma adiponectin when compared to vehicle-treated WKY rats. In addition, consistent with fasting glucose and insulin values, vehicle-treated SHR were more insulin resistant than age-matched vehicle-treated WKY rats. Chronic treatment for 3 weeks with EGCG improved insulin sensitivity, raised plasma adiponectin levels, and reduced food intake and weight gain in SHR. Vehicle-treated SHR showed increased open-field motor activity (both crossings and rearings) when tested after each week of treatment. The overall hyperactivity of vehicle-treated SHR was significantly reduced to the levels of vehicle-treated WKY rats after 2 and 3 weeks of EGCG treatment. Colonic and duodenal preparations obtained from SHR chronically treated in vivo with EGCG showed reduced responses to carbachol (0.05-5 µM) and increased inhibitory response to electrical field stimulation (EFS, 1-10 Hz, 13 V, 1 msec, 10-sec train duration), respectively. In vitro acute EGCG incubation (100 µM, 20 min) of colonic and duodenum strips obtained from untreated SHR and WKY rats showed a reduced contractile colonic response to a fixed dose of carbachol (1.5 µM) only in SHR with respect to its own vehicle, whereas the inhibitory duodenal response to a fixed EFS frequency (5 Hz) was significantly reduced in both WKY rats and SHR groups with respect to their own vehicle.
CONCLUSIONS: These data suggest that EGCG affects body weight gain in rats and this effect seems to be due to the altered intestinal motility and not to increased motor activity.
Keywords: colon; duodenum; green tea; weight gain
References
- Front Microbiol. 2014 Aug 20;5:434 - PubMed
- Am J Physiol Endocrinol Metab. 2013 Sep 15;305(6):E679-86 - PubMed
- Clin Cancer Res. 2005 Jun 15;11(12):4627-33 - PubMed
- Cancer Epidemiol Biomarkers Prev. 2001 Jan;10(1):53-8 - PubMed
- Obes Res. 2004 Nov;12(11):1723-32 - PubMed
- PLoS One. 2014 Feb 03;9(2):e85520 - PubMed
- Obes Res. 2003 Sep;11(9):1088-95 - PubMed
- Br J Nutr. 2011 Dec;106(12 ):1880-9 - PubMed
- Pharmacol Res. 2011 Aug;64(2):123-35 - PubMed
- J Nutr Biochem. 2014 Jan;25(1):1-18 - PubMed
- Nutrients. 2013 Sep 26;5(10):3779-827 - PubMed
- Rev Neurosci. 2011;22(3):365-71 - PubMed
- Am J Clin Nutr. 2010 Jan;91(1):73-81 - PubMed
- Clin Cancer Res. 2003 Aug 15;9(9):3312-9 - PubMed
- Cancer Epidemiol Biomarkers Prev. 1998 Apr;7(4):351-4 - PubMed
- J Nutr Biochem. 2011 Jan;22(1):1-7 - PubMed
- Life Sci. 2014 Nov 24;118(2):200-5 - PubMed
- J Clin Endocrinol Metab. 2000 Jul;85(7):2402-10 - PubMed
- Am J Physiol Endocrinol Metab. 2007 May;292(5):E1378-87 - PubMed
- J Nutr Biochem. 2014 May;25(5):557-64 - PubMed
- Auton Neurosci. 2009 Jan 28;145(1-2):50-4 - PubMed
- Neuropharmacology. 2009 Dec;57(7-8):619-26 - PubMed
- Eur J Pharmacol. 2004 Oct 1;500(1-3):177-85 - PubMed
- Arch Microbiol. 2014 Oct;196 (10 ):681-95 - PubMed
- Neurosci Biobehav Rev. 2000 Jan;24(1):31-9 - PubMed
- Neurogastroenterol Motil. 2008 Nov;20(11):1251-62 - PubMed
- Life Sci. 2010 Mar 13;86(11-12):410-5 - PubMed
- Nutr Metab (Lond). 2014 Jan 07;11(1):3 - PubMed
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