title: High dose astaxanthin lowers blood pressure and increases insulin sensitivity in rats: are these effects interdependent?
abstract: The present investigation in Sprague-Dawley rats (SD) was designed to examine effects of astaxanthin (Asta) at different doses on elevated blood pressure (BP) and glucose-insulin perturbations produced by heavy sucrose ingestion. We also examined effects of Asta on BP during restraint stress. SD were divided into six groups each containing eight rats. All SD ate a basic diet of ground regular rat chow with sucrose added at 30% w/w. The Control group received only the basic diet containing added sucrose, while the other five groups each received the same diet with added test material: captopril, (30 mg/Kg), pioglitazone (15.0 mg/Kg), low Asta (25 mg/Kg), medium Asta (50 mg/kg) or high Asta (100 mg/Kg). Many tests were carried out to examine the mechanisms behind the effects of Asta on BP (serum ACE activity, losartan challenge, and LNAME challenge) and the glucose-insulin system (glucose tolerance, HOMA measurement, and insulin challenge). In SD, a relatively low dose of Asta decreased SBP, but produced no major changes in the glucose-insulin system simulating results from a previous study using Zucker Fatty Rats. Increasing the dose of Asta resulted in both a lowering of elevated systolic BP and enhanced insulin sensitivity determined by many different estimations. BP lowering was consistent with changes in the renin-angiotensin (RAS) and nitric oxide (NO) systems. At the examined doses of each, captopril lowered BP in SD without influencing glucose-insulin metabolism, whereas pioglitazone favorably affected glucose-insulin metabolism while showing essentially no effects on BP. Accordingly, Asta beneficially affects both sucrose-induced elevations of BP and insulin resistance at relatively high doses in SD. Also, Asta at higher doses lessens restraint stress, whereas, captopril and pioglitazone did not at the doses examined, even though they influenced the BP and glucose-insulin systems respectively.
authors.affiliation: Georgetown University Medical Center, Department of Biochemistry, Washington, DC 20057, USA. preusshg@georgetown.edu
authors.forename: Harry G
authors.initials: HG
authors.lastname: Preuss
authors.forename: Bobby
authors.initials: B
authors.lastname: Echard
authors.forename: Eiji
authors.initials: E
authors.lastname: Yamashita
authors.forename: Nicholas V
authors.initials: NV
authors.lastname: Perricone
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001835:Body Weight; D004305:Dose-Response Relationship, Drug; D004327:Drinking Behavior; D005247:Feeding Behavior; D005951:Glucose Tolerance Test; D007333:Insulin Resistance; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D024341:Xanthophylls / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D024341:Xanthophylls; C005948:astaxanthine