Astaxanthin ameliorates features of metabolic syndrome in SHR/NDmcr-cp

被引:115
作者
Hussein, Ghazi
Nakagawa, Takako
Goto, Hirozo
Shimada, Yutaka
Matsumoto, Kinzo
Sankawa, Ushio
Watanabe, Hiroshi
机构
[1] Toyama Univ, Inst Nat Med, Div Med Pharmacol, Fac Med,Dept Japanese Oriental Med, Toyama 9300194, Japan
[2] Int Res Ctr Tradit Med, Toyama 9398224, Japan
关键词
astaxanthin; metabolic syndrome; blood pressure; insulin resistance; lipids; adiponectin; SHR/NDmcr-cp;
D O I
10.1016/j.lfs.2006.09.041
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 [基础医学];
摘要
Glucose and lipid metabolic parameters play crucial roles in metabolic syndrome and its major feature of insulin resistance. This study was designed to investigate whether dietary astaxanthin oil (ASX-O) has potential effects on metabolic syndrome features in an SHR/NDmcr-cp (cp/cp) rat model. Oral administration of ASX (50 mg/kg/day) for 22 weeks induced a significant reduction in arterial blood pressure in SHRcp. It also significantly reduced the fasting blood glucose level, homeostasis index of insulin resistance (HOMA-IR), and improved insulin sensitivity. The results also showed an improved adiponectin level, a significant increase in high-density lipoprotein cholesterol, a significant decrease in plasma levels of triglycerides, and non-esterified fatty acids. Additionally, ASX showed significant effects on the white adipose tissue by decreasing the size of the fat cells. These results suggest that ASX ameliorates insulin resistance by mechanisms involving the increase of glucose uptake, and by modulating the level of circulating lipid metabolites and adiponectin. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:522 / 529
页数:8
相关论文
共 46 条
[1]
The metabolic syndrome - a new worldwide definition [J].
Alberti, KGMM ;
Zimmet, P ;
Shaw, J .
LANCET, 2005, 366 (9491) :1059-1062
[2]
Adiponectin relationship with lipid metabolism is independent of body fat mass:: Evidence from both cross-sectional and intervention studies [J].
Baratta, R ;
Amato, S ;
Degano, C ;
Farina, MG ;
Patanè, G ;
Vigneri, R ;
Frittitta, L .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2004, 89 (06) :2665-2671
[3]
Somatic gene transfer of human apoA-I inhibits atherosclerosis progression in mouse models [J].
Benoit, P ;
Emmanuel, F ;
Caillaud, JM ;
Bassinet, L ;
Castro, G ;
Gallix, P ;
Fruchart, JC ;
Branellec, D ;
Denèfle, P ;
Duverger, N .
CIRCULATION, 1999, 99 (01) :105-110
[4]
Role of fatty acids in the pathogenesis of insulin resistance and NIDDM [J].
Boden, G .
DIABETES, 1997, 46 (01) :3-10
[5]
High-density lipoproteins: A new potential therapeutic target for the prevention of cardiovascular disease [J].
Brewer, HB .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2004, 24 (03) :387-391
[6]
Brunzell JD, 1999, DIABETES CARE, V22, pC10
[7]
The role of non-esterified fatty acids in the deterioration of glucose tolerance in Caucasian subjects: results of the Paris Prospective Study [J].
Charles, MA ;
Eschwege, E ;
Thibult, N ;
Claude, JR ;
Warnet, JM ;
Rosselin, GE ;
Girard, J ;
Balkau, B .
DIABETOLOGIA, 1997, 40 (09) :1101-1106
[8]
The metabolic syndrome [J].
Eckel, RH ;
Grundy, SM ;
Zimmet, PZ .
LANCET, 2005, 365 (9468) :1415-1428
[9]
Proteolytic cleavage product of 30-kDa adipocyte complement-related protein increases fatty acid oxidation in muscle and causes weight loss in mice [J].
Fruebis, J ;
Tsao, TS ;
Javorschi, S ;
Ebbets-Reed, D ;
Erickson, MRS ;
Yen, FT ;
Bihain, BE ;
Lodish, HF .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (04) :2005-2010
[10]
Gavin JR, 1997, DIABETES CARE, V20, P1183