Deleterious effects of sugar and protective effects of starch on cardiac remodeling, contractile dysfunction, and mortality in response to pressure overload

被引:39
作者
Chess, David J.
Lei, Biao
Hoit, Brian D.
Azimzadeh, Agnes M.
Stanley, William C.
机构
[1] Univ Maryland, Dept Med, Div Cardiol, Baltimore, MD 21201 USA
[2] Case Western Reserve Univ, Sch Med, Dept Physiol & Biophys, Cleveland, OH 44106 USA
[3] Case Western Reserve Univ, Sch Med, Dept Med, Cleveland, OH 44106 USA
[4] Univ Maryland, Dept Surg, Baltimore, MD 21201 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2007年 / 293卷 / 03期
关键词
glycemic index; ejection fraction; heart failure; PROTEIN-KINASE ACTIVITY; INSULIN-RESISTANCE; METABOLIC SYNDROME; DOWN-REGULATION; HEART; HYPERTROPHY; DIET; CARBOHYDRATE; HYPERTENSION; OBESITY;
D O I
10.1152/ajpheart.00544.2007
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Little is known about the effects of the composition of dietary carbohydrate on the development of left ventricular (LV) hypertrophy (LVH) and heart failure (HF) under conditions of pressure overload. The objective of this study was to determine the effect of carbohydrate composition on LVH, LV function, and mortality in a mouse model of chronic pressure overload. Male C57BL/6J mice of 6 wk of age (n = 14-16 mice/group) underwent transverse aortic constriction (TAC) or sham surgery and were fed either standard chow ( STD; 32% corn starch, 35% sucrose, 3% maltodextrin, and 10% fat expressed as a percent of the total energy), high-starch chow (58% corn starch, 12% maltodextrin, and 10% fat), or high-fructose chow (9% corn starch, 61% fructose, and 10% fat). After 16 wk of treatment, mice with TAC fed the STD or high-fructose diets exhibited increased LV mass, larger end-diastolic and end-systolic diameters, and decreased ejection fraction compared with sham. The high-starch diet, in contrast, prevented changes in LV dimensions and contractile function. Cardiac mRNA for myosin heavy chain-beta was increased dramatically in the fructose-fed banded animals, as was mortality (54% compared with 8% and 29% in the starch and STD banded groups, respectively). In conclusion, a diet high in simple sugar was deleterious, resulting in the highest mortality and expression of molecular markers of cardiac dysfunction in TAC animals compared with sham, whereas a high-starch diet blunted mortality, increases in cardiac mass, and contractile dysfunction.
引用
收藏
页码:H1853 / H1860
页数:8
相关论文
共 44 条
  • [1] Cardiac hypertrophy with preserved contractile function after selective deletion of GLUT4 from the heart
    Abel, ED
    Kaulbach, HC
    Tian, R
    Hopkins, JCA
    Duffy, J
    Doetschman, T
    Minnemann, T
    Boers, ME
    Hadro, E
    Oberste-Berghaus, C
    Quist, W
    Lowell, BB
    Ingwall, JS
    Kahn, BB
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (12) : 1703 - 1714
  • [2] Inflammatory mediators in chronic heart failure: An overview
    Anker, SD
    von Haehling, S
    [J]. HEART, 2004, 90 (04) : 464 - 470
  • [3] Fructose, insulin resistance, and metabolic dyslipidemia
    Basciano H.
    Federico L.
    Adeli K.
    [J]. Nutrition & Metabolism, 2 (1)
  • [4] Insulin signaling coordinately regulates cardiac size, metabolism, and contractile protein isoform expression
    Belke, DD
    Betuing, S
    Tuttle, MJ
    Graveleau, C
    Young, ME
    Pham, M
    Zhang, DF
    Cooksey, RC
    McClain, DA
    Litwin, SE
    Taegtmeyer, H
    Severson, D
    Kahn, CR
    Abel, ED
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2002, 109 (05) : 629 - 639
  • [5] The epidemic of obesity and changes in food intake: the Fluoride Hypothesis
    Bray, GA
    [J]. PHYSIOLOGY & BEHAVIOR, 2004, 82 (01) : 115 - 121
  • [6] Busserolles J, 2002, BRIT J NUTR, V87, P337, DOI [10.1079/BJN2002524, 10.1079/BJNBJN2002524]
  • [7] Busserolles J, 2003, MAGNESIUM RES, V16, P7
  • [8] Specific and sustained down-regulation of genes involved in fatty acid metabolism is not a hallmark of progression to cardiac failure in mice
    de Brouwer, K. F. J.
    Degens, H.
    Aartsen, W. M.
    Lindhout, M.
    Bitsch, N. J. J. E.
    Gilde, A. J.
    Willemsen, P. H. M.
    Janssen, B. J. A.
    van der Vusse, G. J.
    van Bilsen, M.
    [J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2006, 40 (06) : 838 - 845
  • [9] DENG JY, 2007, AM J PHYSIOL-HEART C, DOI DOI 10.1152/AJPHERT.01002.2006
  • [10] Insulin-resistant heart exhibits a mitochondrial biogenic response driven by the peroxisome proliferator-activated receptor-α/PGC-1α gene regulatory pathway
    Duncan, Jennifer G.
    Fong, Juliet L.
    Medeiros, Denis M.
    Finck, Brian N.
    Kelly, Daniel P.
    [J]. CIRCULATION, 2007, 115 (07) : 909 - 917