Postprandial ghrelin is elevated in black compared with white women

被引:21
作者
Brownley, KA
Light, KC
Grewen, KM
Bragdon, EE
Hinderliter, AL
West, SG
机构
[1] Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA
[2] Univ N Carolina, Dept Med, Chapel Hill, NC 27599 USA
[3] Penn State Univ, Dept Biobehav Hlth, University Pk, PA 16802 USA
关键词
D O I
10.1210/jc.2004-0607
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Ghrelin, a gut-brain peptide that signals hunger, is normally suppressed after meals. Subnormal suppression of postprandial ghrelin, previously noted in obese, insulin-resistant individuals, may contribute to increased food intake. Given the ethnic disparities in obesity and obesity-related cardiovascular morbidity in the United States, the present study compared a single postprandial ghrelin measure in 43 women (22 white, 21 black). Each completed a rigorously controlled 4-d dietary intervention designed to maintain weight and constant daily sodium and potassium intake (220 mEq Na, 40 mEq K). Two hours after consuming a test meal of identical content, blood samples were drawn to assess postprandial ghrelin, leptin, and norepinephrine; resting cardiovascular function was measured; and a 24-h urinary cortisol sample was obtained. Independent of body mass index, postprandial ghrelin was significantly higher in black vs. white women, and higher ghrelin was associated with higher cortisol in blacks, who failed to show the expected inverse relation between ghrelin and central obesity seen in whites. Higher ghrelin was correlated with higher blood pressure but lower norepinephrine in obese women. These findings suggest subnormal postprandial ghrelin suppression (or faster ghrelin rebound) in black women, especially the obese, that might play a role in their increased prevalence of obesity and cardiovascular disorders.
引用
收藏
页码:4457 / 4463
页数:7
相关论文
共 59 条
  • [1] Leptin -: A regulator of islet function?: Its plasma levels correlate with glucagon and insulin secretion in healthy women
    Ahrén, B
    Larsson, H
    [J]. METABOLISM-CLINICAL AND EXPERIMENTAL, 1997, 46 (12): : 1477 - 1481
  • [2] Insulin-dependent modulation of plasma ghrelin and leptin concentrations is less pronounced in type 2 diabetic patients
    Anderwald, C
    Brabant, G
    Bernroider, E
    Horn, R
    Brehm, A
    Waldhäusl, W
    Roden, M
    [J]. DIABETES, 2003, 52 (07) : 1792 - 1798
  • [3] Endocrine activities of ghrelin, a natural growth hormone secretagogue (GHS), in humans: Comparison and interactions with hexarelin, a nonnatural peptidyl GHS, and GH-releasing hormone
    Arvat, E
    Maccario, M
    Di Vito, L
    Broglio, F
    Benso, A
    Gottero, C
    Papotti, M
    Muccioli, G
    Dieguez, C
    Casanueva, FF
    Deghenghi, R
    Camanni, F
    Ghigo, E
    [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2001, 86 (03) : 1169 - 1174
  • [4] Obesity and cortisol
    Björntorp, P
    Rosmond, P
    [J]. NUTRITION, 2000, 16 (10) : 924 - 936
  • [5] Postprandial suppression of plasma ghrelin level is proportional to ingested caloric load but does not predict intermeal interval in humans
    Callahan, HS
    Cummings, DE
    Pepe, MS
    Breen, PA
    Matthys, CC
    Weigle, DS
    [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2004, 89 (03) : 1319 - 1324
  • [6] Ghrelin: The link connecting growth with metabolism and energy homeostasis
    Casanueva F.F.
    Dieguez C.
    [J]. Reviews in Endocrine and Metabolic Disorders, 2002, 3 (4) : 325 - 338
  • [7] WEIGHT-GAIN AS A RISK FACTOR FOR CLINICAL DIABETES-MELLITUS IN WOMEN
    COLDITZ, GA
    WILLETT, WC
    ROTNITZKY, A
    MANSON, JE
    [J]. ANNALS OF INTERNAL MEDICINE, 1995, 122 (07) : 481 - 486
  • [8] DISSOCIATION OF CORTISOL AND ADRENAL ANDROGEN SECRETION IN POORLY CONTROLLED INSULIN-DEPENDENT DIABETES-MELLITUS
    COUCH, RM
    [J]. ACTA ENDOCRINOLOGICA, 1992, 127 (02): : 115 - 117
  • [9] A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans
    Cummings, DE
    Purnell, JQ
    Frayo, RS
    Schmidova, K
    Wisse, BE
    Weigle, DS
    [J]. DIABETES, 2001, 50 (08) : 1714 - 1719
  • [10] De Ambrogi Marco, 2003, Med Sci Monit, V9, pRA217