期刊论文详细信息
Nutrition Journal
The presentation of metabolic dysfunction and the relationship with energy output in breast cancer survivors: a cross-sectional study
Juliette Hussey1  M John Kennedy3  Elizabeth M Connolly2  Emer M Guinan1 
[1] Discipline of Physiotherapy, School of Medicine, Trinity Centre for Health Sciences, St. James’s Hospital, Dublin 8, Ireland;Department of Surgery, St. James’s Hospital, Dublin, Ireland;Academic Unit of Clinical and Medical Oncology, St. James’s Hospital and Trinity College, Dublin, Ireland
关键词: Prognosis;    Physical activity;    Resting metabolic rate;    Metabolic syndrome;    Insulin resistance;    Breast cancer;   
Others  :  806222
DOI  :  10.1186/1475-2891-12-99
 received in 2013-01-16, accepted in 2013-07-05,  发布年份 2013
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【 摘 要 】

Background

Breast cancer prognosis can be adversely influenced by obesity, physical inactivity and metabolic dysfunction. Interventions aimed at improving surrogate markers of breast cancer risk such as insulin resistance may result in improved breast cancer outcomes. The design of such interventions may be improved through increased understanding of metabolic presentation in this cohort. This cross-sectional study aimed to characterise the metabolic profile of breast cancer survivors relative to abdominal obesity and insulin resistance. A secondary aim was to compare measures of energy output across these groups.

Methods

Sixty-nine women (mean (SD) age 53.43 (9.39) years) who had completed adjuvant chemotherapy and radiotherapy for breast cancer were recruited. All measures were completed during one assessment conducted 3.1 (1.0) years post diagnosis. Body composition was measured by bioimpedance analysis and waist circumference (WC). Fasting (12 hour) blood samples were drawn to measure lipid profile, glucose, insulin, glycosylated haemoglobin A1c (HBA1c) and C-reactive protein (CRP). Insulin resistance was estimated by the homeostatic model assessment index (HOMA-IR)). Energy output was evaluated by resting metabolic rate (RMR) measured by indirect calorimetry and physical activity measured by accelerometry. Characteristics were compared across four groups (1. WC <80 cm, not insulin resistant; 2. WC 80–87.9 cm, not insulin resistant; 3. WC >88 cm, not insulin resistant; 4. WC >80 cm, insulin resistant) using ANOVA (p < 0.05).

Results

Group 4 was characterised by significant disturbances in measures of glucose metabolism (glucose, insulin, HOMA-IR and HBA1c) and raised CRP compared to other groups. Group 4 also displayed evidence of dyslipidemia and higher body composition values compared to Groups 1 and 2. Both absolute and adjusted RMR were significantly higher in the Group 4 versus all other groups. Physical activity levels were similar for all groups.

Conclusions

The results from this study suggest that participants who were both centrally obese and insulin resistant showed evidence of dyslipidemia, low-grade inflammation and glucose dysregulation. Metabolic profiles of participants who were centrally obese only were not significantly different from lean participants. Consideration of baseline metabolic presentation may be useful when considering the therapeutic targets for future interventions in this cohort.

【 授权许可】

   
2013 Guinan et al.; licensee BioMed Central Ltd.

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【 参考文献 】
  • [1]Thomson CA, Thompson PA, Wright-Bea J, Nardi E, Frey GR, Stopeck A: Metabolic syndrome and elevated C-reactive protein in breast cancer survivors on adjuvant hormone therapy. J Womens Health (Larchmt) 2009, 18(12):2041-2047.
  • [2]De Haas EC, Oosting SF, Lefrandt JD, Wolffenbuttel BH, Sleijfer DT, Gietema JA: The metabolic syndrome in cancer survivors. Lancet Oncol 2010, 11(2):193-203.
  • [3]Duggan C, Irwin ML, Xiao L, Henderson KD, Smith AW, Baumgartner RN, et al.: Associations of insulin resistance and adiponectin with mortality in women with breast cancer. J Clin Oncol 2011, 29(1):32-39.
  • [4]Goodwin PJ, Ennis M, Pritchard KI, Trudeau ME, Koo J, Taylor SK, et al.: Insulin- and obesity-related variables in early-stage breast cancer: correlations and time course of prognostic associations. J Clin Oncol 2012, 30(2):164-171.
  • [5]Pierce BL, Ballard-Barbash R, Bernstein L, Baumgartner RN, Neuhouser ML, Wener MH, et al.: Elevated biomarkers of inflammation are associated with reduced survival among breast cancer patients. J Clin Oncol 2009, 27(21):3437-3444.
  • [6]Demark-Wahnefried W, Peterson BL, Winer EP, Marks L, Aziz N, Marcom PK, et al.: Changes in weight, body composition, and factors influencing energy balance among premenopausal breast cancer patients receiving adjuvant chemotherapy. J Clin Oncol 2001, 19(9):2381-2389.
  • [7]Irwin ML, Crumley D, McTiernan A, Bernstein L, Baumgartner R, Gilliland FD, et al.: Physical activity levels before and after a diagnosis of breast carcinoma: the Health, Eating, Activity, and Lifestyle (HEAL) study. Cancer 2003, 97(7):1746-1757.
  • [8]Goodwin PJ, Ennis M, Pritchard KI, Trudeau M, Hood N: Risk of menopause during the first year after breast cancer diagnosis. J Clin Oncol 1999, 17(8):2365-2370.
  • [9]Kaaja RJ: Metabolic syndrome and the menopause. Menopause Int 2008, 14(1):21-25.
  • [10]Brochu M, Tchernof A, Dionne IJ, Sites CK, Eltabbakh GH, Sims EA, et al.: What are the physical characteristics associated with a normal metabolic profile despite a high level of obesity in postmenopausal women? J Clin Endocrinol Metab 2001, 86(3):1020-1025.
  • [11]Messier V, Karelis AD, Prud'homme D, Primeau V, Brochu M, Rabasa-Lhoret R: Identifying metabolically healthy but obese individuals in sedentary postmenopausal women. Obesity (Silver Spring) 2010, 18(5):911-917.
  • [12]Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, et al.: Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation 2009, 120(16):1640-1645.
  • [13]Grundy SM: Pre-diabetes, metabolic syndrome, and cardiovascular risk. J Am Coll Cardiol 2012, 59(7):635-643.
  • [14]Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al.: Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute scientific statement: Executive Summary. Crit Pathw Cardiol 2005, 4(4):198-203.
  • [15]Hursting SD, Lashinger LM, Colbert LH, Rogers CJ, Wheatley KW, Nunez NP, et al.: Energy balance and carcinogenesis: underlying pathways and targets for intervention. Curr Cancer Drug Targets 2007, 7(5):484-491.
  • [16]Despres JP, Lemieux I: Abdominal obesity and metabolic syndrome. Nature 2006, 444(7121):881-887.
  • [17]Astrup A, Tremblay A: Energy Metabolism. In Introduction to Human Nutrition. 2nd edition. Edited by Gibney MJ, Lanham-New SA, Cassidy A, Vorster HH. Oxford: Wiley-blackwell; 2009:31-48.
  • [18]Weyer C, Bogardus C, Pratley RE: Metabolic factors contributing to increased resting metabolic rate and decreased insulin-induced thermogenesis during the development of type 2 diabetes. Diabetes 1999, 48(8):1607-1614.
  • [19]Irwin ML, McTiernan A, Manson JE, Thomson CA, Sternfeld B, Stefanick ML, et al.: Physical activity and survival in postmenopausal women with breast cancer: results from the women's health initiative. Cancer Prev Res (Phila) 2011, 4(4):522-529.
  • [20]World Health Organization: Waist Circumference and Waist-Hip Ratio: Report of a WHO Expert Consultation. Geneva: WHO Press; 2008:8-11.
  • [21]Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC: Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985, 28(7):412-419.
  • [22]Balkau B, Charles MA: Comment on the provisional report from the WHO consultation. European Group for the Study of Insulin Resistance (EGIR). Diabet Med 1999, 16(5):442-443.
  • [23]Compher C, Frankenfield D, Keim N, Roth-Yousey L: Best practice methods to apply to measurement of resting metabolic rate in adults: a systematic review. J Am Diet Assoc 2006, 106(6):881-903.
  • [24]Ravussin E, Bogardus C: Relationship of genetics, age, and physical fitness to daily energy expenditure and fuel utilization. Am J Clin Nutr 1989, 49(5 Suppl):968-975.
  • [25]Rowlands AV, Thomas PW, Eston RG, Topping R: Validation of the RT3 triaxial accelerometer for the assessment of physical activity. Med Sci Sports Exerc 2004, 36(3):518-524.
  • [26]Powell SM, Rowlands AV: Intermonitor variability of the RT3 accelerometer during typical physical activities. Med Sci Sports Exerc 2004, 36(2):324-330.
  • [27]Garber CE, Blissmer B, Deschenes MR, Franklin BA, Lamonte MJ, Lee IM, et al.: American College of Sports Medicine position stand. Quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor fitness in apparently healthy adults: guidance for prescribing exercise. Med Sci Sports Exerc 2011, 43(7):1334-1359.
  • [28]Lynch BM, Dunstan DW, Healy GN, Winkler E, Eakin E, Owen N: Objectively measured physical activity and sedentary time of breast cancer survivors, and associations with adiposity: findings from NHANES (2003–2006). Cancer Causes Control 2010, 21(2):283-288.
  • [29]Richardson MT, Leon AS, Jacobs DR Jr, Ainsworth BE, Serfass R: Comprehensive evaluation of the Minnesota Leisure Time Physical Activity Questionnaire. J Clin Epidemiol 1994, 47(3):271-281.
  • [30]Rifai N, Ridker PM: High-sensitivity C-reactive protein: a novel and promising marker of coronary heart disease. Clin Chem 2001, 47(3):403-411.
  • [31]Nieves DJ, Cnop M, Retzlaff B, Walden CE, Brunzell JD, Knopp RH, et al.: The atherogenic lipoprotein profile associated with obesity and insulin resistance is largely attributable to intra-abdominal fat. Diabetes 2003, 52(1):172-179.
  • [32]Piche ME, Weisnagel SJ, Corneau L, Nadeau A, Bergeron J, Lemieux S: Contribution of abdominal visceral obesity and insulin resistance to the cardiovascular risk profile of postmenopausal women. Diabetes 2005, 54(3):770-777.
  • [33]Kershaw EE, Flier JS: Adipose tissue as an endocrine organ. J Clin Endocrinol Metab 2004, 89(6):2548-2556.
  • [34]Pierce BL, Neuhouser ML, Wener MH, Bernstein L, Baumgartner RN, Ballard-Barbash R, et al.: Correlates of circulating C-reactive protein and serum amyloid A concentrations in breast cancer survivors. Breast Cancer Res Treat 2009, 114(1):155-167.
  • [35]Hardy OT, Czech MP, Corvera S: What causes the insulin resistance underlying obesity? Curr Opin Endocrinol Diabetes Obes 2012, 19(2):81-87.
  • [36]Morgan K, McGee H, Watson D, Perry I, Barry M, Shelly E, et al.: SLÁN 2007: Survey of Lifestyle, Attitudes & Nutrition in Ireland. Main Report. Dublin: Department of Health and Children; 2008.
  • [37]World Health Organization: Obesity: preventing and managing the global epidemic. Report of a WHO consultation. World Health Organ Tech Rep Ser 2000, 894:1-253. i-xii
  • [38]Irwin ML, McTiernan A, Bernstein L, Gilliland FD, Baumgartner R, Baumgartner K, et al.: Relationship of obesity and physical activity with C-peptide, leptin, and insulin-like growth factors in breast cancer survivors. Cancer Epidem Biomar Prev 2005, 14(12):2881-2888.
  • [39]Hallal PC, Andersen LB, Bull FC, Guthold R, Haskell W, Ekelund U: Global physical activity levels: surveillance progress, pitfalls, and prospects. Lancet 2012, 380(9838):247-257.
  • [40]Holmes MD, Chen WY, Feskanich D, Kroenke CH, Colditz GA: Physical activity and survival after breast cancer diagnosis. JAMA 2005, 293(20):2479-2486.
  • [41]Irwin ML, Smith AW, McTiernan A, Ballard-Barbash R, Cronin K, Gilliland FD, et al.: Influence of pre- and postdiagnosis physical activity on mortality in breast cancer survivors: the health, eating, activity, and lifestyle study. J Clin Oncol 2008, 26(24):3958-3964.
  • [42]Huang KC, Kormas N, Steinbeck K, Loughnan G, Caterson ID: Resting metabolic rate in severely obese diabetic and nondiabetic subjects. Obes Res 2004, 12(5):840-845.
  • [43]Bitz C, Toubro S, Larsen TM, Harder H, Rennie KL, Jebb SA, et al.: Increased 24-h energy expenditure in type 2 diabetes. Diabetes Care 2004, 27(10):2416-2421.
  • [44]Soares MJ, Cummings NK, Ping-Delfos WL: Energy metabolism and the metabolic syndrome: does a lower basal metabolic rate signal recovery following weight loss? Diabetes Metab Syndr 2011, 5(2):98-101.
  • [45]Buscemi S, Verga S, Caimi G, Cerasola G: A low resting metabolic rate is associated with metabolic syndrome. Clin Nutr 2007, 26(6):806-809.
  • [46]Bandini L, Flynn A: Overnutrition. In Nutrition and Metabolism. Edited by Gibney MJ, Macdonald IA, Roche HM. Oxford: Blackwell Publishing; 2003:324-340.
  • [47]Lynch BM, Friedenreich CM, Winkler EA, Healy GN, Vallance JK, Eakin EG, et al.: Associations of objectively assessed physical activity and sedentary time with biomarkers of breast cancer risk in postmenopausal women: findings from NHANES (2003–2006). Breast Cancer Res Treat 2011, 130:183-194.
  • [48]Protani M, Coory M, Martin JH: Effect of obesity on survival of women with breast cancer: systematic review and meta-analysis. Breast Cancer Res Treat 2010, 123(3):627-635.
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