Evaluation of epicardial adipose tissue in familial partial lipodystrophy

Diabetology & Metabolic Syndrome

Rodrigo O Moreira¹  César Augusto da Silva Nascimento²  Gabriel Cordeiro Camargo²  Rodolfo de Paula Lustosa²  Roberto Luis Zagury¹  Ricardo de Andrade Oliveira¹  Juliana Bonadiman e Bragança¹  Cynthia M Valério¹  Amélio Fernando Godoy-Matos¹ 

[1] Metabolism Unit, State Institute of Diabetes and Endocrinology, IEDE, Rio de Janeiro, Brazil;National Cardiology Institute of Laranjeiras, Rio de Janeiro, Brazil

关键词: Dual energy x-ray absorptiometry;    Metabolic syndrome;    Echocardiography;    Epicardial adipose tissue;    Lipodystrophy;   

Others  :  1174871
DOI  :  10.1186/s13098-015-0024-5

 received in 2014-11-09, accepted in 2015-03-15,  发布年份 2015

【 摘 要 】

Background

Dunnigan type Familial Partial Lipodystrophy (FPLD) is characterized by loss of subcutaneous fat from the limbs and excessive accumulation on the visceral adipose tissue (VAT). Affected individuals have insulin resistance (IR), diabetes, dyslipidemia and early cardiovascular (CV) events, due to their imbalanced distribution of total body fat (TBF). Epicardial adipose tissue (EAT) is correlated with VAT. Hence, EAT could be a new index of cardiac and visceral adiposity with great potential as a marker of CV risk in FPLD.

Objective

Compare EAT in FPLD patients versus healthy controls. Moreover, we aimed to verify if EFT is related to anthropometrical (ATPM) and Dual-Energy X-ray Absorptiometry (DEXA) measures, as well as laboratory blood findings. We postulated that FPLD patients have enlarged EAT.

Methods

This is an observational, cross-sectional study. Six patients with a confirmed mutation in the LMNA gene for FPLD were enrolled in the study. Six sex, age and BMI-matched healthy controls were also selected. EFT was measured by transthoracic echocardiography (ECHO). All participants had body fat distribution evaluated by ATPM and by DEXA measures. Fasting blood samples were obtained for biochemical profiles and also for leptin measurements.

Results

Median EFT was significantly higher in the FPLD group than in matched controls (6.0 ± 3.6 mm vs. 0.0 ± 2.04 mm; p = 0.0306). Additionally, FPLD patients had lower leptin values. There was no significant correlation between EAT and ATPM and DEXA measurements, nor laboratory findings.

Conclusions

This study demonstrates, for the first time, that EAT measured by ECHO is increased in FPLD patients, compared to healthy controls. However, it failed to prove a significant relation neither between EAT and DEXA, ATPM or laboratory variables analyzed.

【 授权许可】

   
2015 Godoy-Matos et al.; licensee BioMed Central.

【 参考文献 】

• [1]Garg A, Agarwal A: Lipodystrophies: Disorders of adipose tissue biology. Biochim Biophys Acta 2009, 1791(6):507-13.
• [2]Garg A, Peshock R, Fleckenstein J: Adipose Tissue Distribution Pattern in Patients with Familial Partial Lipodystrophy (Dunnigan Variety). J Clin Endocrinol Metab 1999, 84:170-174.
• [3]Capeau J, Magré J, Lascols O, Caron M, Béréziat V, Vigouroux C, et al.: Diseases of adipose tissue: genetic and acquired Lipodystrophies. Bioch Soc Trans 2005, 33(5):1073-1077.
• [4]Pandey S, Pungavkar S, Vaidya R, Patkar D, Hegele RA, Sheth FJ, et al.: An Imaging Study of Body Composition Including Lipodeposition Pattern in a Patient of Familial Partial Lipodystrophy (Dunnigan Type). J Assoc Physicians India 2005, 53:897-900.
• [5]Al-Attar SA, Pollex RL, Robinson JF, Miskie BA, Walcarius R, Rutt BK, et al.: Semi-automated segmentation and quantification of adipose tissue in calf and thigh by MRI: a preliminary study in patients with monogenic metabolic syndrome. BMC Medical Imaging 2006, 31:6-11.
• [6]Al-Attar SA, Pollex RL, Robinson JF, Miskie BA, Walcarius R, Little CH, et al.: Quantitative and qualitative differences in subcutaneous adipose tissue stores across lipodystrophy types shown by magnetic resonance imaging. BMC Med Imaging 2007, 12:7. 3
• [7]Addeman BT, Kutty S, Perkins TG, Soliman AS, Wiens CN, McCurdy CM, et al.: Validation of volumetric and single-slice MRI adipose analysis using a novel fully automated segmentation. J Magn Reson Imaging 2015, 41(1):233-41.
• [8]Iacobellis G, Assael F, Ribaudo M, Zappaterreno A, Alessi G, Di Mario U, et al.: Epicardial fat from echocardiography: a new method for visceral adipose tissue prediction. Obes Res 2013, 11:304-310.
• [9]Rabkin SW: Epicardial fat: properties, function and relationship to obesity. Obes Res 2007, 8:253-261.
• [10]Sacks H, Fain J: Human epicardial adipose tissue: A review. Am H J 2007, 153(6):907-917.
• [11]Saura D, Oliva M, Rodriguez D, Pascual-Figal DA, Hurtado JÁ, Pinar E, et al.: Reproducibility of echocardiographic measurements of epicardial fat thickness. Int J Cardiol 2010, 141(3):311-3.
• [12]Mcgavock J, Victor R, Unger R, Szczepaniak L: Adiposity of the Heart, Revisited. Ann Intern Med 2006, 144:517-524.
• [13]Park JS, Choi SY, Zheng M: Epicardial adipose tissue thickness is a predictor for plaque vulnerability in patients with significant coronary artery disease. Atherosclerosis 2013, 226:134-139.
• [14]Iacobellis G, Sharma AM, Pellicelli AM, Grisorio B, Barbarini G, Barbaro B, et al.: Epicardial adipose tissue is related to carotid intima-media thickness and visceral adiposity in HIV-infected patients with highly active antiretroviral therapy-associated metabolic syndrome. Curr HIV Res 2007, 5:275-279.
• [15]Balcioglu AS, Durakoglugil ME, Cicek D, Bal UA, Boyaci B, Muderrisoglu H: Epicardial adipose tissue thickness and plasma homocysteine in patients with metabolic syndrome and normal coronary arteries. Diabetol Metabol Syndr 2014, 6:62-69. BioMed Central Full Text
• [16]Pierdomenico SD, Pierdomenico AM, Cuccurullo F, Iacobellis G: Meta-Analysis of the regulation of echocardiographic epicardial adipose tissue thickness and the metabolic syndrome. Am J Cardiol 2013, 111:73-78.
• [17]Fernandez-Muñoz MJ, BasurtoAcevedo L, Cordoba Perez N, Vazquez Martinez AL, Tepach Gutierrez N, Vega Garcia S, et al.: Epicardial adipose tissue is associated with visceral fat, metabolic syndrome, and insulin resistance in menopausal women. Rev Esp Cardiol 2014, 67:436-441.
• [18]Freitas P, Santos AC, Carvalho D: Fat mass ratio: an objective tool to define lipodystrophy in HIV-infected patients under antiretroviral therapy. J Clin Densitom 2010, 13(2):197-203.
• [19]Hegele RA, Al-Attar SA, Rutt BK: Obstructive sleep apnea in 2 women with familial partial lipodystrophy due to a heterozygous LMNA R482Q mutation. CMAJ 2007, 177(7):743-45.
• [20]Joy T, Kennedy BA, Al-Attar S, Rutt BK, Hegele RA: Predicting abdominal adipose tissue among women with familial partial lipodystrophy. Metabolism 2009, 58(6):828-34.
• [21]Shetty R, Vivek G, Naha K, Nayak K, Goyal A, Dias LS: Correlation of epicardial fat and anthropometric measurements in Asian-Indians: A community based study. Avicenna J Med 2012, 2(4):89-93.
• [22]Okyay K, Balcioglu AS, Tavil Y, Tacoy G, Turkoglu S, Abaci A: A relationship between echocardiographic subepicardial adipose tissue and metabolic syndrome. Int J Cardiovasc Imaging 2008, 24:577-583.
• [23]Malavazos A, Ermetici F, Cereda E, Coman C, Locati M, Morricone L, et al.: Epicardial fat thickness: Relationship with plasma visfatin and plasminogen activator inhibitor-1 levels in visceral obesity. Nutr Metab Cardiovasc Dis 2008, 18(8):523-530.
• [24]Iacobellis G, Sharma A: Epicardial adipose tissue as new cardio-metabolic risk marker and potential therapeutic target in the metabolic syndrome. Cur Pharm Des 2007, 13(21):2180-4.
• [25]Sacks HS, Fain JN, Cheema P: Inflammatory genes in epicardial fat contiguous with coronary atherosclerosis in metabolic syndrome and type 2 diabetes: changes associated with pioglitazone. Diab Care 2011, 34:730-733.
• [26]Park JH, Park YS, Kim YJ: Effects of statins on the epicardial fat thickness in patients with coronary artery stenosis underwent percutaneous coronary intervention: comparison of atorvastatin with simvastatin/ezetimibe. J Cardiovasc Ultrasound 2010, 18:121-126.
• [27]Saura D, Oliva M, Rodrígueza D, Pascual-Figala D, Hurtadoa J, Pinara E, et al.: Reproducibility of echocardiographic measurements of epicardial fat thickness. Int J Cardiol 2010, 141(3):311-313.
• [28]Savage D, Murgatroyd P, Chatterjee V, O’rahilly S: Energy Expenditure and Adaptive Responses to an Acute Hypercaloric Fat Load in Humans with Lipodystrophy. J Clin Endocrinol Metab 2005, 90(3):1446-1452.
• [29]Chan JL, Lutz K, Cochran E, Huang W, Peters Y, Weyer C, et al.: Clinical effects of long-term metreleptin treatment in patients with lipodystrophy. Endocr Pract 2011, 17(6):922-932.
• [30]Chehab F: Minireview: Obesity and Lipodystrophy—Where Do the Circles Intersect? Endocrinol 2008, 149(3):925-934.