Correlation between reduction of superior interventricular groove epicardial fat thickness and improvement of insulin resistance after weight loss in obese men

Liang, Kae‐Woei; Tsai, I-Chen; Lee, Wen‐Jane; Lin, Shih‐Yi; Lee, Wen-Lieng; Lee, I-Te; Fu, Chia-Po; Wang, Jun‐Sing; Sheu, Wayne H‐H

doi:10.1186/1758-5996-6-115

Cited by 10 publications

(11 citation statements)

References 49 publications

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“…Weight loss by diet control or exercise could result in significant reduction of EAT in interventricular groove, which was correlated with improved insulin resistance and insulin sensitivity indexes . Diet control and bariatric surgery induced weight loss in obese individuals was associated with EAT reduction, while no such effect was observed after exercise .…”

Section: Potential Therapiesmentioning

confidence: 92%

Epicardial adipose tissue and atrial fibrillation: Possible mechanisms, potential therapies, and future directions

Zhou

Wang

Chen

et al. 2019

Pacing Clinical Electrophis

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Obesity plays an important role in the pathogenesis of atrial fibrillation (AF). Recently, rather than general fat distribution, epicardial adipose tissue (EAT) gains a growing concern. EAT is the local adipose deposition between myocardium and pericardium. Accumulated evidence revealed several distinguishing characteristics of EAT. It lies contiguously with the myocardium and could infiltration into myocardium, actively secrets cytokines and adipokines mediating inflammation or remodeling, and contains abundant ganglionated plexi. Clinical research also found EAT may be an independent risk factor of AF. Volume or thickness of EAT measured on CT or MRI could be applied as a predictor of presence, severity, and recurrence of AF. Some drugs, like antidiabetic drugs and lipid-lowing drugs, show ability to reduce EAT. Additional surgical ablation of EAT was also proved that it could improve outcome of pulmonary vein isolation for AF. In present review, we summarize recent epidemic, biological, and clinical findings about EAT and its possible role in AF. K E Y W O R D S atrial fibrillation, epicardial adipose tissue, mechanisms, therapies 1 2 THE LINK BETWEEN AF, OBESITY, AND ADIPOSE TISSUE Obesity and AFObesity is an already recognized risk factor of AF. 5,6 It is usually assessed by several indicators, such as body mass index (BMI), waist circumference, waist to hip ratio, and body fat rate. Compared with nonobese people, obese individuals possess higher probability (49%) of suffering AF, which may be associated with atrial enlargement, ventricular diastolic dysfunction, and ectopic fat depot increase. 5 Furthermore, previous literature showed that every 5 kg/m 2 increase in BMI could increase about 10-30% higher risks of AF, and also indicated that every 1 kg/m 2 reduction in BMI was associated with a significant 7% reduction in the risk of AF. 7 These pieces of evidence support that obesity is closely associated with AF occurrence. However, in general, the indicators to measure obesity, such as BMI, are relatively rough to reflect excess adipose; and individuals with similar BMI may have different risks of AF. More precise measurements are needed to predict the occurrence and development of AF.

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Section: Potential Therapiesmentioning

confidence: 92%

Epicardial adipose tissue and atrial fibrillation: Possible mechanisms, potential therapies, and future directions

Zhou

Wang

Chen

et al. 2019

Pacing Clinical Electrophis

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“…[15][16][17] Investigators have reported that epicardial fat is associated with endothelial dysfunction, 18 insulin resistance, 19 and inflammatory markers. 20 According to further study results, EFT is related to subclinical target-organ damage such as aortic stiffness, 21 carotid intima-media thickness, and carotid plaque.…”

Section: Discussionmentioning

confidence: 99%

“…Epicardial fat thickness is associated with insulin resistance, which might be responsible for impaired arterial function. 19 Increased expression of secretory type II phospholipase A 2 in epicardial adipose tissue might be responsible for endothelial dysfunction and increased arterial stiffness. 27 Kim and colleagues, 21 who consecutively enrolled 655 subjects who underwent echocardiography and ankle-brachial pulse-wave velocity measurement, found that individuals with increased velocity and EFT had unfavorable metabolic and lipid profiles, and that EFT was significantly associated with ankle-brachial pulse-wave velocity.…”

Section: Discussionmentioning

confidence: 99%

Increased Epicardial Fat Thickness Correlates with Aortic Stiffness and N-Terminal Pro-Brain Natriuretic Peptide Levels in Acute Ischemic Stroke Patients

Altun¹,

Ünal²,

Başaran³

et al. 2016

Texas Heart Institute Journal

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Epicardial fat, a metabolically active tissue, has emerged as a risk factor and active player in metabolic and cardiovascular diseases. We investigated epicardial fat thickness in patients who had sustained an acute ischemic stroke, and we evaluated the relationship of epicardial fat thickness with other prognostic factors. We enrolled 61 consecutive patients (age, ≥18 yr) who had sustained a first acute ischemic stroke and had been admitted to our hospital within 24 hours of the onset of stroke symptoms. The control group comprised 82 consecutive sex- and age-matched patients free of past or current stroke who had been admitted to our cardiology clinics. Blood samples were taken for measurement of N-terminal pro-brain natriuretic peptide (NT-proBNP) levels at admission. Aortic stiffness indices and epicardial fat thickness were measured by means of transthoracic echocardiography within the first 48 hours. In comparison with the control group, the patients with acute ischemic stroke had significantly higher epicardial fat thickness (4.8 ± 0.9 vs 3.8 ± 0.7 mm; P <0.001), lower aortic distensibility (2.5 ± 0.8 vs 3.4 ± 0.9 cm2·dyn−1; P <0.001) and lower aortic strain (5.5% ± 1.9% vs 6.4% ± 1.8%; P=0.003). We found a significant association between epicardial fat thickness, NT-proBNP levels, and arterial dysfunction in patients who had sustained acute ischemic stroke. Increased epicardial fat thickness might be a novel risk factor and might enable evaluation of subclinical target-organ damage in these patients.

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“…Parts of the results have been published previously. [ 16 – 19 ] In brief, the study enrollment criteria included central obesity, which was defined as waist circumference ≥ 90 cm, in addition to at least 2 other ATP-III MetS criteria. [ 20 ] Patients with DM requiring oral anti-diabetic agents or insulin shots were excluded from the study.…”

Section: Methodsmentioning

confidence: 99%

Regaining body weight after weight reduction further increases pulse wave velocity in obese men with metabolic syndrome

Liang

Lee

et al. 2018

Medicine

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Subjects with metabolic syndrome (MetS) or obesity have worse arterial stiffness. However, there have been no studies addressing time-sequential changes in pulse wave velocity (PWV) after weight loss and then regaining weight in obese non-diabetic men with MetS.We prospectively enrolled 40 obese, non-diabetic men with MetS undergoing a 3-month weight reduction program. Another 26 lean and healthy men were recruited for comparisons. Oral glucose tolerance test and brachial ankle (ba) PWV were assessed in study subjects. Eighteen obese non-diabetic MetS and 15 lean control subjects had follow-ups at the 60th month.The body weight of obese MetS decreased from 94.8 ± 7.6 to 86.1 ± 9.0 (N = 18, P < .001) after a 3-month weight reduction program but regained gradually thereafter to 93.6 ± 11.6 kg at the 60th month (P < .001 versus 3rd month). baPWV decreased after weight loss slightly (P = .240) while weight regain significantly increased the baPWV (from 3rd month, 1358 ± 168 to 60th month 1539 ± 264 cm/sec, P < .001). Systolic and diastolic blood pressure increments correlated with the increment of baPWV after weight regain. At the 60th month, lean controls (N = 15) had increases in body weight while their baPWV increased non-significantly. The increments of baPWV after weight regain in obese MetS were significantly higher than the increment of baPWV in lean controls after weight gain.In conclusion, regaining body weight after weight reduction worsened arterial stiffness with significant increase of baPWV in obese non-diabetic MetS.

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Correlation between reduction of superior interventricular groove epicardial fat thickness and improvement of insulin resistance after weight loss in obese men

Cited by 10 publications

References 49 publications

Epicardial adipose tissue and atrial fibrillation: Possible mechanisms, potential therapies, and future directions

Epicardial adipose tissue and atrial fibrillation: Possible mechanisms, potential therapies, and future directions

Increased Epicardial Fat Thickness Correlates with Aortic Stiffness and N-Terminal Pro-Brain Natriuretic Peptide Levels in Acute Ischemic Stroke Patients

Regaining body weight after weight reduction further increases pulse wave velocity in obese men with metabolic syndrome

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