ArticleDiabetology & metabolic syndrome2015
Evaluation of epicardial adipose tissue in familial partial lipodystrophy.
Article in Diabetology & metabolic syndrome, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Clinical Spectrum ofCells · 2023Pooled it
- Brazilian expert consensus on the diagnosis, classification, screening for complications and treatment of familial partial lipodystrophy.Diabetology & metabolic syndrome · 2025Article
- Looking at New Unexpected Disease Targets inCells · 2020Article
- Massive labial lipomatous hypertrophy in familial partial lipodystrophy seen on computed tomographic angiography.Radiology case reports · 2019Article
- Evaluation of the hypothalamic-pituitary-adrenal axis in a case series of familial partial lipodystrophy.Diabetology & metabolic syndrome · 2019Article
- Pancreatic fat deposition is increased and related to beta-cell function in women with familial partial lipodystrophy.Diabetology & metabolic syndrome · 2018Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDunnigan 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.
objectiveCompare 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.
methodsThis 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.
resultsMedian 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.
conclusionsThis 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.
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