Diabetes, with or without obesity, was associated with increased myocardial (p=0.01) and hepatic (p=0.04) triglyceride content, and impaired myocardial energetics (p=0.04) compared to controls.
Cross-Sectional (n=54)
Do lean and obese patients with Type 2 diabetes exhibit increased ectopic and visceral fat deposition and cardiac/hepatic changes compared to normal-weight controls?
Diabetes is associated with significant abnormalities in cardiac structure, energetics, and steatosis regardless of BMI, though obese patients with T2D show a greater propensity for ectopic and visceral fat deposition.
p-value: p=0.01
BACKGROUND: Type 2 diabetes (T2D) and obesity are associated with nonalcoholic fatty liver disease, cardiomyopathy, and cardiovascular mortality. Both show stronger links between ectopic and visceral fat deposition, and an increased cardiometabolic risk compared with subcutaneous fat. OBJECTIVES: This study investigated whether lean patients (Ln) with T2D exhibit increased ectopic and visceral fat deposition and whether these are linked to cardiac and hepatic changes. METHODS: Twenty-seven obese patients (Ob) with T2D, 15 Ln-T2D, and 12 normal-weight control subjects were studied. Subjects underwent cardiac computed tomography, cardiac magnetic resonance imaging (MRI), proton and phosphorus MR spectroscopy, and multiparametric liver MR, including hepatic proton MRS, T1- and T2*-mapping yielding "iron-corrected T1" cT1. RESULTS: Diabetes, with or without obesity, was associated with increased myocardial triglyceride content (p = 0.01), increased hepatic triglyceride content (p = 0.04), and impaired myocardial energetics (p = 0.04). Although cardiac structural changes, steatosis, and energetics were similar between the T2D groups, epicardial fat (p = 0.04), hepatic triglyceride (p = 0.01), and insulin resistance (p = 0.03) were higher in Ob-T2D. Epicardial fat, hepatic triglyceride, and insulin resistance correlated negatively with systolic strain and diastolic strain rates, which were only significantly impaired in Ob-T2D (p < 0.001 and p = 0.006, respectively). Fibroinflammatory liver disease (elevated cT1) was only evident in Ob-T2D patients. cT1 correlated with hepatic and epicardial fat (p < 0.001 and p = 0.01, respectively). CONCLUSIONS: Irrespective of body mass index, diabetes is related to significant abnormalities in cardiac structure, energetics, and cardiac and hepatic steatosis. Obese patients with T2D show a greater propensity for ectopic and visceral fat deposition.
Levelt et al. (Mon,) conducted a cross-sectional in Type 2 Diabetes (n=54). Type 2 Diabetes (with or without obesity) vs. Normal-weight controls was evaluated on Myocardial triglyceride content, hepatic triglyceride content, and myocardial energetics (p=0.01). Diabetes, with or without obesity, was associated with increased myocardial (p=0.01) and hepatic (p=0.04) triglyceride content, and impaired myocardial energetics (p=0.04) compared to controls.