The prevalence and incidence of metabolic-associated fatty liver disease (MAFLD), a clinically heterogeneous disease whose primary clinical therapies include dietary control and exercise therapy, is increasing worldwide and constitutes a significant medical burden. Gut microbes influence the physiopathological processes of the liver through different mechanisms based on the gut-liver axis. Exosomes are essential carriers of intercellular communication. Most previous studies have focused on adipocyte- and hepatocyte-derived exosomes, while the critical role of microbial-derived exosomes and the molecular mechanisms behind them in MAFLD have received little attention. Therefore, we searched and screened the latest relevant studies in the PubMeb database to elucidate the link between microbial-derived exosomes and the pathogenesis of MAFLD, mainly in terms of insulin resistance, intestinal barrier, inflammatory response, lipid metabolism, and liver fibrosis. The aim was to provide a theoretical framework and support for clinical protocols and innovative drug development.

Background and AimNon-alcoholic fatty liver disease (NAFLD) is closely related to cardiovascular diseases (CVD). A newly proposed definition is metabolic dysfunction-associated fatty liver disease (MAFLD), which was changed from NAFLD. The clinical effect of this change on abnormalities of cardiac structure and function is yet unknown. We aimed to examine whether MAFLD is associated with left ventricular (LV) diastolic dysfunction (LVDD) and cardiac remolding and further identify the impact of different subgroups and severity of MAFLD.MethodWe evaluated 228 participants without known CVDs. Participants were categorized by the presence of MAFLD and the normal group. Then, patients with MAFLD were subclassified into three subgroups: MAFLD patients with diabetes (diabetes subgroup), overweight/obesity patients (overweight/obesity subgroup), and lean/normal-weight patients who had two metabolic risk abnormalities (lean metabolic dysfunction subgroup). Furthermore, the severity of hepatic steatosis was assessed by transient elastography (FibroScan®) with a controlled attenuation parameter (CAP), and patients with MAFLD were divided into normal, mild, moderate, and severe hepatic steatosis groups based on CAP value. Cardiac structure and function were examined by echocardiography.ResultsLVDD was significantly more prevalent in the MAFLD group (24.6% vs. 60.8%, p < 0.001) compared to the normal group. The overweight subgroup and diabetes subgroup were significantly associated with signs of cardiac remolding, including interventricular septum thickness, LV posterior wall thickness, left atrial diameter (all p < 0.05), relative wall thickness, and LV mass index (all p < 0.05). Additionally, moderate-to-to severe steatosis patients had higher risks for LVDD and cardiac remolding (all p-values < 0.05).ConclusionMAFLD was associated with LVDD and cardiac remolding, especially in patients with diabetes, overweight patients, and moderate-to-to severe steatosis patients. This study provides theoretical support for the precise prevention of cardiovascular dysfunction in patients with MAFLD.

Background: Cardiovascular disease is the leading cause of death from Cushing’s syndrome (CS). Primary bilateral macronodular adrenal hyperplasia (PBMAH), a rare cause of CS, is clinically distinct from the other common types of CS, but its cardiac characteristics have been poorly studied. Methods: The clinical data, steroid hormones and echocardiographic variables were collected in 17 PBMAH patients. Twenty-one CS patients with cortisol-producing adenoma (CPA) were collected as controls. Results: In the PBMAH group, the proportion of female was lower (35.30 vs 100.00%), the age was older (55.76 ± 2.42 years vs 39.57 ± 2.72 years), and the course of disease was longer [13.00 (5.00, 21.50) years vs 1.58 (1.00, 5.00) years]. The proportion of PBMAH patients with hypertension was higher than that of CPA patients (100.00% vs 61.90%). Plasma cortisol and 24h urinary free cortisol (24h UFC) were lower in PBMAH patients than that in CPA patients [morning cortisol 19.50 (15.35, 24.48) μg/dl vs 28.30 (22.88, 29.89) μg/dl, 24h UFC 106.20 (65.35, 156.58) vs 506.23 (292.53, 712.18) μg]. The PBMAH group had longer right ventricular diameter (24.06 ± 1.23 mm vs 20.48 ± 0.83 mm), left atrial diameter (39.41 ± 1.15 mm vs 32.86 ± 0.76 mm), and a higher rate of diastolic dysfunction (76.50% vs 38.10%) than the CPA group. Univariate regression analysis showed that combination of hypertension and duration of hypertension had significant effects on left atrial diameter (b=6.383, P=0.001; b = 0.276, P<0.001, respectively) and E/A ratios (b=-0.496, P< 0.001; b=0.022, P<0.001, respectively). Multivariate regression analysis showed that corticosterone level had a significant effect on systolic blood pressure (b=6.712, P=0.025). Conclusion: Comparing to the CPA, ventricular diastolic dysfunction was common in PBMAH patients under relatively lower cortisol level. PBMAH had a high corticosterone level which may play a role in the development of hypertension and further heart changes.