ABSTRACT
PURPOSE OF REVIEW: To update information about the relationship between metabolic dysfunction-associated steatotic liver disease (MASLD) and atherosclerosis. This review emphasizes the potential mechanisms linking MASLD with atherosclerosis and the possible causal relationships between these conditions. RECENT FINDINGS: An increased risk of cardiovascular disease is related to MASLD. Several molecular, cellular, and metabolic mechanisms have been described to explain the development of atherothrombosis in MASLD patients. These include atherogenic dyslipidemia, low-grade vascular inflammation, endothelial dysfunction, foam cell formation, proliferation of vascular smooth muscle cells, insulin resistance, gut microbiota dysbiosis, activation of renin-angiotensin and sympathetic nervous systems, hypercoagulability, and decreased fibrinolysis. Also, there is recent evidence suggesting an association between genetically driven liver fat and coronary heart disease mediated by the causal effect of apoB-containing lipoproteins. Several meta-analyses and systematic reviews have reported a strong association between MASLD and cardiovascular outcomes. MASLD is an important and independent risk factor for atherosclerosis development. Multiple mechanisms may be involved in this association. Further research is required to establish a causal association between MASLD and atherosclerosis.
Subject(s)
Atherosclerosis , Humans , Atherosclerosis/etiology , Atherosclerosis/complications , Fatty Liver/complications , Fatty Liver/metabolism , Fatty Liver/etiology , Risk Factors , Insulin ResistanceABSTRACT
OBJECTIVE: To compare the efficacy of liraglutide monotherapy with glimepiride monotherapy in subjects with DM2 inadequately controlled by previous treatment of diet/exercise or oral antidiabetic drug. METHODS: A 52-week, double-blinded, active-controlled, parallel-group, multi-centre, prospective trial, involving 746 subjects was conducted in the USA and Mexico. In Mexico, 171 subjects were rando-mised (1:1:1) to once daily liraglutide (either 1.2, or 1.8 mg/day injected subcutaneously) or glimepiride (8 mg/day orally). RESULTS: Hb1Ac reduced by 0.64%, 1.31% and 0.30% with glimepiride, liraglutide 1.8 mg and 1.2 mg, respectively. Body weight decreased with both liraglutide doses while a weight gain of 0.94 kg was observed with glimepiride. FPG reduced by 27.9 mg/dL with liraglutide 1.8 mg, whereas a FPG increase of 9.54 mg/dL was shown with glimepiride. No major hypoglycaemic episodes were reported in this trial. CONCLUSIONS: in Mexican subjects with DM2, liraglutide monotherapy can provide greater reduction in HbA1c, weight loss and lower risk of hypoglycaemia in comparison with glimepiride.
