A 55-year-old man with metabolic syndrome presents with BP 148/92 mmHg, HR 88/min, and fasting labs showing triglycerides 450 mg/dL, HDL 32 mg/dL, glucose 118 mg/dL, and elevated apoB levels. Abdominal ultrasound shows no hepatic steatosis. He denies alcohol use. VLDL particle analysis reveals small, dense particles with reduced triglyceride content per particle. Which mechanism best explains small, dense VLDL particle production in this metabolic context?
- A)Enhanced clearance of apoB-100-containing particles by LDL receptors
- B)Impaired esterification of cholesterol by LCAT in HDL particles
- C)Decreased activity of lipoprotein lipase in adipose tissue
- D)Increased hepatic uptake of remnant particles via apoE receptors
- E)Increased hepatic re-esterification of free fatty acids and impaired apoB-100 secretionGABARITO
Explicação
In insulin resistance and metabolic syndrome, increased hepatic fatty acid re-esterification provides excess triglyceride substrate. However, apoB-100 secretion is suppressed, so the same number of VLDL particles must carry more triglycerides, creating small, ... Ver explicação completa e trilha adaptativa →