Sepsis-induced liver dysfunction: Impact on lipid metabolism and pathophysiology

Despite advances in medical technology, sepsis remains a significant cause of mortality in intensive care units. The pathophysiology of sepsis is complex and involves increased activity of molecules that regulate vascular tone, including nitric oxide, hydrogen sulfide, endothelin-1, and carbon monoxide. These molecular changes contribute to the high mortality associated with sepsis. Moreover, as a systemic inflammatory response to infection, sepsis leads to reduced neutrophil levels, impairing the body’s ability to combat the disease effectively. The impact of sepsis on lipid metabolism and liver function is profound. The liver, a vital organ involved in various physiological processes, experiences enzyme production under septic conditions. Proinflammatory cytokines overload the liver during sepsis, impairing its normal functions and disrupting lipid metabolism. Altered circulating lipid levels, particularly triglycerides and cholesterol, may further exacerbate organ failure associated with sepsis. This review aims to explore the intricate relationship between sepsis, liver function, and lipid metabolism, offering a comprehensive understanding of the mechanisms behind sepsis-induced liver dysfunction and lipid abnormalities. A deeper insight into these processes may pave the way for developing effective therapeutics to counteract the detrimental consequences of sepsis. By highlighting the current knowledge gaps and elucidating the underlying mechanisms, this review seeks to contribute to improving sepsis management and patient outcomes.