Kanchana Ngaosuwan1, Natnicha Houngngam1, Pichapa Limpisook1, Wanee Plengpanich1, Weerapan Khovidhunkit2. 1. Hormonal and Metabolic Disorders Research Unit, Excellence Center for Diabetes, Hormone, and Metabolism, and Division of Endocrinology and Metabolism, Department of Medicine, Faculty of Medicine, Chulalongkorn University, and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Patumwan, Bangkok 10330, Thailand. 2. Hormonal and Metabolic Disorders Research Unit, Excellence Center for Diabetes, Hormone, and Metabolism, and Division of Endocrinology and Metabolism, Department of Medicine, Faculty of Medicine, Chulalongkorn University, and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Patumwan, Bangkok 10330, Thailand. Electronic address: wkhovid@gmail.com.
Abstract
PURPOSE: During critical illnesses, alterations in lipid metabolism occur. We examined levels of apolipoprotein A-V, a novel regulator of triglyceride metabolism, during sepsis in humans. METHODS: Seventy-five cases of sepsis and 75 cases of acute illnesses not associated with infection were recruited. Lipids and apolipoprotein A-V levels were measured by enzymatic methods and enzyme-linked immunosorbent assay, respectively, within 24 hours of diagnosis. Fifty healthy controls were also enrolled. RESULTS: During sepsis and acute illnesses, serum total cholesterol and high-density lipoprotein cholesterol levels were significantly lower than those in controls. Serum triglyceride levels, however, were not significantly different. Similarly, serum apolipoprotein A-V levels during sepsis were not significantly different from those during acute illnesses and those in controls (expressed as median [interquartile range]: 149.6 [97.5-257.1] vs 157.9 [98.4-238.2] and 155.9 [91.5-253.8] ng/mL, respectively; P = .98); and they were not correlated with serum triglyceride levels. Low apolipoprotein A-V levels were associated with higher mortality, but the association became nonsignificant after adjusting for high-density lipoprotein cholesterol levels. CONCLUSIONS: During sepsis or acute illnesses, serum apolipoprotein A-V levels were not significantly different from those in controls. Furthermore, apolipoprotein A-V levels were not linearly correlated with triglyceride levels, suggesting that it might not be a major determinant of triglyceride levels during sepsis.
PURPOSE: During critical illnesses, alterations in lipid metabolism occur. We examined levels of apolipoprotein A-V, a novel regulator of triglyceride metabolism, during sepsis in humans. METHODS: Seventy-five cases of sepsis and 75 cases of acute illnesses not associated with infection were recruited. Lipids and apolipoprotein A-V levels were measured by enzymatic methods and enzyme-linked immunosorbent assay, respectively, within 24 hours of diagnosis. Fifty healthy controls were also enrolled. RESULTS: During sepsis and acute illnesses, serum total cholesterol and high-density lipoprotein cholesterol levels were significantly lower than those in controls. Serum triglyceride levels, however, were not significantly different. Similarly, serum apolipoprotein A-V levels during sepsis were not significantly different from those during acute illnesses and those in controls (expressed as median [interquartile range]: 149.6 [97.5-257.1] vs 157.9 [98.4-238.2] and 155.9 [91.5-253.8] ng/mL, respectively; P = .98); and they were not correlated with serum triglyceride levels. Low apolipoprotein A-V levels were associated with higher mortality, but the association became nonsignificant after adjusting for high-density lipoprotein cholesterol levels. CONCLUSIONS: During sepsis or acute illnesses, serum apolipoprotein A-V levels were not significantly different from those in controls. Furthermore, apolipoprotein A-V levels were not linearly correlated with triglyceride levels, suggesting that it might not be a major determinant of triglyceride levels during sepsis.
Authors: Alexander C Reisinger; Max Schuller; Michael Holzer; Julia T Stadler; Gerald Hackl; Florian Posch; Gunther Marsche; Harald Sourij; Robert Ekart; Kathrin Eller; Philipp Eller Journal: Front Med (Lausanne) Date: 2020-10-22