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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Altered hepatic production of apolipoproteins B and E in the fasted septic rat: factors in the development of hypertriglyceridemia.

The etiology of hypertriglyceridemia associated with sepsis remains unclear, but we will attempt to elucidate its character by studying the hepatic production of apolipoproteins B and E. Male Lewis rats (260-330 g) were assigned to two groups, control (n = 5) and septic (n = 5). The septic group was injected with 2 x 10(8) live Escherichia coli colonies/100 g body wt. Food was removed from all rats after injections. Twenty-four hours later a recirculating in situ liver perfusion was performed for 120 min with KRB buffer, containing L-[35S]methionine. The production of apolipoprotein B (apo B), apolipoprotein E (apo E), albumin, and transferrin was determined by immunoprecipitation. The septic rats showed a protein-specific response to sepsis. The total protein secreted increased throughout each perfusion, septic greater than control. Apo B production was increased 2.6-fold in the septic versus control groups (P = 0.037), while apo E production was decreased by 2.9 times control (P = 0.036). Albumin production was decreased 2-fold in the septic group (P = 0.002). The increased hepatic production of apo B represents an increased number of very low density lipoprotein (VLDL) particles and contributes to the elevated VLDL triglyceride levels seen in sepsis. In contrast, decreased apo E production may result in a diminished ability for peripheral and/or hepatic receptor recognition of VLDL and VLDL remnants, respectively. Each of these changes are factors in the development of hypertriglyceridemia in sepsis.[1]


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