Interleukin-6 stimulates hepatic triglyceride secretion in rats

Katsunori Nonogaki, Gerald M. Fuller, Nelson L. Fuentes, Arthur H. Moser, Ilona Staprans, Carl Grunfeld, Kenneth R. Feingold

Research output: Contribution to journalArticlepeer-review

245 Citations (Scopus)


Interleukin-6 (IL-6) not only regulates a variety of immune functions, but also is the most potent cytokine in inducing the hepatic acute phase proteins. We determined the effect of IL-6 on serum lipid levels and the mechanism of IL-6-induced hypertriglyceridemia in rats. Intravenous administration of IL-6 (0.1 10 μg/200 g BW) increased serum triglyceride levels in a dose-dependent manner. One hour after IL-6 administration, serum triglyceride levels were increased, with peak values at 2 h (2.2-fold increase). Serum cholesterol levels also increased, but the effect was delayed, first occurring at 4 h and peaking at 8 h (1.24-fold increase). IL- 6 treatment increased hepatic triglyceride secretion without decreasing the clearance of triglyceride-rich lipoproteins, indicating that the hypertriglyceridemia was due to increased secretion by the liver. Furthermore, IL-6 stimulates lipolysis, and the increased delivery of FFA to the liver significantly contributed to the IL-6-induced hypertriglyceridemia. Neither α1- nor β-adrenergic receptor antagonists affected the hypertriglyceridemia induced by IL-6, whereas previous studies have shown that endotoxin-induced hypertriglyceridemia was blocked by α-adrenergic receptor antagonists. These results demonstrate that IL-6 induces hypertriglyceridemia by stimulating hepatic triglyceride secretion independent of endogenous catecholamines. Thus, changes in hepatic triglyceride metabolism are another acute phase response that can be induced by IL-6.

Original languageEnglish
Pages (from-to)2143-2149
Number of pages7
Issue number5
Publication statusPublished - 1995


Dive into the research topics of 'Interleukin-6 stimulates hepatic triglyceride secretion in rats'. Together they form a unique fingerprint.

Cite this