Ethanol intake increases plasma concentrations of
triglycerides and chronic
ethanol use impairs lipid metabolism and causes chronic
inflammation. The gut plays an important role in metabolic handling of nutrients, including
lipids, and a leaky gut associated with alcohol intake, allowing inflammatory signals to the portal vein, has been proposed to constitute a mechanism by which
ethanol induces hepatic
inflammation. We compared the effects of enteral and parenteral administration of
ethanol on a range of circulating
inflammation markers (including soluble CD163, a marker of liver macrophage activation),
lipids,
cholecystokinin (CCK) and
fibroblast growth factor 19 (FGF19) as well as gallbladder volume. On two separate and randomized study days, we subjected healthy men (n = 12) to double-blinded intragastric
ethanol infusion (IGEI) and isoethanolemic intravenous
ethanol infusion (IVEI). Blood was sampled and ultrasonographic evaluation of gallbladder volume was performed at frequent intervals for 4 h after initiation of
ethanol administration on both days. Little or no effects were observed on plasma levels of
inflammation markers during IGEI and IVEI, respectively. Circulating levels of total,
low-density lipoprotein and
high-density lipoprotein cholesterol decreased after
ethanol administration independently of the administration form.
Triglyceride and
very low-density lipoprotein (
VLDL) cholesterol concentrations increased more after IGEI compared to IVEI. IVEI had no effect on plasma CCK and caused an increased gallbladder volume whereas IGEI elicited a CCK response (P < 0.0001) without affecting gallbladder volume. Circulating FGF19 concentrations decreased equally in response to both
ethanol administration forms. In conclusion, by evaluating a range of circulating
inflammation markers during IGEI and IVEI we were not able to detect signs of systemic low-grade
inflammation originating from the presence of
ethanol in the gut. IVEI increased gallbladder volume whereas IGEI increased plasma CCK (with neutral effect on gallbladder volume), increased plasma
VLDL cholesterol and
triglyceride concentrations; indicating that the enteral route of administration may influence
ethanol's effects on lipid metabolism.