Objective: Both insulin-like growth factor (IGF)-1 and insulin-like growth factor-binding protein (IGFBP)-1 are synthesized by the liver. It is well known that chronic alcohol abuse impairs liver function, but less is known about how an acute intake of moderate quantities of alcohol affects hepatic production of IGF-1 and IGFBP-1. The objective of the present investigation was to study this issue by measuring serum levels of IGF-1 and IGFBP-1 in normal subjects before, during and after ingestion of a moderate dose of ethanol.
Subjects and design: Eight healthy subjects were tested on two occasions. On one occasion (experiment A), three 150-ml doses of ordinary drinking-water were given at 08.00, 09.30, and 11.00 h. On another occasion (experiment B), three 150-ml drinks of diluted ethanol were given instead of water. Each drink contained 0.45 g ethanol/kg b.w. Experiments A and B were performed in random order, 1 week apart. Blood samples were collected before, during and after the drinks over a period of 7 h (08.00-15.00 h). One blood sample was also drawn at 08.00 h the following day.
Measurements: Blood glucose and serum concentrations of ethanol, insulin, growth hormone (GH), IGF-1 and IGFBP-1 were determined.
Results: When alcohol had been ingested, the serum ethanol concentration rose to a peak value of 28.6 +/- 0.9 mmol/l (mean +/- SEM). The serum IGF-1 level declined significantly toward the end of the 7-h period. The serum IGFBP-1 level increased promptly in response to ethanol, and reached a maximum 2.7 times above basal as the ethanol level peaked. Neither IGF-1, nor IGFBP-1 levels changed significantly after water intake. The IGF-1 : IGFBP-1 ratio declined markedly after ethanol (from 15.7 +/- 3.9 to 3.9 +/- 0.6; P < 0.01), but not after water intake. The blood glucose and serum levels of insulin and GH were unaffected by both ethanol and water.
Conclusions: Ingestion of moderate amounts of alcohol by healthy individuals results in an acute and profound increase in the serum IGFBP-1 level and a protracted and less powerful decline in the IGF-1 level. The mechanism behind the IGFBP-1 increase is probably a direct effect on the liver, since neither insulin, nor glucose or GH concentrations changed significantly in response to the ethanol challenge.