Abstract
Summary: To date, no information is available on whether human growth hormone (hGH) exerts an influence on digestive processes in man. To test this, we studied the composition of the aqueous (micellar) phase during the digestion of two consecutive meals in growth hormone-deficient individuals and in control subjects, before and after replacement therapy with hGH.
Before treatment, the average micellar bile acid concentration was 5.0 ± 0.6 mM (normal adults and controls subjects: 6–15 mM) during the first meal, and 3.5 ± 0.9 mM (normal adults and control subjects 5–10 mM) during the second meal. After 1 year of treatment, the mean micellar bile acid concentration increased to 9.7 ± 1.0 mM (P < 0.02) during the First, and to 7.1 ± 0.3 mM (P < 0.01) during the second meal. Concomitantly with an increased micellar bile acid concentration, micellar lipid increased as well (effect of treatment: (1) fatty acid, first meal 6.3 ± 0.6 mM to 13.0 ± 0.7 mM, P < 0.001; second meal 4.5 ± 1.5 mM to 8.5 ± 0.3 mM, P < 0.05; (2) monoglyceride, as percentage of total fatty acids: first meal 25 ± 10 to 53 ± 7, P < 0.02; second meal 31 ± 7 to 62 ± 6, P 0.02).
Short term treatment (10 days) did not have an effect on the concentration of micellar bile acids and lipids in the control subjects. There was no significant difference in the physical state of bile acids and lipids between patients and control subjects before and after treatment.
Speculation: The digestion of dietary lipid involves a sequence of important steps: after emulsification, lipolysis generates fatty acids and monoglyceride, which require dispersal by bile acids (above their critical micellar concentration) for transport through the aqueous milieu to the membrane of the enterocyte. The “physiologic micellar concentration” of bile acids in the intestine during a meal for the efficient micellar dispersal of lipid is between 3 and 4 mM.
The increase of the intestinal micellar bile acid concentration from borderline to normal adult levels after replacement therapy with growth hormone could be explained as follows. The increased concentrations of bile acids in the intestine after treatment was the result of an increased hepatobiliary secretion of bile acids. This could have been effected by a growth hormone-mediated increase of hepatic bile acid synthesis, or through increased storage capacity of the gallbladder. The latter is probably best explained by a growth hormone-stimulated secretin effect, rather than an effect of gallbladder emptying. Further, increased availability of bile acids for lipid digestion could also result from their improved intestinal conservation (absorption).
The clinical implications of the results reported in this study are indirect, but may point towards an interrelationship between hormonal stimulation and certain aspects of hepatobiliary function, which influence digestive processes.
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Poley, J., Smith, J., Thompson, J. et al. Improved Micellar Dispersal of Dietary Lipid by Bile Acids during Replacement Therapy in Growth Hormone-deficient Children. Pediatr Res 11, 1186–1191 (1977). https://doi.org/10.1203/00006450-197712000-00004
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DOI: https://doi.org/10.1203/00006450-197712000-00004