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Background: Diabetes mellitus (DM) is a potential contributor to the muscle abnormalities and poor physical functioning of the dialysis population., Methods: Thirty-three dialysis patients without DM (non-DM group) were compared with 25 dialysis patients with DM (DM group). Measures were made of cross-sectional area and composition of the leg muscles by using proton T1-weighted magnetic resonance imaging; body composition by means of dual-energy X-ray absorptiometry; leg muscle strength by means of isokinetic knee extension; isometric dorsiflexor maximum voluntary contraction by means of force plate; physical activity by means of 3-dimensional accelerometry; and functional capacity by using various functional tests., Results: The DM group was older, weaker, more atrophic, and had a greater amount of intramuscular fat compared with the non-DM group. However, when the overall analysis was adjusted for age and sex, there were no differences between the 2 groups with respect to muscle cross-sectional area, leg strength, or physical activity. To further account for sex and age differences, a paired analysis was performed after matching patients by age (within 5 years) and sex (N = 16/group). In the matched analysis, only intramuscular fat and leg adipose tissue were different between the 2 groups., Conclusion: DM is associated with more fat within muscles of dialysis patients, but is unrelated to muscle size or strength. Demographic differences between the DM and non-DM groups on dialysis therapy likely are responsible for the general perception that patients with DM are more debilitated.

The purpose of this study was to examine and quantify hepatic uptake and degradation of gastrin and cholecystokinin peptides. Rat livers were perfused in situ, without recirculation, with Krebs-Ringer bicarbonate (pH 7.4) containing 10% bovine erythrocytes, gassed with 95% O2-5% CO2. Gastrin and cholecystokinin peptide fragments of various lengths were injected into a portal vein via a sidearm syringe for over 1 min, and hepatic venous effluent was collected every minute for 20 min. After injection of 125I-labeled gastrin peptides more than eight amino acids in length, greater than 95% radioactivity appeared in the hepatic venous effluent, all of which was intact peptide, as determined by immunoprecipitation, trichloroacetic acid precipitation, and Sephadex gel chromatography. Decreasing the chain length to eight or less amino acids resulted in progressive increases in hepatic uptake and degradation of gastrin fragments. Injected cholecystokinin peptides greater than seven amino acids in length traversed the liver intact, whereas smaller cholecystokinin peptides were cleared by the liver. The liver eliminated greater than 90% of the biologically active carboxyl-terminal tetrapeptide amide common to gastrin and cholecystokinin. The results of this study indicate that gastrin and cholecystokinin peptides longer than seven amino acids traverse the liver without significant degradation, however, smaller peptides are progressively cleared during hepatic transit. Therefore, if small gastrin and cholecystokinin peptides from antral and intestinal mucosa are released and reach the portal venous circulation, hepatic inactivation would appear to prevent them from reaching the systemic circulation, precluding their significant contribution to gastric acid secretion and other physiologic functions.

The present studies were directed toward examining the effect of somatostatin on gastrin release and acid secretion by the isolated vascularly perfused rat stomach. Rat stomachs were perfused in situ with Krebs-Ringer bicarbonate buffer containing 10% ovine erythrocytes and gassed with 95% O2-5% CO2. Inclusion of pentagastrin in the perfusion buffer increased acid output from 2.2 +/- 0.4 microEq H+/h during control perfusion to 18.8 +/- 1.8 microEq H+/h (p less than 0.01). In order to determine the effect of somatostatin on acid secretion and gastrin release, specific antibodies to somatostatin were included in the perfusate. Inclusion of antibodies to somatostatin in the buffer without pentagastrin did not significantly enhance acid output; however, gastrin concentration in the portal venous effluent increased from 15.1 +/- 2.0 to 25.2 +/- 5.2 pg/ml at 45 min (p less than 0.05). When antibodies to somatostatin were perfused in the presence of pentagastrin, acid output increased by 32% to 24.9 +/- 1.2 microEq H+/h (p less than 0.05); however, no change in gastrin concentration over basal was detected in the portal effluent. Results of these studies indicate that the capacity of the isolated rat stomach to secrete acid permits direct assessment of factors involved in the regulation of acid secretion. Under the conditions of these experiments, gastric somatostatin inhibits basal gastrin release and directly inhibits pentagastrin-stimulated acid secretion without affecting gastrin release.