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Copyright of Gefaesschirurgie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Gefaesschirurgie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Der Diabetologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of ProCare is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The influence of postprandial-like plasma insulin levels on intestinal calcium absorption (CaA) was studied in 9 healthy men. On separate occasions, they received either an i.v. infusion of 40 mU/m2 minute synthetic human insulin as well as a variable glucose infusion in order to clamp the plasma glucose at the baseline level (= glucose clamp), or insulin- and glucose-free vehicle infusions (= vehicle). During these infusions, an oral load containing 326 mg Ca in the form of Ca chloride was administered and CaA was determined thereafter with a 47Ca/85Sr double tracer method. During glucose clamp, mean plasma insulin was 172 +/- (1 SEM) 10 as compared to 6 +/- 1 microU/ml during vehicle infusions. During the clamp, 3-hour cumulative CaA rose significantly by 14% as compared to vehicle (39.2 +/- 2.5 vs. 34.4 +/- 2%, P less than 0.02). AT the same time, serum potassium and phosphorus dropped significantly, whereas serum parathyroid hormone (PTH) and 1,25(OH)2D levels were unchanged as compared to vehicle. The urinary excretions of potassium, sodium, and inorganic phosphorus, as well as the urinary specific activity of 47Ca, dropped significantly during glucose clamp, whereas the urinary excretion of cAMP was unchanged as compared to vehicle. The results suggest that, under the conditions of euglycemic hyperinsulinemic clamp, insulin stimulates CaA of healthy humans in a PTH- and 1,25(OH)2D-independent manner. Insulin may thus possibly be regarded as a factor participating in the regulation of CaA in humans. [ABSTRACT FROM AUTHOR]

Using in situ perfusion in the rat, we studied the duodenal bidirectional fluxes (LP, lumen-to-plasma; PL, plasma-to-lumen) and the net absorption of calcium (Ca) at progressive molar citrate: Ca ratios (1∶1, 2.1∶1, 8.5∶1) and three pH levels (pH 5.0, 6.25, 7.0) of the Ca-containing (4 mmol/liter) perfusion solution. Rats perfused with pH-adjusted, citrate-free solutions served as controls. LP-flux and net calcium absorption (net CaA) fell dose-dependently with increasing citrate concentrations. Also, at a given citrate:Ca ratio, LP-flux and net CaA fell with increasing pH of the perfusion solution. PL-fluxes did not change from control values, irrespective of the composition of the perfusion solution. The concomitant serum Ca and parathyroid hormone levels as well as blood pH and bicarbonate, were largely unchanged under any of the citrate-containing perfusion solutions. In conclusion, citrate inhibits duodenal CaA of the rat pH- and dose-dependently, without changing intestinal Ca secretion. This effect is not related to changes in the acid-base status or to suppressed parathyroid gland function of the animals and may be best explained by dose- and pH-dependent intraluminal complex formation between Ca and citrate. [ABSTRACT FROM AUTHOR]