To better define the normal metabolism of the trace element chromium, we studied its diurnal variation and its response to an oral glucose challenge in nine healthy volunteers. Plasma and urine chromium concentrations were measured by electrothermal atomic-absorption spectroscopy and plasma insulin by radioimmunoassay. A significant inverse relationship was found between plasma chromium and plasma insulin concentrations both over a 24-h period (P less than 0.001) and after a 75-g glucose load (P less than 0.01). This interesting observation, suggesting the removal of chromium from the plasma compartment after meals (confirmed by glucose tolerance test), is not explained simply by increased urinary loss but might be explained by transient changes in uptake or binding of chromium by insulin-sensitive tissues.
Evidence in the literature suggests that the trace element chromium may have a role in glucose homeostasis through the regulation of insulin action. We have previously reported a significant reduction in plasma chromium levels in healthy individuals, following a 75 g oral glucose load, and after meals and glucose-dependent uptake of chromium in insulin-dependent tissues in vitro. However, in vivo it is unclear whether the changes in plasma chromium relate to changes in plasma glucose or insulin. The present study describes a series of euglycaemic hyperinsulinaemic clamps designed to attempt to define the initiator of changes in plasma chromium levels in ten healthy individuals. The data showed a significant (P < 0.01) reduction in fasting plasma chromium levels following glucose infusion and an initial bolus of insulin. Significant (P < 0.02) increases in post-clamp urinary chromium excretion were insufficient to explain the decrease in plasma levels. During the recovery phase of an extended two-phase clamp protocol we found plasma insulin levels decreased by 70% within 10 min, associated with an increase in plasma chromium levels of 30% and no significant change in plasma glucose level. These data indicate that alterations in plasma glucose are unlikely to be directly related to changes in plasma chromium, whilst supporting the hypothesis that plasma insulin may influence plasma levels of this trace element. In contrast, plasma zinc was unaffected throughout these clamp studies.
The concentration of phosphate (Pi) in plasma, Pi excretion, and the tubular threshold of Pi resorption (TmP/GFR) all increase throughout the day from about 1100 to 0300 h. For plasma [Pi], cosinor analysis yielded the following estimates of the parameters of this pattern (with 95% confidence limits): amplitude = 0.17 (0.07-0.26) mmol/L, phase = peak at 0201 (1127-0342) h, and MESOR = 1.14 (1.11-1.18) mmol/L. The increase in TmP/GFR reflects an underlying change in renal Pi handling, which is not attributable to changes in parathyrin concentrations. The changes in Pi excretion work both for and against the changes in plasma [Pi], at different times. The calculated net nonrenal flux of Pi into the extracellular fluid increases in the morning and remains high until 0300 h, and neither it nor Pi excretion nor plasma [Pi] shows any relation to meals. This illustrates the importance of transient net fluxes of Pi between intracellular and extracellular spaces in the control of hour-to-hour changes of plasma [Pi].
We report here on a method for the determination of urine iodine by ICP-MS. The method proved to be fast, reliable and precise (within batch CVs v2.5%) and to have a low limit of detection (0.000 38 mmol L 21 ). Iodine was determined in a total of 379 urine samples from 86 healthy pregnant women who gave samples at intervals of 4 weeks from 16 weeks pregnancy to 10 weeks post-partum. Fifty-®ve control urine samples were analysed from age-matched non-pregnant females. Iodine excretion (mmol of iodine per mol of creatinine) increased signi®cantly from 28±40 weeks of pregnancy (pv0.05), returning to non-pregnant control levels by 10 weeks post-partum. This study con®rms the ability of our ICP-MS method to analyse large numbers of patient samples with the speed and performance acceptable for a routine assay.
Previous work from this and other laboratories has suggested that the trace element chromium plays some role in glucose homeostasis. In this study, we sought to characterise an in vitro cell culture model in which the effects of chromium on insulin-dependent glucose uptake could be studied. Mouse C2C12 myoblasts were differentiated to form myotubes in culture in chromium-replete or chromium-poor media. Chromium levels in standard media were 0.56 +/- 0.01 micrograms/l (mean +/- S.E.M.) compared with 0.09 +/- 0.01 micrograms/l in chromium-poor media. In chromium-poor media, insulin-stimulated uptake of radiolabelled glucose was reduced by almost 50% compared with that found in chromium-replete media. This decreased response could be restored by the addition of physiologically relevant (0.3 micrograms/l) concentrations of inorganic chromium (P < 0.001). The sensitivity of these cells to insulin was reduced dramatically by a reduction in the chromium content of the medium and was again increased (P < 0.001) by chromium addition. The concentrations of chromium required to restore the sensitivity to insulin were of the same order as those found physiologically; much higher concentrations of chromium could also stimulate glucose uptake in the absence of insulin but such concentrations were supra-physiological.
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