Serum chromium does not predict glucose tolerance in late pregnancy.

BACKGROUND: Chromium is an essential element in human nutrition. Serum concentrations of chromium are not well characterized during pregnancy or in gestational diabetes mellitus. OBJECTIVE: The objective of this study was to determine whether low plasma chromium concentrations (< or =3 nmol/L) are associated with altered glucose, insulin, or lipid concentrations during pregnancy. DESIGN: The study was conducted prospectively and took place at the medical obstetric clinic of a tertiary referral hospital. Seventy-nine women with abnormal results of a 50-g glucose challenge test in the third trimester of pregnancy were studied. All women had a formal 75-g oral-glucose-tolerance test, and fasting insulin, lipid, and chromium concentrations were determined. Chromium was measured by graphite furnace atomic absorption spectrometry. RESULTS: The median chromium concentration was 2 nmol/L (95% CI: 0, 12). There were no significant differences in age, plasma glucose, insulin, lipids, calculated insulin resistance, or calculated ss cell function between women with normal and those with abnormal (< or =3 nmol/L) chromium concentrations. CONCLUSIONS: Plasma chromium during pregnancy does not correlate with glucose intolerance, insulin resistance, or serum lipids. Plasma chromium concentrations may not accurately reflect tissue stores of chromium. Several trials showed a beneficial effect of chromium supplementation on glucose tolerance, insulin, and lipids. A method for assessing body chromium stores is required to allow further study.

Iodine deficiency in ambulatory participants at a Sydney teaching hospital: is Australia truly iodine replete?

OBJECTIVE: To assess iodine status in four separate groups--pregnant women, postpartum women, patients with diabetes mellitus and volunteers. DESIGN AND SETTING: Prospective cross-sectional study at a tertiary referral hospital in Sydney. PARTICIPANTS: 81 pregnant women attending a "high risk" obstetric clinic; 26 of these same women who attended three months postpartum; 135 consecutive patients with diabetes mellitus attending the diabetes clinic for an annual complications screen; and 19 volunteers. There were no exclusion criteria. METHODS: Spot urine samples were obtained, and urinary iodine was measured by inductively coupled plasma mass spectrometer. OUTCOME MEASURES: Iodine status based on urinary iodine concentration categorised as normal (> 100 micrograms/L), mild deficiency (51-100 micrograms/L) and moderate to severe deficiency (< 50 micrograms/L). RESULTS: Moderate to severe iodine deficiency was found in 16 pregnant women (19.8%), five postpartum women (19.2%), 46 patients with diabetes (34.1%) and five volunteers (26.3%). Mild iodine deficiency was found in an additional 24 pregnant women (29.6%), nine postpartum women (34.6%), 51 patients with diabetes (37.8%) and 9 normal volunteers (47.4%). Median urinary iodine concentration was 104 micrograms/L in pregnant women, 79 micrograms/L in postpartum women, 65 micrograms/L in patients with diabetes mellitus and 64 micrograms/L in volunteers. CONCLUSIONS: The high frequency of iodine deficiency found in our participants suggests that dietary sources of iodine in this country may no longer be sufficient. Further population studies are required.

An analysis for blood manganese used to assess environmental exposure.

In this graphite-furnace atomic-absorption spectrometric method for measuring manganese in whole blood, we use a pyrolytic platform to minimize interference by sample matrix. For optimal sample ashing we denature the sample within the furnace with nitric acid and use oxygen as the purge gas at low temperatures. The mean manganese concentration found in blood from 15 unexposed city dwellers was 215 (2 SD 135) nmol/L. By comparison, the range of manganese concentrations in blood sampled from a group of Australian aborigines living near a surface manganese ore deposit on Groote Eylandt, Northern Territory, was much higher (median 405 nmol/L, range 175 to 990 nmol/L).

Modification of renal and tissue cation transport by cholecystokinin octapeptide in the rabbit.

1. Reports that gastric sodium loads cause a greater natriuresis than those administered intravenously, suggest that a gastric or portal sodium monitor exists which releases a humoral natriuretic factor. To determine whether cholecystokinin octapeptide (CCK-8) had direct renal natriuretic effects (and was therefore a candidate for this gut-derived natriuretic factor) we compared the natriuretic response to CCK-8 infused intravenously with that infused directly into the renal artery of six conscious male rabbits. 2. CCK-8 produced a significant log dose-dependent decrease in the fractional excretions of calcium (P less than 0.05) and magnesium (P less than 0.005) and a log dose-dependent increase in fractional sodium excretion (P less than 0.025). The significant decreases in the fractional excretions of calcium and magnesium were accompanied by log dose-dependent falls in their plasma levels (calcium, P less than 0.05, and magnesium, P less than 0.005), indicating movement of calcium and magnesium to extravascular sites. Studies of tissue calcium and magnesium levels in response to CCK-8 infusion showed that calcium accumulated in kidney and skeletal muscle. 3. We conclude that CCK-8 has direct renal natriuretic effects at the tubular level and could be the gut-derived natriuretic factor. In addition to its effects on sodium excretion, CCK-8 causes renal retention and increased gut absorption of calcium and magnesium with movement of these ions to extravascular sites.

High aluminium content of infant milk formulas.

The aluminium content of several commercially available infant milk formulas was measured by electrothermal atomic absorption spectrometry. Results were compared with those for fresh breast milk, cow's milk, and local tap water. Differences in aluminium concentration of greater than 150-fold were found, with the lowest concentrations in breast milk.

Serotoninergic agents in the treatment of isolated sleep paralysis.

The authors report three cases of isolated sleep paralysis controlled by L-tryptophan with or without amitriptyline. Both agents increase CNS 5-hydroxytryptamine availability, whereas imipramine, which was ineffective in the one case in which it was tried, affects predominantly norepinephrine reuptake.