Change in pancreatic B-cell function (HOMA-B) varies in different populations with similar genetic backgrounds but different environments.

OBJECTIVE: To determine whether pancreatic B-cell function varies in different populations with similar genetic backgrounds but different environments. RESEARCH DESIGN/METHODS: We compared a specific migrant Gujarati community in the UK (n = 205) with people still resident in the same villages of origin in Gujarat, India (n = 246). Pancreatic B-cell function (HOMA-B) was determined and the influence of age, migration and other factors was explored. RESULTS: As anticipated, there was an age-related decline in log(HOMA-B) in both groups. However, the age-related fall in log(HOMA-B) was more pronounced in the UK than in Gujarat (normalized beta-0.29 vs. -0.14, P for difference = 0.03). The decline of HOMA-B with age persisted after adjustment for body mass index (UK beta = -0.31; Gujarat beta = -0.16, P = 0.015, P < 0.001). There was no significant change in insulin sensitivity (HOMA-S) with age at either site, although insulin sensitivity was lower in the UK. Fasting non-estrified fatty acid (NEFA) levels rose with age in the UK but not in Gujarat (P = 0.003 for difference in gradients). In multiple linear regression analysis, lower log(HOMA-B) was independently associated with higher fasting log(NEFA) levels; normalized beta = -0.24, P < 0.001, age; beta = -0.16, P = 0.005, higher log(insulin-like growth factor binding protein-1); beta = -0.19, P = 0.007 and lower body mass index; beta = 0.26, P = 0.001. This model accounted for 25% of the variability in HOMA-B. CONCLUSIONS: HOMA-B as a measure of B-cell function declines more rapidly with age in the migrant UK group than in Gujarat. This may be a direct consequence of chronically higher NEFA exposure in the UK group.

Isolation of a biologically active low-molecular-mass chromium compound from rabbit liver.

A low-molecular-mass chromium-binding substance (LMCr), which is recognized as a detoxification ligand of chromium, was isolated from the livers of rabbits injected intravenously with K2Cr2O7 (200 mumol Cr/kg body wt) as a biologically active form. LMCr appears as an anionic, organic Cr compound with a relative molecular mass of 1500. It is composed of glutamic acid or glutamine, glycine, cysteine and aspartic acid or asparagine with a Cr/amino-terminal residue ratio of 4:1. The purified LMCr (10-300 ng Cr/ml) shows in vitro activities comparable to those of glucose tolerance factor in relation to insulin action. In the presence of insulin it enhances [U-14C]glucose conversion to 14CO (23-30% up) in rat epididymal adipocytes above the value obtained with insulin alone. LMCr also stimulates the rate of [3-3H]glucose incorporation into lipid by 30-40% with insulin or by 15-23% without insulin, as compared with the basic value obtained with insulin alone or without insulin. These findings suggest that LMCr plays essential roles in both glucose metabolism and detoxification of invaded Cr in the body.

Chromium deficiency and cardiovascular risk.

Recent measurements have demonstrated that plasma chromium levels in patients with coronary artery disease are very much lower than in normal subjects. A review of the literature concerning the physiological functions of chromium (or GTF) shows it to be implicated in most of the known factors of cardiovascular risk, via its effect on insulin levels and activities. Chromium deficiency leads to impaired lipid and glucide metabolism and results in high circulating insulin levels, the probable consequences of which suggest that chromium deficiency may be a primary risk factor in cardiovascular disease.

Ketamine potentiates the responses of the rat superior cervical ganglion to GABA.

The responses of the rat superior cervical ganglion to gamma-aminobutyric acid (GABA) were recorded in vitro using extracellular electrodes. Ketamine was found to increase the amplitude of these responses by up to 100%. This potentiation was seen at ketamine concentrations as low as 18 microM, reached maximum at 180 microM and then declined as the concentration was raised further. Ketamine (90 microM and over) depressed the nicotinic responses of the ganglia. The log concentration-effect curve to GABA was shifted to the left, and the maximum response increased, by ketamine. Inhibition of glial uptake of GABA did not prevent the effect of ketamine. The effects of 3-aminopropane sulphonic acid, which has a very low affinity for this GABA uptake mechanism, were also increased by ketamine. We conclude that ketamine, at concentrations which are found during general anaesthesia, potentiates the responses of the ganglion to GABA, by a mechanism other than inhibition of uptake, and suggest this may be due to action at the GABA receptor site.

The relationship of chromium to the glucose tolerance factor. II.

After incubation with CrCl3 X 6H2O (or 51CrCl3 X 6H2O) for 25 days, a sterile growth medium, whole yeast cells harvested after growth on a similar chromium-containing medium for the same period, and the spent growth medium remaining after removal of the yeast were each subjected to the separation procedure reported previously [S. J. Haylock. P. D. Buckley and L. F. Blackwell, J. Inorg. Biochem., in press]. The results obtained showed that most of the eleven chromium-containing fractions isolated previously were artifacts formed as a result of direct reaction between the chromium and components of the medium. An anionic complex (which was the major chromium-containing fraction isolated) was identified as a chromium-glucose complex, but one possessing no biological activity. The biologically active chromium-containing fractions (P-3 and P-4) that were only present after yeast had been grown in the medium were further purified, however, during the purification steps, the biological activity was cleanly separated from the chromium material for both P-3 and P-4. Fraction P-4 was subsequently shown to consist of approximately 90% tyramine, but pure tyramine was not active in the yeast bioassay. Although the structure of the glucose tolerance factor-active component in fraction P-3 could not be determined due to the presence of high concentrations of salt that could not be separated on gel filtration columns, the results show that the glucose tolerance factor from brewer's yeast can no longer be regarded as a chromium complex.

Role of placenta in maternal-fetal vitamin transfer in humans.

Vitamins B12, B6, biotin, folate, thiamine, riboflavin, pantothenate, and nicotinate were determined in maternal and fetal blood and placental tissue of normovitaminemic and hypovitaminemic mothers who disclaimed supplemental vitamin intake during pregnancy. No biotin or pantothenate deficits were observed in the gravidas. Hypovitaminemic mothers transferred less B12, folate, and B6 to the fetus and placenta than normovitaminemic mothers. Vitamins given by mouth increased maternal fetal, and placental levels of folate, but B6 increased only in maternal blood and the placenta; biotin and pantothenate increased only in fetal blood. Except for riboflavin, nicotinate, and pantothenate, the intramuscular administration of vitamins increased the levels of other vitamins in maternal and fetal blood and placental tissue. Results suggest that the placenta stores vitamins and the tissue vitamin receptors must be saturated before adequate transfer of vitamins to the fetus occurs.

Dietary niacin requirements for channel catfish.

Channel catfish fingerlings were fed purified diets containing five levels (0, 25, 50, 100, and 150 mg/kg) and six levels (0, 5, 10, 25, 50, and 100 mg/kg) of supplemental niacin in 20 and 12 weeks feeding studies, respectively. The dietary niacin level required to provide maximal growth in rapidly growing channel catfish fingerlings was found to be approximately 14 mg/kg of diet. Fish fed unsupplemented diets (niacin content of 1.6 mg/kg diet) demonstrated poor growth, anemia, skin and fin lesions and hemorrhages, exophthalmia and total mortality in 20 weeks. Mortality and gross deficiency signs were prevented by 11.6 mg niacin/kg diet and anemia was prevented by 6.6 mg/kg. No histological abnormalities were observed in the heart, hepatopancreas, kidney, lateral muscle, gastrointestinal tract and gill tissues of deficient fish.