Blood rheology and microalbuminuria in type I diabetes mellitus.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J M Court.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Pancreatic function was investigated in neonatal suckling offspring of caffeine-ingesting dams, with or without maternal sucrose supplementation, throughout pregnancy and lactation. In offspring of rats ingesting caffeine without sucrose supplementation, there was initial hyperinsulinaemia, followed by a progressive fall of plasma insulin to subnormal levels. This fall in plasma insulin coincided with depletion of pancreatic insulin stores. Both the fall in plasma insulin and depletion of pancreatic insulin stores were prevented by sucrose supplementation of caffeine-ingesting dams. Offspring of dams fed sucrose alone and control offspring also maintained pancreatic insulin stores and circulating insulin levels over the first 14 days of postnatal life. Pancreases from offspring of caffeine-exposed animals tested in vitro showed enhanced sensitivity of the insulin release process to glucose. This was reflected in the glucose concentration required to elicit half-maximal insulin release (2.4 +/- 0.2 mmol/l for caffeine offspring, 2.3 +/- 0.2 mmol/l for caffeine with sucrose, 3.8 +/- 0.3 mmol/l for sucrose and 4.1 +/- 0.3 mmol/l for control offspring, mean +/- SEM). In contrast, offspring of sucrose-supplemented (with or without caffeine) dams showed increased sensitivity of the proinsulin biosynthetic process to glucose, whereas offspring of dams ingesting caffeine alone showed no significant enhancement of the biosynthetic process compared with control offspring. Thus enhanced sensitivity of the insulin secretory process to glucose without a change in the sensitivity of the biosynthetic process in the offspring of the caffeine ingesting (non-sucrose supplemented) dams could explain the progressive depletion of pancreatic insulin stores and eventual hypoinsulinaemia seen in this group.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Studies were made of steroid metabolites excreted in the urine of 17 obese girls 11.4 to 16.8 yr and 17 normal girls 11 to 17 yr. Creatinine excretion (muscle mass), total body water (or deuterium space), lean body mass and body fat were determined in the obese girls. Extracellular volume (corrected bromide space) was also measured and by difference with body water, intracellular water or soft tissue cell mass was calculated. In normal girls 24-h creatinine excretion was determined, but body water was predicted from height and weight. It was found, as in previous studies, that the obese girls had excess muscle mass and soft tissue cell mass for height. The excess growth of muscle, lean tissue, and body length in obese girls correlated with increments in oxosteroid (17 ketosteroid) excretion. The overall weight increase correlated with increased excretion of corticosteroid metabolites--a finding of interest since a physiological Cushing's syndrome was postulated for fat girls many years ago. When the normal and obese girls were divided by age at 14 yr and the subgroups compared (normal obese) the younger girls showed differences with respect to height, weight, total body water, fat and percentage fat. Differences in steroid metabolites were not found. In older girls the same findings were made again, but here it was clear that the increments in body size, particularly muscle mass, correlated with augmented oxosteroid excretion. Evidence is cited that these findings are not just related to a larger steroid pool in obese girls.
When caffeine (1,3,7-trimethylxanthine) was introduced into the diet of rats throughout pregnancy and lactation at levels of consumption of 10 mg/kg/day, offspring of successive pregnancies showed growth reductions. This finding was not accompanied by teratogenic effects. However, following four pregnancies severely reduced offspring growth and neonatal mortality was demonstrated. The birthweights of these offspring were 72.5% of control. This study mimicked the mode of intake and quantities of caffeine consumed in many societies.
Reduced offspring growth was found following introduction of caffeine into the normal diet of rats during pregnancy and lactation. When maternal caffeine (10 mg/kg/day) was consumed together with supplementary sucrose (7 g/kg/day) the expected offspring growth reduction attributed to caffeine did not occur. It is concluded that maternal nutritional status may determine the outcome of caffeine exposure at low concentrations which mimic human usage.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Age, sex, and estimated time of onset of insulin-dependent diabetes were determined for children in Pittsburgh (N = 673), Gainesville (N = 976), Galveston (n = 741), and Melbourne (N = 851). The US cities had a decrease in new cases during the summer and peak incidence in January through April. In Melbourne, monthly trends were reversed: there were more cases during May through August. In US cities, but not in Melbourne, children less than 6 years old showed a greater variation by season than children 6 years old and older. Observations of the same fall and winter onset (in different calendar months) of insulin-dependent diabetes in Australia and the United States, and exaggeration of seasonal differences in young US children, suggest that onset of insulin-dependent diabetes is associated with seasonally varying viral diseases. Mumps and rubella infections do not seem to be responsible for much of the seasonal variation. Seasonal peaks of mumps and rubella are later than those observed for insulin-dependent diabetes, and immunization with live mumps and rubella viruses has not been associated with changes in incidence of insulin-dependent diabetes. An increase in disease incidence in boys over girls below age 6 years and in girls over boys at ages 6 through 11 years was consistently observed but not explained.
De novo lipid synthesis can be demonstrated in human fetal subcutaneous tissue cells which are in the initial stages of liquid accumulation. Lipogenic capacity measured as ability to incorporate acetate into neutral lipid was shown to increase with gestational age. This lipogenic capacity was accompanied by an increased activity of acetyl co-enzyme A carboxylase. Insulin, which is known to activate this enzyme in mature adipose tissue, increased neutral lipid synthesis in fetal subcutaneous tissue. When tissue insulin levels were determined, insulin was found from 16 wk gestation. At this time triglyceride content of the tissue was also increasing. Thus de novo fatty acid synthesis is a means by which the developing adipose cell initiates lipid accumulation.
Explore the source record for details and available documents.
In developing adipose tissue, cells of size less than 25 micron may make a major contribution to adipose tissue cell populations. This study reports the separation, identification, and sizing of infant and foetal adipose tissue small cells. Subcutaneous adipose tissue was taken from the anterior abdominal wall of children aged 2 months and 22 months. Subcutaneous tissue was also obtained from a paraumbilical site in 4 fetuses of gestational age 16 weeks. Tissue samples were fixed in buffered osmium tetroxide solution containing collidine. Aliquots of cell preparations suspended in saline on microscope slides were viewed and separated using a dissecting microscope. A diameter distribution of particle size was obtained using at least 200 cells for each preparation. There was a substantial number of cells that were smaller than 20 micron. Their modal cell size was remarkably constant in fetuses and in 2-month-old and 22-month-old infants. Ultrastructural studies show that the tissue is composed of a relatively uniform population of cells within sparsely collagenous connective tissue. Although some of the cells show no intracytoplasmic aggregates of lipid material, others show variable amounts of lipid material which can occupy a very large part of the cell volume.
Studies on the development of adipose tissue in infancy would seem essential to test the hypothesis that adult fat stores relate to the numbers of fat cells developed during early childhood. Thirty infants aged from 1-28 months and 13 fetuses of approximately 11-16 weeks of gestation obtained at therapeutic abortion and two preterm infants of 28 weeks of gestation were studied. The cells of both fetal and infant adipose tissue were separated from connective tissue and fixed by treatment with osmium tetroxide in buffered collidine using a method modified from Hirsch and Gallian (J. Lipid Res.,9:100(1968) for estimation of cell size and number. In fetal and early infancy there are two populations of cells in adipose tissue. Small cells found in tissue before birth and the first months of postnatal life do not contain fat. The larger cells, which are fat containing, represent maturing fat cells. They are cells which include fat cells recognized by previous workers but up to 24.6% were found to be less than 25 micron in diameter. Small cells in the early stages of fat accumulation may make an important contribution to the cell population of fat mass. It is apparent that increasing fat accumulation in the first 6-12 months of life, as demonstrated by increased skinfold thickness measurements, is associated with increasing fat cell size and that this association bears a linear relationship.
Explore the source record for details and available documents.