Showing papers by "K. G. M. M. Alberti published in 1986"
TL;DR: There is a good case for retaining the term tropical diabetes until there is more information on clinical and biochemical features and on aetiology.
136 citations
TL;DR: It is concluded that hyperglycemia per se reduces delta I/ delta G and must be considered when assessing insulin responses and noninsulin-dependent diabetic subjects have defective first- and second-phase responses.
Abstract: Stepwise glucose clamps were used to study beta-cell insulin response to glucose in normal and noninsulin-dependent diabetic subjects and to study changes in response after hyperglycemia. In normal subjects, insulin increment, delta I, correlated with glucose increment above basal, delta G, during the first 6 min of hyperglycemia, r = 0.748, P less than 0.0001. After 1 h of hyperglycemia, mean delta I/ delta G was reduced from 50 to 23 (mean difference 23 +/- 5) pmol/mmol, P = 0.0002; but delta I/% change in glucose (delta G') was unaltered (2.3 vs. 1.7, mean difference 0.4 +/- 0.3 pmol/%). Second-phase response correlated with mean glucose elevation (r = 0.835, P less than 0.0001), and no plateau was reached after 3 h at 3 mmol/l above basal glucose (rate of change of insulin concentration = 0.5; range, 0.3-0.8 pmol . l-1 . min-1). In diabetic subjects, delta I/ delta G was 20% of normal, while delta I/ delta G' was 63% of normal and second-phase response 30% of normal. We conclude that hyperglycemia per se reduces delta I/ delta G and must be considered when assessing insulin responses. Noninsulin-dependent diabetic subjects have defective first- and second-phase responses.
30 citations
TL;DR: The demonstration that insulin is less effective in promoting glucose disappearance in NlDDM* does not mean that the question of insulin secretion can be answered by default because the insulin resistance may be due to changes in insulin secretion.
Abstract: Twenty-five years after Yalow and Berson’ showed how to measure insulin we still do not know if non-insulindependent diabetes mellitus (NIDDM) is essentially a disease of the pancreatic beta cell. The problem i s important because rational prevention and treatment of NIDDM depend on knowing its pathogenesis. The demonstration that insulin is less effective in promoting glucose disappearance in NlDDM* does not mean that the question of insulin secretion can be answered by default because the insulin resistance may be due to changes in insulin secretion. Indeed both abnormalities may be necessary for NIDDM, or NIDDM may be due to different defects in different patients. The answers have proved elusive. In 32 studies3 of insulin secretion in subjects of normal weight with NIDDM and fasting hyperglycaemia, 16 concluded that secretion was reduced whilst 15 concluded that it was normal or increased. The reason for this disturbing discord and ways to resolve it are examined.
16 citations
Journal Article•
TL;DR: It is concluded that AER is lower in children than in adults and that the levels of albumin excretion which are predictive of clinical diabetic nephropathy in adults may not be applicable to children.
Abstract: Microalbuminuria has been shown to predict end-stage renal failure in adults with insulin-dependent diabetes. We have measured albumin excretion rates (AER) in 106 normal adults, 64 normal children and 68 children with insulin-dependent diabetes. The median AER's in both groups of children were similar and both were significantly lower than in the adult population. In normal and diabetic children there was a significant positive correlation of AER with age, but not with duration of disease or HbA1 in the diabetic group. We conclude that AER is lower in children than in adults and that the levels of albumin excretion which are predictive of clinical diabetic nephropathy in adults may not be applicable to children.
10 citations
TL;DR: This work describes here a simple and cheap method for impregnation of filter paper which inhibits further glycosylation of haemoglobin, enabling clinically suitable HbAl determination up to 4 weeks after sampling.
Abstract: Glycosylated haemoglobin (HbAl) assay is now widely used as a measure of diabetic control, but problems with sample collection and storage limit the overall usefulness of the measurement. These factors are of importance in screening programmes, and for patient care in remote areas. In hospital practice, analysis of samples is not usually possible during an out-patient clinic and prior home-blood sampling would enable a recent result to be available for the patient's visit. Sending blood samples is inconvenient, and filter paper\" spots would be preferable. However, further glycosylation of haemoglobin during the storage and transport of dried blood must be prevented. We describe here a simple and cheap method for impregnation of filter paper which inhibits further glycosylation of haemoglobin, enabling clinically suitable HbAl determination up to 4 weeks after sampling. Blood spots were taken from 16 diabetic and four non-diabetic subjects onto Blood Collection Cards (Sigma Chemical Co., St Louis, MI, USA), which were previously impregnated with citrate buffer (0,5 molar, pH 4,5) containing semicarbazide (60 mmol/L) and aniline (25 mmol/L) to trap glucose present in the sample. Filter paper blood spots were left to air dry and stored in plastic bags at room temperature until assayed. Parallel blood samples were taken into standard EDTA tubes for reference measurement. Red blood cell haemolysates (1:20 dilution in distilled water) were prepared from the reference samples and stored at 4°C for 18 h to remove the unstable aldimine fraction. HbAl was measured using the Glyco-Gel Test KitTM (Pierce Chemical Co., Rockford, IL, USA) affinity chromatography method (betweenbatch CV 3,5%). For dried blood analysis 9 mm
5 citations