For different reasons interest in dietary protein intake has recently increased in diabetes research. Manipulation of protein ingestion has been used to slow down diabetic nephropathy [1]. Furthermore, epidemiological studies indicate that the quantity and quality of protein ingestion affects the expression of Type I (insulin-dependent) diabetes mellitus [2,3]. We have previously shown that a high protein diet accelerates the progression of the autoimmune loss of endogeneous insulin secretion in patients with Type I diabetes [4,5]. In general, high protein ingestion could be more detrimental in clinical situations with impaired glucose tolerance than is recognized; there is evidence that high protein intake promotes diabetes. Therefore, more knowledge is needed to decide in what way high dietary protein intake changes glucose metabolism in humans.The protein supplied by a meal is a major stimulator of insulin secretion [6]. Dietary protein potential- Diabetologia (2000) Results. Glucose-stimulated insulin secretion was increased in the high protein group (516 45 pmol/l vs 305 32, p = 0.012) due to reduced glucose threshold of the endocrine beta cells (4.2 0.5 mmol/l vs 4.9 0.3, p = 0.031). Endogeneous glucose output was increased by 12 % (p = 0.009) at 40 pmol/l plasma insulin in the high protein group, but not at higher insulin concentration whereas overall glucose disposal was reduced. Fasting plasma glucagon was 34 % increased in the high protein group (p = 0.038). Fractional gluconeogenesis was increased by 40 % in subjects receiving a high protein diet as determined by both methods. Conclusion/interpretation. High protein diet is accompanied by increased stimulation of glucagon and insulin within the endocrine pancreas, high glycogen turnover and stimulation of gluconeogenesis. [Diabetologia (2000

A new high-pressure NMR probehead designed for a 400 MHz widebore NMR spectrometer is described. For the first time, the electrical leads of the rf circuit, the tubes for the thermostating liquid and the high-pressure 'fluid, as well as the wires of the Pt-100 resistor for temperature control, are all fitted at the bottom of the high-pressure vessel. The sample can easily be removed through a top plug, which allows a relatively fast exchange of the sample. A rather simple design leads to a low-cost construction. The high-pressure vessel and the rf circuit are placed inside a standard probehead jacket, such that the high-pressure probehead can be fitted into the superconducting magnet in the same way as a commercial probehead.

This prospective study was designed to validate a novel biopsy urease test as well as a simplified ¹³C-urea breath test for the detection of Helicobacter pylori. In addition, the hypothesis was tested that both the reaction velocity of the urease test and the ¹³CO₂ excess of the urea breath test may allow a prediction of the severity of gastritis. Seventy dyspeptic patients with unknown H. pylori status were included. The H pylori status was assessed by means of culture and histology after Warthin and Starry stain. One antral and one body biopsy specimen were separately analyzed by the novel biopsy urease test (HUT). Also, a ¹³C-urea breath test using 75 mg ¹³C-labelled urea and orange juice as test meal was performed in all patients. Forty-seven patients (67%) were H. pylori positive as judged from histology and culture. In 46 patients, H. pylori infection was also detected by the novel biopsy urease test and by the urea breath test as well (sensitivity 97.9%). False-positive results were not observed by either method (specificity 100%). Both the reaction velocity of the urease test and the ¹³CO₂ excess of the breath test significantly correlated with H. pylori density and grade and activity of gastritis. The determination coefficients, however, indicated that both methods allow a reliable prediction of the severity of gastritis only in about 40-50% of the patients. In conclusion, the novel biopsy urease test and the simplified ¹³C-urea breath test proved to be highly accurate in diagnosing H. pylori infection. Despite a significant correlation, neither the reaction velocity of the urease test nor the ¹³CO₂ excess of the breath test are clinically useful for the prediction of the severity of gastritis.

Approximately 1 in 400 neonates in Turkey is affected by inherited metabolic diseases. This high prevalence is at least in part due to consanguineous marriages. Standard screening in Turkey now covers only three metabolic diseases (phenylketonuria, congenital hypothyroidism, and biotinidase deficiency). Once symptoms have developed, tandem-MS can be used, although this currently covers only up to 40 metabolites. NMR potentially offers a rapid and versatile alternative.We conducted a multi-center clinical study in 14 clinical centers in Turkey. Urine samples from 989 neonates were collected and investigated by using NMR spectroscopy in two different laboratories. The primary objective of the present study was to explore the range of variation of concentration and chemical shifts of specific metabolites without clinically relevant findings that can be detected in the urine of Turkish neonates. The secondary objective was the integration of the results from a healthy reference population of neonates into an NMR database, for routine and completely automatic screening of congenital metabolic diseases.Both targeted and untargeted analyses were performed on the data. Targeted analysis was aimed at 65 metabolites. Limits of detection and quantitation were determined by generating urine spectra, in which known concentrations of the analytes were added electronically as well as by real spiking. Untargeted analysis involved analysis of the whole spectrum for abnormal features, using statistical procedures, including principal component analysis. Outliers were eliminated by model building. Untargeted analysis was used to detect known and unknown compounds and jaundice, proteinuria, and acidemia. The results will be used to establish a database to detect pathological concentration ranges and for routine screening.