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

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Recent studies have shown that systemic lupus erythematosus (SLE) is associated with a loss of trabecular bone. However, these changes have not been not described in patients with SLE at the time of diagnosis. To investigate the markers of bone metabolism 20 female patients with a recently manifested clinical picture of SLE were selected. All patients included in this study met the ARA criteria (for classification) of SLE. For comparison, 35 female patients with SLE, which had previously manifested itself and which had been treated with glucocorticoids, were included in a second group. A control group (III) consisting of 20 healthy individuals of the same age was formed to compare the results obtained. Test parameters comprised both serum levels of osteocalcin (OC) as the marker for bone formation and crosslinks excretion (CE) in urine as a specific marker for bone resorption. The bone density (BMD) was examined by dual energy X-ray absorption (DEXA) of the vertebral column (L2-L4), femoral neck, Ward's triangle and trochanter. The patients under study received either no medication or nonsteroidal antirheumatic drugs. The BMD of the vertebral column was significantly lower than expected in SLE-afflicted subjects of group II when compared with the age-matched normal female controls. The reduction of BMD in female patients with SLE was related to the significantly increased excretion of urinary pyridinoline, to hypoparathyroidism, and to the decrease in serum OC. Bone loss in women with fresh manifestation of SLE (I) increases to a degree similar to that of patients in group II. Lowered BMD predicts an increased risk for bone fractures. Therefore, female premenopausal SLE patients should be monitored for osteoporosis.