K. FRANK, S. KORTH-SCHÜTZ and R. ZIEGLER
H. Minne, S. Bellwinkel and R. Ziegler
F. Raue, H. Minne, S. Klüber and R. Ziegler
F. Raue, H. Minne, S. Bellwinkel and R. Ziegler
S. T. PARVIZI, H. W. MINNE, F. BAUSS and R. ZIEGLER
B Guerci, S Hadjadj, D Quilliot, O Ziegler and P Drouin
This study was done to elucidate the relationship between postprandial leptin and obesity, and the possible influence of the circadian rhythm on the dynamic leptin response to an oral fat load (OFLT). In experiment 1, we measured the leptin and insulin responses to an oral fat load in 16 non-diabetic obese subjects and in 16 healthy controls, matched for age and gender. In experiment 2, we measured the leptin and insulin responses to an OFLT according to the time of fat load ingestion: 0700 h (diurnal (D) test) or 2200 h (nocturnal (N) test) in nine normal-weight healthy males. Baseline leptin concentration was correlated with the body mass index, body fat mass and percentage of body fat mass in both experiments. The leptin concentrations were higher in women than in men (P<0.001). In experiment 1, the leptin concentrations were higher in obese subjects than in controls, but did not change over time in either group. The plasma insulin concentrations at baseline and during the postprandial state, as well as the area under the curve (AUC) of insulin, were higher in obese subjects than in controls (P<0.05-0. 0001). There was no correlation between postprandial insulin responses and postprandial leptin responses in either obese or control groups. In experiment 2, leptin (D vs N, 2.9+/-1.4 vs 2. 9+/-1.0 ng/ml) and insulin (D vs N, 41+/-18 vs 25+/-9 pmol/l) concentrations were similar at the beginning of the D and N tests after a 10 h fast. The leptin concentrations did not change after D or N tests and were not statistically different for D and N tests. Our results indicate that the leptin concentration in healthy controls and in obese patients is not acutely influenced by a high fat load.
H. Minne, F. Raue, S. Bellwinkel and R. Ziegler
The strain of Walker carcinosarcoma 256 described induces hypercalcaemia, hyperphosphataemia and hyperuraemia in tumour bearing rats. Changes in calcium and phosphorus excretion are observed as well as accompanying calcification of soft tissue organs and loss of bone calcium. These changes in calcium metabolism disappear after removal of the tumour, so that long-range action of the tumour can be stated. The results are discussed in comparison with three other animal models of tumour dependent hypercalcaemia.