Objective: The severity of obesity is often more determined by the distribution of fat depots rather than by body weight itself. Therefore, the effect of rimonabant on fat distribution pattern was investigated in female candy-fed Wistar rats. Design: Female Wistar rats were fed a high fat, high carbohydrate (candy-) diet for 12 weeks. During the last 6 weeks rats were treated with rimonabant. Food intake and body weight development were investigated, as well as effects on total body fat, especially visceral fat and ectopic lipid accumulation in skeletal muscle and liver, determined by in vivo magnetic resonance imaging/magnetic resonance spectroscopy. Results: Candy-diet increased body weight, which was predominantly due to the increased total fat mass with predominance of visceral fat accumulation. Treatment with rimonabant fully reversed the weight gain and fat deposition in the visceral cavity and skeletal muscle, in contrast to pair feeding. In spite of an only transient reduction of food intake, body weight reduction, as well as normalized body fat, reduced visceral fat and intramyocellular lipids were maintained over the treatment period. Conclusions: We conclude that additional factors other than reduced caloric intake must be responsible for the improvements in these lipid parameters. The complete cluster of results is consistent with increased lipid oxidation caused by rimonabant.

Intact as well as neuromuscular affected skeletal muscles can be precisely analysed by MR tomography with high magnetic field strengths. The substitution of muscle by adipose tissue under atrophic conditions is seen most clearly in fat images, while the morphology of small structures is predominantly shown by water images. The aim of in-vivo spectroscopy is an identification and quantification of metabolites. A relative increase in the amount of adipose tissue within atrophic muscles was confirmed by the 1-H spectrum. As concluded from 13-C and 31-P spectra there was neither a change in adipose tissue composition nor a modification of energy metabolism.

31-phosphorus spectroscopy was used to control the results of chemotherapy in a patient with an osteogenic sarcoma. The findings were compared with conventional imaging methods (DSA, MRT and conventional radiography). The imaging methods do not provide reliable information regarding growth of tumour tissue during treatment, whereas the determination of phosphate concentration in the tumour provides direct information concerning tumour metabolism.

Altered renal cellular phosphate (P_i) homeostasis may be involved in disturbed regulation of lα,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃] production in chronic renal failure. To assess cytoplasmic concentrations of P_i and other phosphate metabolites in uremia, phosphorus-magnetic resonance spectroscopy (³¹P-MRS) studies were carried out in vivo in rat remnant kidney. Five-sixths-nephrectomized animals (Nx, n = 8, serum creatinine 1.28 ± 0.18 mg/ dl) and sham-operated control animals (n = 8) were pair-fed a high-phosphate diet (1.6% phosphate, 1.0% calcium) for 19 days. In both remnant and intact kidneys, ³¹P-magnetic resonance spectra displayed six major peaks: phospho-monoesters (PME), P_i, phosphodiesters, and adenosine triphosphate (ATP)-γ -α, and -β. Phosphocreatine was absent. The relative intensity of the renal γATP signal was comparable between the remnant kidney in Nx and the sham-operated kidney in control animals and was, therefore, used as the internal standard to assess the P_i/γATP ratio. The P_i/γATP ratio was significantly (p < 0.05) increased in the remnant kidney as compared to the sham-operated control kidney (0.97 ± 0.24 in Nx vs. 0.75 ± 0.12 in sham-operated controls; means ± SE). Similarly, the PME/γATP ratio was significantly increased in Nx (p < 0.01), whereas the relative intensities of other phosphate metabolite signals were not altered in Nx. Mean serum 1,25(OH)₂D₃ concentrations were 62 pg/ml for Nx and 93 for sham-operated controls (p < 0.05); mean serum phosphate levels were 4.35 mmol/l for Nx and 2.61 for sham-operated controls (p < 0.01). The pH in the remnant kidneys was 7.20 ± 0.06 (mean ± SE, n = 8), whereas the pH in intact kidneys was 7.29 ± 0.05 (n = 8, p < 0.05). To examine the contribution of blood cells to ³¹P-magnetic resonance spectra, an exchange transfusion with a fluorocarbonated oxygen carrier (to a final hematocrit of 8%) was carried out, while animals (n = 5) were monitored by MRS. This did not significantly change the relative intensities of phosphate metabolite peaks, indicating that blood phosphorus did not measurably contribute to the renal P_i signal. The data suggest that intrarenal P_i concentration is elevated in renal failure. This could inhibit 25-hydroxyvitamin D₃-1 α-hydroxylase activity and thus have some relevance for pathogenesis of renal hyperparathyroidism.