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The raccoon dog (Nyctereutes procyonoides) is a middle-sized canid with profound autumnal fattening followed by winter sleep. This study investigated the effects of prolonged fasting-induced winter sleep on the fat and nitrogen metabolism of the species. Half of the animals were treated with continuous-release melatonin implants to induce artificial short photoperiod. Autumnal accumulation of fat was characterized by low plasma free fatty acid (FFA), diacylglycerol (DG), and triacylglycerol (TG) levels. After transition to winter catabolism, the circulating lipid levels increased due to enhanced lipolysis. Two months of fasting resulted in a steady 3.1 kg weight loss (28% of body mass, 0.47% day-1). Storage fat was mobilized during the winter sleep reflected by the elevated FFA and DG concentrations. The lowered insulin levels could be a stimulator for TG hydrolysis. The plasma total amino acid concentrations, urea levels, and urea-creatinine ratios decreased due to fasting, whereas ammonia and total protein concentrations remained stable. The effects of melatonin on energy metabolism were modest. The results indicate that the raccoon dog is well adapted to long-term wintertime fasting utilizing fat as the principal metabolic fuel. The species can maintain its protein catabolism constant for at least 60 days. Decreased cortisol and thyroid hormone concentrations may contribute to protein sparing. [ABSTRACT FROM AUTHOR]

A high sucrose diet reduces dentin apposition of growing rats. The mechanisms of reduction are unclear, but disturbances in calcium balance or in mineralization of predentin may explain them. In this experiment, 29 Sprague-Dawley rats, 21 days old, were weaned and randomized into calcium-deficient, high-sucrose or standard-diet groups for 3 weeks. They were given food and water ad libitum. During the experiment, animals were individually housed in metabolic cages where urine samples were collected. At ages of 21 and 40 days mineralizing dentin was marked using I.P. injections of oxytetracycline hydrochloride. At 42 days of age, the animals were anesthetized and their blood was collected by cardiac puncture. Right hemimandibles were sectioned sagittally and left hemimandibles were fixed, decalcified, and cut into histological sections. Dentin appositions were measured planimetrically, predentin width, from histological sections. Ca, K, and Na levels of serum and urine were measured flame photimetrically and P levels were measured by the UV method. Statistical analyses were done using one-way analysis of variation (ANOVA) Tuckey's HSD t test. In the calcium-deficient group, hypocalcemia, reduced dentin apposition, and increased predentin width were noticed when compared with the control group (P<0.05). Also, the increase in predentin width, caused by calcium deficiency, was significant compared with sucrose-fed animals (P<0.05). Sucrose diet reduced dentinogenesis, increased Ca excretion to urine, but also reduced urinary levels of P, K, and Na, and the differences were significant for the controls (P<0.05). In conclusion, despite the same kind of reduced dentinogenesis in calcium-deficient and high-sucrose groups, calcium imbalance or reduced mineralization of predentin does not explain reduced dentinogenesis in sucrose-fed animals. [ABSTRACT FROM AUTHOR]

Three parameters of hepatic drug metabolism, cytochrome P-450 (P-450) content, antipyrine metabolism and urinary excretion of glucaric acid (GA) were investigated in 161 patients who underwent diagnostic liver needle biopsy. P-450 and antipyrine metabolism, but not GA were related to histological changes in liver. All the parameters were significantly increased in subjects treated with enzyme-inducing drugs, the extent of induction being related to alterations in liver histology. The largest responses were seen in subjects with an intact liver and the smallest in those with hepatitis or cirrhosis. Therapy with inducers partly compensated for the impairement in drug metabolism caused by the disease process; thus, some patients with altered liver had normal values in the tests if they had been treated with inducers. There were significant correlations between in vivo and in vitro parameters of drug metabolism, but in the interpretation of data selection of the material and the parameters influenced the results. Thus, the antipyrine plasma clearance rate was directly related to P-450 and GA values, whereas the correlation between the latter and the drug half-life was non-linear. Also, comparison of selected groups of patients resulted in better correlations between the indices of drug metabolism than in the entire series. The results demonstrate that the overall picture of hepatic drug metabolism in man is largely determined by histological changes in the liver and by exposure to drugs, which are reflected differently in various assays of hepatic drug metabolism. Quantitative evaluation of these factors, and selection of the appropriate assay method, seem to be of importance in investigating hepatic drug metabolism in man. [ABSTRACT FROM AUTHOR]