In April 1996, an outbreak of toxic polyneuropathy in cats occurred in the Netherlands. All cats had been fed one of two brands of dry cat food from one manufacturer. Chemical analyses of these foods, stomach contents, and liver and kidney of affected cats revealed contamination with the ionophor salinomycin. Epidemiologic and clinical data were collected from 823 cats, or about 1% of the cats at risk. In 21 affected cats, postmortem examination was performed. The affected cats had acute onset of lameness and paralysis of the hindlimbs followed by the forelimbs. Clinical and pathologic examination indicated a distal polyneuropathy involving both the sensory and motor nerves.

Hepatic cholesterol metabolism was studied in rats fed purified diets supplemented (9% wt/wt) with either fish oil (FO) (n-3 fatty acids) or corn oil (CO) (n-6 fatty acids) for 4 wk. Rats were equipped with permanent catheters in heart, bile duct, and duodenum to allow studies under normal feeding conditions. [3H, cholesteryl oleate-labeled small unilamellar liposomes, which are rapidly endocytosed by hepatocytes, were intravenously injected to label intrahepatic cholesterol pools, and plasma and bile were collected. FO as compared to CO induced a lowering of plasma cholesterol levels by 38% and oftriglyceride levels by 69%. This reduction in plasma lipids in FO rats was accompanied by: (a) an increased bile acid pool size (28%); (b) a fourfold increase in the ratio cholic acid/chenodeoxycholic acid in bile; (c) increased biliary excretion of cholesterol (51%) (d) accelerated excretion of endocytosed free cholesterol into bile; (e) accelerated incorporation ofendocytosed cholesterol in bile acids; (f) a significant increase in the bile acid-independent fraction of bile flow, and (g) a threefold increase in hepatic alkaline phosphatase activity. The results show that FO induces changes in transport and metabolic pathways of cholesterol in the rat liver, which result in a more rapid disposition of plasmaderived cholesterol into the bile. (J. Clin. Invest. 1991. 88:943-951.)

SummaryTo contribute to the assessment of the degree of discomfort in rats after orbital puncture, we have examined the histological changes in the intraorbital tissues caused by this technique of blood sampling. Orbits were studied from rats euthanized either within 1 min, 4 days, 28 days or S6 days after puncture while under diethyl-ether anaesthesia. The techniques of 2 animal technicians were compared, one using a broken haematocrit capillary and the other using an intact Pasteur's pipette. Non-punctured orbits served as controls.Microscopic slides containing the eye in situ at 2 horizontal levels in the orbital region were examined for 37 parameters; the slides were scored blind and in random order. Orbital puncture caused haemorrhages in the puncture track and, depending on the technique used, also in the periosteum. Four days after puncture, inflammatory reactions were present in the puncture track. Depending on the technique of puncture, these reactions were also seen in the eye muscles and periosteum or in the Harderian gland. Within 4 weeks after puncture, the lesions had healed without detectable scars. The different histological effects of the·2 techniques of orbital puncture are discussed in the light of the characteristics of these techniques.

The present study describes the effect of replacement of digestible starch by resistant starch (RS) on dietinduced thermogenesis (DIT), postprandial glucose and insulin responses, and colonic fermentation. Ten healthy males consumed three test meals, consisting of diluted, artificially-sweetened fruit syrup and either 50 g raw potato starch (550 g RS/kg), or 50 g pregelatinized potato starch (0 g RS/kg) or 30 g pregelatinized potato starch plus 20 g lactulose (670 g indigestible disaccharide/kg). The meals were served in the morning after an overnight fast. Each volunteer consumed each meal twice on six separate days in random order. Metabolic rate was measured by indirect calorimetry in the fasting state for 15 min and postprandially for 5 h. Shortly before and hourly up to 7 h after consumption of the test meal, end-expiratory breath samples were obtained for H, and CH, analysis. Shortly before the meal and 30, 60, 180, and 300min postprandially, blood samples were taken for glucose and insulin analyses. Postprandial increases in glucose and insulin levels were proportional to the amount of digestible carbohydrate in the meal. Breath H, and CH, concentrations indicated that the pregelatinized starch was not fermented and that lactulose was fermented rapidly. Fermentation of the raw starch started only 6 to 7 h after consumption, resulting in a rise in breath H, but not in CH,. The replacement of 27 g digestible starch by RS in a single meal lowered DIT by on average 90 kJ/5 h, as could also be calculated by assuming that RS does not contribute to DIT. The ingestion of lactulose resulted in a substantial rise in DIT which was most probably caused by its fermentation.Diet-induced thermogenesis: Glucose : Insulin: Resistant starch Diet-induced thermogenesis (DIT) depends on the composition of the meal, including the type of carbohydrate (Sharief & MacDonald, 1982;Schwarz et al. 1989). About 60-70 % of DIT comprises the obligatory energy costs of ingesting, digesting, absorbing and metabolizing the food consumed. The rest of the DIT can be ascribed to a facultative thermogenic effect of the food (Himms-Hagen, 1989). A meal with a high content of rapidly digestible and absorbable carbohydrate, resulting in relatively high postprandial blood glucose concentrations and hence relatively high insulin responses, may increase the facultative part of the DIT via stimulation of the sympathetic nervous system (Landsberg & Young, 1983).Resistant starch (RS) is not absorbed in the small intestine of healthy humans (Englyst et al. 1992). Therefore, RS consumption represents a lower net energy intake compared with an identical amount of digestible starch. This might be of benefit for the obese. Furthermore, because of its indigestible character, RS consumption may result in lower available at https://www.cambridge.org/core/terms. https://doi

SummaryIt has been previously reported that in 2 C57BL mouse sublines a dark pigmentation of the cranial part of the spleen occurs in up to 30% of the animals within the populations. It was not clear whether this discoloration is caused by melanosis, lipofuscinosis or haemosiderosis. With the use of light and electron microscopy of stained spleen sections, we identified the pigment in 14 out of 60 C57BL mice aged 8-lOwks. In the mice with pigmented spleens there was accumulation of melanin, predominantly in melanophores. Literature data indicate that apart from melanin, lipofuscin and haemosiderin can be observed in splenic macrophages provided that the mice are older than those studied by us. We conclude that melanin is the principal pigment causing spleen discoloration in young C57BL mice. Splenic melanosis displays inter-individual variation, but its relevance from a pathophysiological point of view remains obscure. Keywords