Search

Previous studies show that a high sucrose diet reduces the rate of primary dentinogenesis and increases dental caries, although their cause-effect relationship is still obscure. The purpose of this study was to explore whether the effect of sucrose load on the dentinogenesis and dental caries of young rat molars is mediated by systemic (intragastric) or by systemic and local (dietary) factors. At weaning (19 days), animals were randomized into the control, intragastric sucrose, and dietary sucrose groups for 4 weeks. The areas of dentin appositions and dentinal caries lesions were measured planimetrically. Caries was also determined with Shiffs staining and the width of predentin by histology. Urinary Ca, K, and Na levels were measured by flame photometry, urinary P levels using an UV method, and serum insulin levels using radioimmunoassay. Systemic and local sucrose load reduced dentin appositions and intragastric sucrose increased urinary Ca excretion. No differences in the width of predentin were noticed. Only dietary sucrose enhanced the occurrence and progression of caries. The present findings show that sucrose load reduces dentinogenesis by impairing the synthesis of dentin matrix, but also point out the crucial importance of the local sucrose challenge in the initiation of dental caries. [ABSTRACT FROM AUTHOR]

Skin prick tests (SPT) with freeze-dried spices and 5% (w/v) spice extracts were performed on 50 patients with 2+ or stronger SPT reactions to spices per se, and RAST were performed on 10 of them. Freeze-dried extracts produced mostly equal or stronger SPT reactions than corresponding whole spices, but 5% (w/v) extracts produced weaker reactions and also remained totally negative in some patients. Positive RAST results were seen in all 10 patients tested. The correlation between the RAST and SPT results was good for mustard and paprika, but poor for cayenne, coriander, caraway and white pepper. Five patients with positive SPT and RAST for spices contracted rhinitis from powdered spices in their working environments, and one patient suffered from gastrointestinal pains caused by spiced food. The others had noticed no clinical symptoms caused by spices. The present results thus indicate that both SPT and RAST should include purified spice extracts. [ABSTRACT FROM AUTHOR]

The European polecat (Mustela putorius) is a naturally lean carnivore prone to excessive weight gain in captivity. This study assessed its suitability to investigate the natural history of the obese phenotype displayed in overweight humans, domestic animals, and seasonally obese wild mammals. Ten farm-bred polecats were subjected to a 5-day fast with 10 controls. Obesity (40% body fat) was associated with an unfavorable plasma lipid profile and high glucose and insulin concentrations. The polecats were in phase II of fasting with normoglycemia, low liver carbohydrate stores, and decreased plasma concentrations of urea and most amino acids. Although the plasma nonesterified fatty acid (NEFA) levels were elevated, the adipose tissue lipase activities suggested a blunted lipolytic response. Lipid mobilization was more efficient from intraabdominal fat. The animals developed hepatic lipidosis with elevated NEFA influx into the liver and losses of n-3 polyunsaturated fatty acids and arginine as hypothetical etiological factors. The plasma leptin, insulin, and triiodothyronine levels decreased but were not accompanied by reduced sex steroid or increased stress hormone concentrations. The blunted lipolytic response often encountered in obesity suggests that the organism is trying to defend the obese phenotype. Liver lipidosis and decreased insulin and triiodothyronine levels seem to be among the most consistent responses to fasting manifested in diverse mammalian orders and different levels of body fatness. The polecat could be recommended as an easily accessible carnivorean model to study the natural history of the obese phenotype and its comorbidities.

The aim of this study was to investigate whether the actively wintering Palearctic sable Martes zibellina has evolved physiological adaptations to tolerate nutritional scarcity. Sixteen farm-bred male sables were divided into a fed control group and an experimental group fasted for 4 days. The rate of weight loss in the sable was similar to other medium-sized mustelids. Fasting led to hypoglycaemia and to a decreased lymphocyte percentage. The sable derived metabolic energy from both subcutaneous and intraabdominal white adipose tissues and the relative decrease in fat mass was the largest for the retroperitoneal and subcutaneous depots. Metabolic energy derived partly from body proteins indicated by the increased plasma levels of urea, uric acid and total essential amino acids. Triacylglycerols accumulated in the livers of the fasted sables and the increased plasma aminotransferase activities suggested hepatic dysfunction. The decreased plasma insulin concentrations and the elevated cortisol levels probably contributed to stimulated lipolysis and protein catabolism. Moreover, fasting increased the plasma ghrelin concentrations of the sables and down-regulated the thyroid activity.

This study investigated the physiological adaptations to fasting using the farmed blue fox (Alopex lagopus) as a model for the endangered wild arctic fox. Sixteen blue foxes were fed throughout the winter and 32 blue foxes were fasted for 22 d in Nov-Dec 2002. Half of the fasted blue foxes were food-deprived again for 22 d in Jan-Feb 2003. The farmed blue fox lost weight at a slower rate (0.97-1.02% body mass d(-1)) than observed previously in the arctic fox, possibly due to its higher initial body fat content. The animals experienced occasional fasting-induced hypoglycaemia, but their locomotor activity was not affected. The plasma triacylglycerol and glycerol concentrations were elevated during phase II of fasting indicating stimulated lipolysis, probably induced by the high growth hormone concentrations. The total cholesterol, HDL- and LDL-cholesterol, urea, uric acid and total protein levels and the urea:creatinine ratio decreased during fasting. Although the plasma levels of some essential amino acids increased, the blue foxes did not enter phase III of starvation characterized by stimulated proteolysis during either of the 22-d fasting procedures. Instead of excessive protein catabolism, it is liver dysfunction, indicated by the increased plasma bilirubin levels and alkaline phosphatase, alanine aminotransferase and aspartate aminotransferase activities, that may limit the duration of fasting in the species.

The aim of this study was to investigate the adaptations of protein metabolism to seasonal fasting in an actively wintering boreal carnivore. Fifty farm-bred male American minks Mustela vison were divided into a fed control group and four experimental groups fasted for 2, 3, 5 or 7 days. The responses of nitrogen metabolism to wintertime food deprivation were determined by measuring the rate of weight loss, the tissue total protein concentrations and the plasma amino acid, urea, ammonia, uric acid and total protein levels. The mink has relatively poor adaptations to food deprivation, as it is not able to prolong phase II of fasting with fat as the major metabolic fuel. Instead, the species has to derive a part of its energy requirements from the breakdown of body proteins. The end product of protein catabolism--urea--accumulates in its circulation, and the mink may not be able to recycle urea-N. Although the mink can still have a high body fat percent at the end of the 7-day fast, it appears to enter phase III of fasting with stimulated proteolysis during this period.

Low-grade chronic inflammation, reflected in elevated levels of serum C-reactive protein (CRP), has recently been linked to obesity, insulin resistance syndromes such as polycystic ovary syndrome (PCOS), and an increased risk of cardiovascular disease. Because the insulin sensitizer metformin has been shown to improve metabolic disturbances in PCOS, it was of particular interest to examine serum CRP levels during metformin therapy. Twenty nonobese women [body mass index (BMI) /==" BORDER="0"> 27 kg/m(2)) with PCOS were randomized to receive either metformin (500 mg twice daily for 3 months, then 1000 mg twice daily for 3 months) or ethinyl estradiol (35 micro g)-cyproterone acetate (2 mg) oral contraceptive pills. The serum concentrations of CRP were significantly higher in obese than in nonobese subjects at baseline [4.08 +/- 0.53 (SE) vs. 1.31 +/- 0.28 mg/liter; P < 0.001] and correlated to BMI and to a lesser extent waist-hip ratio, suggesting that the elevated CRP levels may be related to obesity and not only to PCOS itself. During metformin treatment, serum CRP levels decreased significantly from 3.08 +/- 0.7 mg/liter to 1.52 +/- 0.26 mg/liter at 6 months in the whole study population (P = 0.006) and especially in obese subjects. In contrast, the treatment with ethinyl estradiol-cyproterone acetate increased serum CRP levels from 2.91 +/- 0.68 mg/liter to 4.58 +/- 0.84 mg/liter (P < 0.001). Whether this effect is related to estrogen action in the liver or whether it reflects increased inflammation process and possible risks for cardiovascular disease remains unclear. The decrease of serum CRP levels during metformin therapy is in accordance with the known beneficial metabolic effects of this drug and suggests that CRP or other inflammation parameters could be used as markers of treatment efficiency in women with PCOS.

Optima from KONE Instruments Corporation is a new selective laboratory analyzer for turbidimetric, colorimetric and ion selective electrode measurements. Overall analytical performance of Optima and reagents provided by KONE was evaluated according to ECCLS guidelines, in a multicentre study involving four different laboratories, including substrates (cholesterol, high-density lipoprotein-cholesterol, creatinine), specific proteins (transferrin, IgG), enzyme activities (gamma-glutamyltransferase, alanine aminotransferase) and electrolytes (sodium, potassium, chloride). The results obtained attest good precision of the system for all the analytes tested: the range of within-run CV is 0.5 %-4.3 %, and range of between-day CV % is 0.8 %-7.9 % (median of four laboratories). Except for total cholesterol (5 % overestimation compared to the reference method) accuracy of measurement is adequate. Creatinine and uric acid assays were subjects of interference (defined as deviation > 10 % from target value) by bilirubin and haemoglobin respectively.

Elective cesarean section was performed in a consecutive series of 30 patients with full-term pregnancies who were not in labor. Epidural (lidocaine, 1.5 per cent, with epinephrine, 1:200,000) and general anesthesia (thiopental, nitrous oxide-oxygen, succinylcholine infusion) was used alternately. Neonatal acid-base values and Apgar scores showed no significant difference between the two anesthetic groups, and most infants were vigorous at birth. The neurologic recoveries of the infants showed no significant difference between the two groups. In the group receiving epidural anesthesia, there was a significant correlation between maternal hypotension and weak rooting and sucking reflexes of the infants during the first two days. All infants of high-risk obstetric patients in the series, independent of anesthetic technique used, had abnormal neurologic activity, as evidenced by either depression of muscle tone and the reflexes or all the tested variables. Neurologic assessment as followed in this series is a sensitive indicator of the effects of fetal stress factors acting during cesarean section.

To clarify the role of insulin receptors in the macrosomia and the tendency to hypoglycemia in infants of mothers with insulin-treated diabetes mellitus (IDM) we studied insulin binding in erythrocytes from mixed umbilical blood and from peripheral venous blood collected when the infants were 3-14 days old. Normal infants were matched for gestational and postnatal age. The IDM infants were macrosomic, with significantly higher birth weights relative to gestational age than the control infants. Plasma free insulin concentrations in cord blood were 15-fold higher in the IDM than in the normal infants and more than 3-fold higher in the peripheral venous blood at the median age of 4 days. Hypoglycemia occurred in 12 of the 17 IDM and in none of the normal infants. In umbilical blood insulin binding to erythrocytes was similar in the IDM and normal infants. In both groups insulin binding decreased during the first postnatal weeks, but the decrease was significantly greater in the IDM than in the normal infants. The decrease in insulin binding to erythrocytes was a consequence of decreased receptor affinity as well as decreased receptor concentration in the IDM infants, but was mainly due to decreased receptor concentration in the normal infants. We conclude that insulin binding to its erythrocyte receptor in cord blood in IDM infants is similar to that in normal infants in spite of the simultaneous gross hyperinsulinemia in the IDM infants. The resulting increase in insulin action would then contribute to the tendency toward hypoglycemia and may be partly responsible for the macrosomia in IDM infants. The marked postnatal decrease in insulin binding in IDM infants is a possible explanation for their diminishing risk of hypoglycemia after the first few days of life in spite of persisting hyperinsulinemia.

Propionic acidaemia is a defect of propionyl-CoA-carboxylase activity characterized by urinary excretion of propionic acid, its metabolites and hyperglycinaemia. The clinical picture of this autosomally, recessively inherited disorder, which has been reported in the literature in 63 patients varies from overwhelming metabolic crisis in the neonate to an almost asymptomatic disease responding to protein restriction and biotin supplementation. The first Finnish patient with propionic acidaemia had a severe type of disease with neonatal onset simulating nonketotic hyperglycinaemia. In spite of protein restriction and biotin supplementation this infant developed progressive psychomotor retardation and died of intercurrent infection at the age of 8.5 months. The definite, correct diagnosis was not reached until a severe infection occurred, during which the pathognomonic organic aciduria manifested. This delay in the diagnosis illustrates the importance of performing the analysis of urinary excretion of organic acids during stress situations, such as infections, since the metabolic block may be undetectable under normal conditions.

It is established that PRL secretion is regulated by estrogens. Glucocorticoids, on the other hand, suppress estrogen secretion during pregnancy and may also inhibit PRL by direct hypothalamopituitary action. In this study PRL and estradiol were determined with specific radioimmunoassays in 14 women during gestational weeks 28 to 34 prior to, during, and following short-term intramuscular dexamethasone administration (12, 8, and 4 mg on three consecutive days) used for prophylaxis of RDS in preterm infants. There were no significant alterations in PRL serum concentrations; estradiol showed a significant drop (P less than 0.001) during all 3 days of treatment, returning to the pretreatment level on posttreatment day 1. The PRL and TSH responses to 200 micrograms of intravenous TRH on day 2 or 3 of dexamethasone treatment in six women during late pregnancy were not inhibited. Short-term dexamethasone treatment with pharmacologic doses does not suppress the physiologic secretion and release of PRL or the release induced by TRH during late pregnancy.