57 resultados para Prolonged fasting


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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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On day 64 after artificial insemination, a six-year-old primiparous briard bitch whelped three live pups between 05.00 and 08.00. It was presented at 11.00 on the same day with failure to complete parturition. on ultrasound examination, a normal live fetus was observed and the bitch was treated with oxytocin three times during the day (1(.)0, 2(.)0 and 2(.)0 iu intramuscularly), with no effect. The following day, a higher dose of oxytocin (5(.)0 iu) was administered intramuscularly at 11.00, after a uterine ultrasound examination confirmed viability of the fetus. At 18.00 of the same day, the bitch whelped the fourth normal live pup, 37 hours after initiation of parturition and 34 hours after expulsion of the last fetus. Effectiveness of oxytocin and normal versus prolonged parturition due to uterine inertia are discussed.

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This in vitro study evaluated the effect of a prolonged erosive pH cycling on the superficial microhardness change (SMHC) and the erosive wear of different restorative materials. Eighty enamel specimens with prepared cavities of 1.5 x 1.5 mm were randomly divided into eight groups according to the restorative materials used for the fillings (RMGI - resin-modified glass-ionomer, CGI - conventional glass-ionomer, CR- composite resin, A - amalgam) and immersion media used (ERO - erosive medium or SAL - artificial saliva). During 35 days, half of the specimens were immersed in a cola drink (ERO), for 5 min, three times a day, and they remained in SAL between the erosive cycles. The other half of the specimens was immersed in SAL only, for the entire experimental period (control). Data were tested for significant differences by anova and Tukey's tests (P < 0.05). Scanning electron microscopy images were made to illustrate the enamel erosive wear and restorative materials alterations. The mean SMHC (%) and mean erosive wear (mu m) of the materials were: RMGI-ERO (30/0.5); CGI-ERO (37/0.5); CR-ERO (-0.3/0.3); A-ERO (-4/0.3); RMGI-SAL (4/0.4); CGI-SAL (-6/0.4); CR-SAL (-3/0.2) and A-SAL (2/0.4). Scanning electron microscopy images showed pronounced enamel erosive wear on groups submitted to erosive pH cycling when compared with groups maintained in saliva. In conclusion, the prolonged pH cycling promoted significantly higher alterations (SMHC and erosive wear) on the glass-ionomer cements than the CR and amalgam.

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We tested the correlation between growth rate before and after a food deprivation phase in twelve single held Nile tilapias, Oreochromis niloticus. The experiment was divided into three phases: before food deprivation (phase 1: 15 d), food deprivation (phase 2: 12 d) and refeeding (phase 3: 15 d). The specific growth rate - SGR, food conversion efficiency - FCE and feed ingestion increased significantly during phase 3. Positive and significant correlations were found either to SGR or to feed ingestion between Phase 1 and 3 but not for FCE. The SGR on phase 3, moreover, were positively correlated to FCE and feed ingestion, while on phase 1 SGR was positively correlated to FCE only. Thus, high pre-fasting SGR or feed ingestion reflects in likewise high post-fasting SGR or feed ingestion values. Moreover, since SGR and FCE are correlated to each other in both phase 1 and 3, but phase 3 SGR is also correlated to feed ingestion; we could suppose that hyperphagic behaviour could be the main compensatory mechanism. Accordingly, we suggest that a fish with an elevated growth performance shall display a proportionally raised post-fasting growth response in order to normalize its predetermined growth trajectory and resume its normal growth rate.

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Metabolic changes during the transition from post-feeding to fasting were studied in Brycon cephalus, an omnivorous teleost from the Amazon Basin in Brazil. Body weight and somatic indices (liver and digestive tract), glycogen and glucose content in liver and muscle, as well as plasma glucose, free fatty acids (FFA), insulin and glucagon levels of B. cephalus, were measured at 0, 12, 24, 48, 72, 120, 168 and 336 h after the last feeding. At time 0 h (the moment of food administration, 09.00 h) plasma levels of insulin and glucagon were already high, and relatively high values were maintained until 24 h post-feeding. Glycemia was 6.42 +/- 0.82 mM immediately after food ingestion and 7.53 +/- 1.12 MM at 12 h. Simultaneously, a postprandial replenishment of liver and muscle glycogen reserves was observed. Subsequently, a sharp decrease of plasma insulin occurred, from 7.19 +/- 0.83 ng/ml at 24 h of fasting to 5.27 +/- 0.58 ng/ml at 48 h. This decrease coincided with the drop in liver glucose and liver glycogen, which reached the lowest value at 72 h of fasting (328.56 +/- 192.13 and 70.33 +/- 14.13 mumol/g, respectively). Liver glucose increased after 120 h and reached a peak 168 h post-feeding, which suggests that hepatic gluconeogenesis is occurring. Plasma FFA levels were low after 120 and 168 h and increased again at 336 h of fasting. During the transition from post-feeding to fast condition in B. cephalus, the balance between circulating insulin and glucagon quickly adjust its metabolism to the ingestion or deprivation of food. (C) 2002 Elsevier B.V. All rights reserved.

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OBJETIVO: O objetivo deste estudo foi analisar os efeitos da corrida contínua prolongada realizada na intensidade correspondente ao início do acúmulo do lactato no sangue (OBLA) sobre o torque máximo dos extensores do joelho analisado em diferentes tipos de contração e velocidade de movimento em indivíduos ativos. MÉTODO: Oito indivíduos do gênero masculino (23,4 ± 2,1 anos; 75,8 ± 8,7 kg; 171,1 ± 4,5 cm) participaram deste estudo. Primeiramente, os sujeitos realizaram um teste incremental até a exaustão voluntária para determinar a velocidade correspondente ao OBLA. Posteriormente, os sujeitos retornaram ao laboratório em duas ocasiões, separadas por pelo menos sete dias, para realizar 5 contrações isocinéticas máximas para os extensores do joelho em duas velocidades angulares (60 e 180º.s-1) sob as condições excêntrica (PTE) e concêntrica (PTC). Uma sessão foi realizada após um período de aquecimento padronizado (5 min a 50%VO2max). A outra sessão foi realizada após uma corrida contínua no OBLA até a exaustão voluntária. Essas sessões foram executadas em ordem randômica. RESULTADOS: Houve redução significante do PTC somente a 60º.s-1 (259,0 ± 46,4 e 244,0 ± 41,4 N.m). Entretanto, a redução do PTE foi significante a 60º.s-1 (337,3 ± 43,2 e 321,7 ± 60,0 N.m) e 180º.s-1 (346,1 ± 38,0 e 319,7 ± 43,6 N.m). As reduções relativas da força após o exercício de corrida foram significantemente diferentes entre os tipos de contração somente a 180º.s-1. CONCLUSÃO: Podemos concluir que, em indivíduos ativos, a redução no torque máximo após uma corrida contínua prolongada no OBLA pode ser dependente do tipo de contração e da velocidade angular.

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In order to investigate whether prolonged stress interferes with the onset of sexual behavior at puberty and with fertility at adulthood, prepubertal male Wistar rats (40 days of age) were immobilized 6 h a day for 15 days (up to early puberty) or for 60 days (until sexual maturity). Pubertal stressed rats showed a two-fold increase in the latency for the first mount (probably due to repeated aversive experience in which a change of environment was always followed by immobilization) and a 2.5-fold increase in the frequency of thrusting (indicative of enhanced sexual performance). The apparently stimulatory effect of prolonged stress on the onset of sexual behavior is discussed in terms of increased testosterone level and interference with the complex interchanges between the neurotransmitters/neuropeptides involved in the central control of male sexual activity. Adult stressed animals were mated with normal females, which became pregnant but exhibited a more than two-fold increase in both pre-implantation and post-implantation loss, probably due to a smaller rate of fertilization and/or fertilization with damaged spermatozoa.

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The present study examined the role of branchial and orobranchial O-2 chemoreceptors in the cardiorespiratory responses, aquatic surface respiration (ASR), and the development of inferior lip swelling in tambaqui during prolonged (6 h) exposure to hypoxia. Intact fish (control) and three groups of denervated fish (bilateral denervation of cranial nerves IX+X (to the gills), of cranial nerves V+VII (to the orobranchial cavity) or of cranial nerves V alone), were exposed to severe hypoxia (Pw(O2) = 10 mmHg) for 360 min. Respiratory frequency (fR) and heart rate (fH) were recorded simultaneously with ASR. Intact (control) fish increased fR, ventilation amplitude (V-AMP) and developed hypoxic bradycardia in the first 60 min of hypoxia. The bradycardia, however, abated progressively and had returned to normoxic levels by the last hour of exposure to hypoxia. The changes in respiratory frequency and the hypoxic bradycardia were eliminated by denervation of cranial nerves IX and X but were not affected by denervation of cranial nerves V or V+VII. The VAMP was not abolished by the various denervation protocols. The fH in fish with denervation of cranial nerves V or V+VII, however, did not recover to control values as in intact fish. After 360 min of exposure to hypoxia only the intact and IX+X denervated fish performed ASR. Denervation of cranial nerve V abolished the ASR behavior. However, all (control and denervated (IX+X, V and V+VII) fish developed inferior lip swelling. These results indicate that ASR is triggered by O-2 chemoreceptors innervated by cranial nerve V but that other mechanisms, such as a direct effect of hypoxia on the lip tissue, trigger lip swelling.

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The effects of prolonged oral administration (21 days) of fumonisin B(1) (FB(1)) and aflatoxin B(1) (AFB(1)) were evaluated on male Wistar rats. The animals were housed in individual metabolic cages and submitted to the following treatments: 1-0 mug AFB(1) + 0 mg FB(1)/100g bw.; 2-72 mug AFB(1)+ 0 mg FB(1)/100 g bw; 3-0 mug AFB(1) + 0.5 mg FB(1) g bw; 4-0 mug AFB(1) + 1.5 mg FB(1)/100 g bw; 5-72 mug AFB(1) + 0.5 mg FB(1)/100g bw; 6-72 mu gAFB(1) + 1.5 mg FB(1)/100g bw. on day 21, the rats were sacrificed for evaluation. The results showed that treated animals presented differences in body weight and absolute/relative weights of liver and kidney as well as altered hepatic function and cholesterol blood levels. Rats fed with the greatest doses of AFB(1) and FB(1) gained less weight (2.79 g/day) at the end of the experimental period; their blood concentrations of liver enzymes aspartate aminotransferase (AST) and alkaline phosphatase (AP) were above control levels (130.35 mu /l and 471.00 mu /l, respectively). Blood cholesterol increased in the groups treated with the highest dose of FB(1) or FB(1) associated with AFB(1). Histopathology revealed the occurrence of apoptosis in the liver of rats exposed to FB(1). The association of aflatoxin B(1) with fumonisin B(1) at higher dose probably potentiated the effects of the higher dose of fumonisin B(1)acting singly.

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In a cross-sectional study, we assessed beta-cell function and insulin sensitivity index (ISI) with hyperglycemic clamps (10 mmol/l) in 24 subjects with impaired fasting glycemia (IFG, fasting plasma glucose [FPG] between 6.1 and 7.0 mmol/l), 15 type 2 diabetic subjects (FPG >7.0 mmol/l), and 280 subjects with normal fasting glycemia (NFG, FPG <6.1 mmol/l). First-phase insulin release (0-10 min) was lower in IFG (geometric mean 541 pmol/l (.) 10 min; 95% confidence interval [CI] 416-702 pmol/l (.) 10 min) and in type 2 diabetes (geometric mean 376 pmol/l (.) 10 min; 95% CI 247-572 pmol/l (.) 10 min) than NFG (geometric mean 814 pmol/l (.) 10 min; 95% CI 759-873 pmol/l (.) 10 min) (P < 0.001). Second-phase insulin secretion (140-180 min) was also lower in IFG (geometric mean 251 pmol/l; 95% CI 198-318 pmol/l; P = 0.026) and type 2 diabetes (geometric mean 157 pmol/l; 95% CI 105-235 pmol/l; P < 0.001) than NFG (geometric mean 295 pmol/l; 95% CI 276-315 pmol/l): IFG and type 2 diabetic subjects had a lower ISI (0.15 +/- 0.02 and 0.16 +/- 0.02 mumol/kg fat-free mass [FFM]/min/ pmol/l, respectively) than NFG (0.24 +/- 0.01 mumol/kg FFM/min/pmol/l, P < 0.05). We found a stepwise decline in first-phase (and second-phase) secretion in NFG subjects with progressive decline in oral glucose tolerance (P < 0.05). IFG subjects with impaired glucose tolerance (IGT) had lower first-phase secretion than NFG subjects with IGT (P < 0.02), with comparable second-phase secretion and ISI. NFG and IFG subjects with a diabetic glucose tolerance (2-h glucose >11.1 mmol/l) had a lower ISI than their respective IGT counterparts (P < 0.05). We conclude that the early stages of glucose intolerance are associated with disturbances in beta-cell function, while insulin resistance is seen more markedly in later stages.

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We performed hyperglycemic clamps in 283 nondiabetic Caucasians and, with multiple linear regression, determined the contribution of beta-cell function and tissue insulin sensitivity to variations in glycemia and insulinemia during oral glucose tolerance tests (OGTTs). Impaired glucose tolerance (IGT) subjects had reduced insulin sensitivity(P < .02) and beta-cell function (P < .0001). Normal glucose tolerance (NGT) subjects with first-degree type 2 diabetic relatives had reduced first and second phase insulin secretion (both, P < .05), but normal insulin sensitivity(P = .37). beta-Cell function and insulin sensitivity accounted for one fourth of the variability in glucose tolerance. Fasting plasma glucose in subjects with NGT (n = 185) was a function of both phases of insulin secretion and of insulin sensitivity tall, P < .05), whereas, in IGT subjects (n = 98), it was a function of first phase insulin secretion and insulin sensitivity(P < .01). Two-hour glycemia was a function of second phase secretion and insulin sensitivity (P < .01). Fasting and 2-hour plasma insulin levels were determined by insulin sensitivity land glycemia) in NGT subjects (P < .001), but by second phase secretion in IGT (P < .001). We conclude that beta-cell function is reduced in subjects with IGT; glycemia and insulinemia are not regulated by the same mechanisms in IGT and NGT; insulin sensitivity does not contribute to insulinemia in IGT; family history of diabetes influences beta-cell function, but not insulin sensitivity in Caucasians. Copyright (C) 2000 by W.B. Saunders Company.