Seasonal changes in haematology and metabolic resources in the tench

Significant variations in the number of white and red blood cells, haematocrit and haemoglobin were found throughout the year in sexually mature male and female tench Tinca tinca . In general, the lowest values were observed during autumn–winter and the highest during summer, with males exhibiting higher values than females. Plasma glucose, cholesterol and triglycerides were lower during the winter than during the summer–autumn seasons in both sexes. Gonado-somatic and hepato-somatic indices were inversely correlated in female tench throughout the year. Seasonal patterns in liver metabolic resources were very similar for both sexes. For males and females, liver glycogen and proteins increased during the autumn, whereas the liver stored lipid during spring. Dorsal muscle mainly deposited glycogen, whereas lipid was mainly stored in the ventral muscle. Relations between seasonal changes in environmental factors, such as feeding and temperature are discussed.     

Gluconeogenic pathway in liver and muscle glycogen synthesis after exercise

To determine whether prior exercise affects the pathways of liver and muscle glycogen synthesis, rested and postexercised rats fasted for 24 h were infused with glucose (200 mumol.min-1.kg-1 iv) containing [6-3H]glucose. Hyperglycemia was exaggerated in postexercised rats, but blood lactate levels were lower than in nonexercised rats. The percent of hepatic glycogen synthesized from the indirect pathway (via gluconeogenesis) did not differ between exercised (39%) and nonexercised (36%) rats. In red muscle, glycogen was synthesized entirely by the direct pathway (uptake and phosphorylation of plasma glucose) in both groups. However, only approximately 50% of glycogen was formed via the direct pathway in white muscle of exercised and nonexercised rats. Therefore prior exercise did not alter the pathways of tissue glycogen synthesis. To further study the incorporation of gluconeogenic precursors into muscle glycogen, exercised rats were infused with either saline, lactate (100 mumol.min-1.kg-1), or glucose (200 mumol.min-1.kg-1), containing [6-3H]glucose and [14C(U)]lactate. Plasma glucose was elevated one- to twofold and three- to fourfold by lactate and glucose infusion, respectively. Plasma lactate levels were elevated by about threefold during both glucose and lactate infusion. Glycogen was partially synthesized via an indirect pathway in white muscle and liver of glucose- or lactate-infused rats but not in saline-infused animals. Thus participation of an indirect pathway in white skeletal muscle glycogen synthesis required prolonged elevation of plasma lactate levels produced by nutritive support.     

Glucose infused through the portal vein enhances liver gluconeogenesis and glycogenesis from [3-14C]pyruvate in the starved rat

After a pulse of [3-14C]pyruvate, 24 hr starved rats were infused through the portal vein with two different doses of glucose (7.8 or 20.8 mg/min) or the medium, and blood was collected from the inferior cava vein at the level of the suprahepatic veins. The highest dose of glucose enhanced the appearance of [14C]glucose in blood from the 2nd to the 20th min after tracer delivery. It also enhanced production of [14C]glycogen and concentration of glycogen in the liver after 5 and 20 min. At 20 min of glucose infusion the appearance of [14C]glyceride glycerol in liver as well as liver lactate concentration and lactate/pyruvate ratio were increased. The low dose of glucose used enhanced liver values of [14C]glycogen, [14C]glycogen specific activity and glycogen concentration. Our results support the hypothesis that in the starved rat glucose is converted into C3 units prior to being deposited as liver glycogen and based on the liver zonation model (Jungermann et al., 1983) it is proposed that glucose stimulated gluconeogenesis by shifting the liver to the cytosolic redox state as a secondary consequence of increased glycolytic activity.     

不同游泳速度条件下瓦氏黄颡幼鱼的有氧和无氧代谢反应

在(25±1)℃的条件下,测定瓦氏黄颡(Pelteobagrus vachelli Richardson)幼鱼体重(4.34±0.13)g的临界游泳速度(Ucrit),然后分别以临界游泳速度的不同百分比(20、40、60、80、100%Ucrit)将实验鱼分为5个速度处理组,另外设置静止对照组和高速力竭对照组。处理组实验鱼在不同游泳速度下分别游泳20min,在此过程中测定并计算运动代谢率(Activity metabolic rate,AMR),随后测定肌肉、血液和肝脏中的乳酸、糖原和葡萄糖含量。结果显示:实验鱼的绝对临界游泳速度为(48.28±1.02)cm/s,相对临界游泳速度为(6.78±0.16)BL/s;随着游泳速度的提高AMR显著增加(Pcrit时肌乳酸和血乳酸含量显著高于80%Ucrit的水平(P0.05);100%Ucrit时肝糖原含量显著低于40%Ucrit的水平(P0.05)。经计算瓦氏黄颡幼鱼到达临界游泳速度时的无氧代谢功率比例仅为11.0%,表明其游泳运动主要以有氧代谢供能;实验鱼的无氧代谢大约在80%Ucrit才开始启动,与其他鱼类比较启动时间较晚,说明其游泳运动对无氧代谢的依赖程度较低。研究提示瓦氏黄颡幼鱼是一种有氧运动能力较强的鱼类,这一能量代谢特征可能与提高其生存适合度有关。       

Tissue glycogen and lactate handling by the developing domestic fowl

The levels of glycogen and lactate in liver, intestine, yolk sac membrane and leg and breast muscle of domestic fowl from day 10 of "in ovo" development to day 5 after hatching compared with adults have been measured and compared with the circulating concentrations in blood of glucose and lactate. Glycogen stores in most tissues increased before hatching to attain a minimum around the eclosion and then increased to adult values in muscle and liver. Lactate maintained its plasma concentrations with higher effectiveness than plasma glucose, which increased steadily up to adult levels from hatching. The study of tissue vs plasma lactate concentration ratios suggests a general activation of lactate metabolism from hatching, coinciding with the ingestion of carbohydrate-based food. Both muscles studied, as well as intestine, seem to be net lactate producers; blood cells can speculatively be considered as lactate users and liver maintains its concentration of lactate very close to that of plasma, suggesting a fast utilization of this material as well as liver being the main site for control of circulating lactate.     

Tissue glycogen and lactate handling by the developing domestic fowl

The levels of glycogen and lactate in liver, intestine, yolk sac membrane and leg and breast muscle of domestic fowl from day 10 of "in ovo" development to day 5 after hatching compared with adults have been measured and compared with the circulating concentrations in blood of glucose and lactate. Glycogen stores in most tissues increased before hatching to attain a minimum around the eclosion and then increased to adult values in muscle and liver. Lactate maintained its plasma concentrations with higher effectiveness than plasma glucose, which increased steadily up to adult levels from hatching. The study of tissue vs plasma lactate concentration ratios suggests a general activation of lactate metabolism from hatching, coinciding with the ingestion of carbohydrate-based food. Both muscles studied, as well as intestine, seem to be net lactate producers; blood cells can speculatively be considered as lactate users and liver maintains its concentration of lactate very close to that plasma, suggesting a fast utilization of this material as well as liver being the main site for control of circulating lactate.     

不同季节高原鼢鼠乳酸脱氢酶活力和同工酶谱

目的:探讨高原鼢鼠对洞道低氧高二氧化碳环境的代谢适应机制。方法:用酶活力分析法,分析春季、夏季和秋季高原鼢鼠血清乳酸脱氢酶(LDH)活力、乳酸含量和组织LDH活力,用聚丙烯酰胺凝胶电泳法分析血清和组织LDH同工酶谱。结果:高原鼢鼠血清LDH活力在春夏秋三季具有明显的差异,春季高于夏季,夏季高于秋季,血清乳酸含量表现出同样的变化趋势;春季血清中五种同工酶条带都清晰可见,夏季血清中LDH5和LDH4清晰可见,秋季血清中只能看见LDH5带。骨骼肌、心肌和脑组织LDH活力较高,而且从春季到秋季显著降低;肝、肾和肺组织LDH活力较低,肝组织LDH活力春季显著高于夏季和秋季,夏秋两季之间没有明显差异;肾和肺组织LDH活力在春季与夏季之间没有明显差异,但秋季明显降低。心、肝、肺、肾、脑和肌肉组织LDH同工酶谱,在春夏秋三季都显示出五条带,并表现出明显的组织差异;各组织同工酶含量也有不同程度的季节差异。结论:高原鼢鼠体内糖酵解过程具有明显的季节性变化,从春季到秋季依次降低,这与它们的季节性活动特点和洞道中氧气和二氧化碳的季节性波动有关。     

The influence of insulin and of contraction on glucose metabolism in the perfused diaphragm muscle from normal and streptozotocin-treated rats

1. The metabolism of [U-(14)C]glucose in perfused resting and contracting diaphragm muscle from normal rats and rats made diabetic with streptozotocin was studied in the presence and absence of insulin. 2. The incorporation of [U-(14)C]-glucose into glycogen and oligosaccharides was stimulated by insulin under all experimental conditions studied. 3. In the normal perfused resting diaphragm muscle the incorporation of radioactivity from [(14)C]glucose into lactate and CO(2) was not affected by insulin. 4. Periodic contractions, induced by electrical stimulation of the perfused diaphragm muscle in the absence of insulin, caused an increased incorporation of (14)C into glycogen and hexose phosphate esters, whereas incorporation of (14)C into lactate was greatly decreased. Production of (14)CO(2) in the contracting muscle was not significantly different from that in resting muscle. Addition of insulin to the perfusion liquid caused a further increase in formation of [(14)C]-glycogen in contracting muscle to values reached in the resting muscle in the presence of insulin. Formation of [(14)C]lactate was also stimulated by insulin, to values close to those found in the resting muscle in the presence of insulin. 5. In the diabetic resting muscle the rate of glucose metabolism was very low in the absence of insulin. Insulin increased formation of [(14)C]glycogen to the value found in normal muscle in the absence of insulin. Production of (14)CO(2) and formation of [(14)C]hexose phosphate remained unchanged. 6. In the diabetic contracting muscle production of (14)CO(2) was increased to values approaching those found in normal contracting muscle. Formation of [(14)C]lactate and [(14)C]glycogen was also increased by contraction, to normal values. Only traces of [(14)C]hexose phosphate were detectable. Addition of insulin to the perfusion medium stimulated formation of [(14)C]glycogen, to values found in normal contracting muscle. Production of [(14)C]hexose phosphate was stimulated by insulin, to approximately the values found in the normal contracting muscle. Production of (14)CO(2) and [(14)C]lactate, however, was not significantly affected by insulin. 7. These results indicate that the defects of glucose metabolism observed in perfused resting diabetic diaphragm muscle can be partially corrected by contraction, and in the presence of insulin the contracting diabetic muscle has a completely normal pattern of glycogen synthesis and lactate production, but CO(2) production remains impaired.     

不同剂量玛咖对力竭运动致大鼠运动性低血糖的保护作用

目的：探讨不同剂量玛咖对力竭运动致大鼠运动性低血糖的保护作用。方法：采用递增负荷力竭游泳训练的方法建立运动性低血糖动物模型。55只42 d龄雄性Wistar大鼠随机分为5组：①静止对照组（C组）,②运动对照组（M组）,③~⑤运动+低、中、高剂量玛咖组（LM I、LM Ⅱ,LM Ⅲ组）,每组10只（剔除不符合实验要求的大鼠5只）。每天灌胃（ig）1次,LM各组灌胃玛咖的剂量为0.2,0.4,1.2 g/kg体重,灌胃体积为5 ml/kg体重,C、M组灌胃等体积生理盐水。运动大鼠采用递增负荷力竭游泳训练42 d,42 d力竭游泳训练后,测定体重、力竭游泳时间,取血、肝脏及深层股四头肌检测相关生化指标。结果：与C组比较,M组体重、血糖水平、肌糖原与肝糖原含量、肝细胞磷酸烯醇式丙酮酸羧激酶（phosphoenol pyruvate carboxy kinase,PEPCK）表达、肝细胞阳性染色累计吸光度均值等均明显降低（P<0.05或P<0.01）;力竭游泳时间无明显差异;血乳酸含量明显升高（P<0.01）。与M组比较,LM各组体重、血糖水平、肌糖原与肝糖原含量、肝细胞PEPCK表达、肝细胞阳性染色累计吸光度均值等均明显升高（P<0.05或P<0.01）,力竭游泳时间明显延长（P<0.01）,血乳酸含量明显降低（P<0.01）。与LM I组比较,LMⅢ组体重无明显差异,LM Ⅲ组血糖水平、肌糖原与肝糖原含量、肝细胞PEPCK表达、肝细胞阳性染色累计吸光度均值等均明显升高（P<0.05）,力竭游泳时间明显延长,血乳酸含量明显降低（P<0.05）。结论：高剂量玛咖可有效抑制和延缓长时间、大负荷运动导致的运动性低血糖和运动性疲劳的发生与发展,其机制可能与优化肌糖原和肝糖原的储备量及上调糖异生限速酶PEPCK的表达,提高PEPCK活性,促进糖异生有关。     

Effects of handling and electrofishing on plasma glucose and whole blood lactate of Leuciscus cephalus

Chub Leuciscus cephalus exposed to simulated pulsed direct current electrofishing operations exhibited rapid elevations in plasma glucose and blood lactate levels. Plasma glucose levels were significantly higher 0·5 h after simulated electrofishing operations, and peaked 2 h after treatment. Glucose levels remained high for up to 4 h. No changes in plasma glucose were evident following handling. Simulated electrofishing operations and handling induced an immediate lactacidosis in chub. Initial responses to both treatments were similar except that blood lactate was significantly higher in fish exposed to simulated electrofishing operations than in handled fish 5 and 15 min after treatment. Blood lactate remained elevated in fish exposed to simulated electrofishing operations for 2 h, while blood lactate of handled fish returned to levels similar to those in the control fish within 0·5 h post‐treatment.     

Short-term insulin infused through the portal vein enhances liver gluconeogenesis and glycogenesis from [3-14C]pyruvate in the starved rat

Insulin infusion through the portal vein immediately after a pulse of [3-14C]pyruvate in 24 hr starved rats enhanced the appearance of [14C]glucose at 2, 5 and 10 min and glucose specific activity at 1, 2 and 20 min in blood collected from the cava vein at the level of the suprahepatic veins. Insulin infusion for 5 min decreased liver pyruvate concentration and enhanced both liver and plasma lactate/pyruvate ratio, and it decreased the plasma concentration of all amino acids. When insulin was infused together with glucose, [14C]glucose levels and glucose specific activity decreased in blood but there was a marked increase in liver [14C]glycogen, glycogen specific activity and glycogen concentration, and an increase in liver lactate/pyruvate ratio. The effect of insulin plus glucose infusion on plasma amino acids concentration was smaller than that found with insulin alone. It is proposed that insulin effect enhancing liver gluconeogenesis is secondary to its effect either enhancing liver glycolysis which modifies the liver's cytoplasmic oxidoreduction state to its more reduced form, increasing liver amino acids consumption or both. In the presence of glucose, products of gluconeogenesis enhanced by insulin are diverted into glycogen synthesis rather than circulating glucose. This together with results of the preceding paper (Soley et al., 1985), indicates that glucose enhances liver glycogen synthesis from C3 units in the starved rat, the process being further enhanced in the presence of insulin.     

Effect of maternal exercise on fetal liver glycogen late in gestation in the rat

To determine the effect of maternal exercise on fetal liver glycogen content, fed and fasted rats that were pregnant for 20.5 or 21.5 days were run on a rodent treadmill for 60 min at 12 m/min with a 0% grade or 16 m/min up a 10% grade. The rats were anesthetized by intravenous injection of pentobarbital sodium, and fetal and maternal liver and plasma samples were collected and frozen. Fetal liver glycogenolysis did not occur as a result of maternal exercise. Fetal blood levels of lactate increased 22-60%, but glucose, plasma glucagon, and insulin were unchanged during maternal exercise. Maternal liver glycogen decreased as a result of exercise in all groups of rats except the fasted 20.5-day-pregnant group. Plasma free fatty acids increased in all groups and blood lactate increased in fed (20.5 days) and fasted (21.5 days) pregnant rats. Maternal glucose, glucagon, and insulin values remained constant during exercise. The fetus appears to be well-protected from metabolic stress during moderate-intensity maternal exercise.     

Effect of stress and sampling site on metabolite concentration in rat plasma

The effect of mild stress on various plasma metabolites in the rat has been studied. Mild stress resulted in significant decreases in liver size and glycogen content, as well as in an increase of blood glucose. In addition, plasma lactate, insulin, glycerol and urea, as well as a number of amino acids were altered by stress. These data indicate that minimal stress can have major effects upon the composition of blood, and suggest the need for strict precautions on the handling of animals during blood sampling. The site of blood extraction--tail tip vs. neck--was also found to have a significant effect on plasma lactate, glucose and urea concentrations. In stressed animals the differences between tail- and neck blood composition were increased.     

Bioassay of insulin activity of pancreatic tissue in active and aestivated African lungfish, Protopterus annectens (Owen)

The insulin activity of the pancreatic tissues of free-swimming and aestivated African lungfish, P. annectens (Owen), was bioassayed against standard insulin in rabbits. The hepatic glycogen content and plasma glucose concentration in free-swimming and aestivated lungfish were also estimated. The liver glycogen content was 64·47 ± 6·32 and 7·19 ± 2·68 mgg⁻¹ net wt and the plasma glucose concentration was 37·62 ± 4·22 and 6·39 ± 1·29% in free-swimming and aestivated lungfish, respectively.
Extracts of pancreatic tissue of the lungfish produced a dose-dependent decrease in the plasma glucose concentration in rabbits. The magnitude of the decrease in plasma glucose concentration produced by extracts from aestivated specimens was significantly smaller (about 26%) compared to that produced by pancreatic extracts from free-swimming active lungfish (about 37%). The insulin activity of the pancreatic tissue was 0·82 ± 0·02 and 1·27 ± 0·25 iu mg⁻¹ dry pancreatic tissue weight in aestivated and free-swimming lungfish, respectively.     

Effects in vivo of food deprivation and 3-mercaptopicolinate in the glycogen-storage-disease (gsd/gsd) rat.

Intraperitoneal injection of 3-mercaptopicolinate into 24 h-food-deprived 27-week-old female control (GSD/GSD) rats lowered the concentration of circulating glucose by 66%, but glycerol and lactate concentrations were increased up to 3- and 4-fold respectively. In phosphorylase b kinase-deficient (gsd/gsd) rats the corresponding changes for blood glucose, lactate and glycerol were half those observed in the controls. Although the concentration of liver glycogen (approx. 12%, w/w) in the gsd/gsd rats was not altered during food deprivation, total hepatic glycogen was decreased by 17%. It is suggested that the gradual breakdown of the extensive hepatic glycogen stores during starvation assists in the maintenance of normoglycaemia in the gsd/gsd rat.     

Effect of cocaine on exercise endurance and glycogen use in rats

To determine the effects of cocaine on exercise endurance, male rats were injected intraperitoneally with cocaine (20 mg/kg body wt) or saline and then run to exhaustion 20 min later at 22 m/min and 15% grade. Saline-injected animals ran 74.9 +/- 16.5 (SD) min, whereas cocaine-treated rats ran only 29 +/- 11.6 min. The drug had no effect on resting blood glucose or lactate levels, nor did it affect resting glycogen levels in liver or red and white vastus muscle. However, it did reduce resting soleus glycogen content by 30%. During exercise liver and soleus glycogen depletion occurred at the same rate in saline- and cocaine-treated animals. In contrast, the rate of glycogen depletion during exercise in red and white vastus was markedly increased in cocaine-treated rats with a corresponding elevation in blood lactate (12 vs. only 5 mM in saline group) at exhaustion. These data suggest that cocaine administration (20 mg/kg) before submaximal exercise dramatically alters glycogen metabolism during exercise, and this effect has a negative impact on exercise endurance.     

Fasting and refeeding in carp,Cyprinus carpio L.: the mobilization of reserves and plasma metabolite and hormone variations

Summary Carp, Cyprinus carpio, were subjected to a short term of fasting (2 months) and 12 days of refeeding. The early changes produced in plasma metabolites and hormones (insulin and glucagon) and their respective energy contribution in liver and muscle during fasting and refeeding was studied. Two phases of fasting were differentiated. The first phase (until day 8 of fasting) was characterized by a reduction in the hepatosomatic index mainly due to glycogen mobilization. A transitory increase in plasma glucose and lactate suggested an initial increase in energy demand. No changes were produced in the percentage of glycogen and protein in muscle, but musculosomatic index and the total body muscle protein decreased. Although the most depleted tissue in this phase was the liver, the loss of energy content of total muscle was higher. Stabilization of liver glycogen content, plasma glucose and lactate levels, decreased muscle protein levels and a reduction in the rate of body weight loss characterized the second phase (from day 8 of fasting). Protein content in whole muscle decreased by 22%, similar to the first phase. The energy expenditure of both liver and muscle was lower in this phase. Plasma insulin levels decreased two-fold and plasma glucagon three-fold in the first phase and remained low in the second phase of fasting. Twelve days of refeeding produced a greater increase in daily growth rate than in the control group and a recovery of plasma insulin, glucagon and glucose levels. Liver completely recovered. In contrast, musculosomatic index, protein and lipid content indicated that muscle did not completely recover from the 2 months of fasting, although and overshoot of muscle glycogen was observed.Abbreviations ANOVA analysis of variance - bw body weight - D1, D2, D5, D8, D19, D50 1, 2, 5, 8, 19 and 50 days of fasting, respectively - GSI gonadosomatic index - HSI hepatosomatic index - MSI musculosomatic index - P-DNA deoxyribonucleic acid phosphorus     

Metabolic effects of testosterone during prolonged physical exercise and fasting

Previous studies have shown a decrease in plasma testosterone during prolonged physical exercise and 72 h fasting in rats. To determine whether this hormonal change has an influence upon energy metabolism, two experiments were carried out, in which the plasma levels of testosterone were elevated during prolonged physical exercise and fasting in male wistar rats. The effects of acute and chronic increases in the levels of circulating testosterone were studied, on the one hand after human chorionic gonadotropin (H.C.G.) injection, and on the other by prolonged testosterone perfusion with an osmotic minipump. Blood and tissue sampling were performed to evaluate blood glucose, alanine, and lactate, and tissue glycogen. The results in fed and rest control rats showed no changes in blood parameters under the effect of hypertestosteronemia but there was an increase in muscle glycogen after testosterone perfusion. In 72 h fasted rats both types of hypertestosteronemia were associated with a decrease in blood alanine and lactate ranging from 25% to 35%. Only testosterone perfusion was associated with higher concentrations of muscle glycogen. After 7 h of treadmill running, testosterone perfusion and H.C.G. injection induced a 35% decrease in blood alanine and a slight decrease in blood glucose, with no change in other parameters. Whereas an elevation in the level of testosterone can induce muscle glycogen compensation in the fed resting state, it cannot counteract the exhaustion of muscle glycogen during running.