Somatotropin-induced protein anabolism in hindquarters and portal-drained viscera of growing pigs

To differentiate the effect of somatotropin (ST) treatment on protein metabolism in the hindquarter (HQ) and portal-drained viscera (PDV), growing swine (n = 20) treated with ST (0 or 150 microg x kg(-1) x day(-1)) for 7 days were infused intravenously with NaH(13)CO(3) and [(2)H(5)]phenylalanine and enterally with [1-(13)C]phenylalanine while in the fed state. Arterial, portal venous, and vena cava whole blood samples, breath samples, and blood flow measurements were obtained for determination of tissue and whole body phenylalanine kinetics under steady-state conditions. In the fed state, ST treatment decreased whole body phenylalanine flux, oxidation, and protein degradation without altering protein synthesis, resulting in an improvement in whole body net protein balance. Blood flow to the HQ (+80%), but not to the PDV, was increased with ST treatment. In the HQ and PDV, ST increased phenylalanine uptake (+44 and +23%, respectively) and protein synthesis (+43 and +41%, respectively), with no effect on protein degradation. In ST-treated and control pigs, phenylalanine was oxidized in the PDV (34-43% of enteral and arterial sources) but not the HQ. In both treatment groups, dietary (40%) rather than arterial (10%) extraction of phenylalanine predominated in gut amino acid metabolism, whereas localized blood flow influenced HQ amino acid metabolism. The results indicate that ST increases protein anabolism in young, growing swine by increasing protein synthesis in the HQ and PDV, with no effect on protein degradation. Differing results between the whole body and the HQ and PDV suggest that the effect of ST treatment on protein metabolism is tissue specific.     

Metabolic flux measurements across portal drained viscera, liver, kidney and hindquarter in mice

A method was developed to measure metabolic fluxes across either portally-drained viscera (PDV) and liver or kidney and hindquarter (HQ) in anesthetized mice. The method includes a primed-constant infusion of ketamine-medetomidine anaesthesia to stabilize the mice for the surgical procedures. For measurement of metabolic fluxes across PDV and liver, blood sampling catheters were inserted in the carotid artery, portal vein and hepatic vein and infusion catheters in the jugular vein and mesenteric vein. For measurement of metabolic flux across kidney and HQ, blood sampling catheters were inserted in the carotid artery, renal vein and caval vein and infusion catheters in the jugular vein and abdominal aorta. 14C-PAH was infused to enable plasma flow measurement using an indicator dilution method. In addition, we developed a blood sampling procedure without waste of blood. We measured plasma flow and metabolic fluxes across PDV, liver, kidney and HQ. Mean plasma flow in post-absorptive mice was: PDV: 0.9+/-0.2, liver: 1.2+/-0.3, kidney: 1.0+/-0.1, HQ: 1.1+/-0.3 ml/10 g body weight (b.w.)/min. Significant glutamine release by the HQ and uptake of glutamine by the kidney and PDV was observed. In PDV, citrulline is produced from glutamine and is in turn used by the kidney for the production of arginine. In conclusion, the described model enables measurement of metabolic fluxes across PDV, liver, kidney and HQ in mice. The availability of such a small animal model allows the potential for measuring metabolic parameters in transgenic and knockout mice, and therefore may lead to an important refinement in metabolic research.     

Fatty acid synthetase in control, starved and refed Richardson's ground squirrels

1. Starvation for 6 days reduced whole body mass and total body lipids to 76 and 71%, respectively, of pre-starvation levels in weight-gain phase ground squirrels. After 4 days of refeeding, body mass increased to 86% of pre-starvation level but total body lipids had not changed from starvation levels. 2. Compared to the fed state, fatty acid synthetase (FAS) activity in white adipose tissue (WAT) was 15 and 31% in starved and refed 4-day animals, respectively, and in liver was 26 and 21% in starved and refed 4-day animals, respectively. Lipids depleted by starvation during prehibernatory fattening were not rapidly restored in Richardson's ground squirrels. 3. Changes in these parameters with starvation and refeeding were similar in weight-loss phase animals. 4. In control animals of both phases, WAT accounted for at least 90% of total FAS activity and liver nearly all of the remainder.     

Changes in lipoprotein lipase modulate tissue energy supply during stress.

We studied the variations caused by stress in lipoprotein lipase (LPL) activity, LPL-mRNA, and local blood flow in LPL-rich tissues in the rat. Stress was produced by body immobilization (Immo): the rat's limbs were taped to metal mounts, and its head was placed in a plastic tube. Chronic stress (2 h daily of Immo) decreased total LPL activity in mesenteric and epididymal white adipose tissue (WAT) and was accompanied by a weight reduction of these tissues. In limb muscle, heart, and adrenals, total LPL activity and mRNA levels increased, and, in plasma, LPL activity and mass also increased. Acute stress (30-min Immo) caused a decrease in total LPL activity only in retroperitoneal WAT and an increase in preheparin plasma active LPL, but the overall weight of this tissue did not vary significantly. We propose an early release of the enzyme from this tissue into the bloodstream by some unknown extracellular pathways or other local mechanisms. These changes in this key energy-regulating enzyme are probably induced by catecholamines. They modify the flow of energy substrates between tissues, switching the WAT from importer to exporter of free fatty acids and favoring the uptake by muscle of circulating triacylglycerides for energy supply. Moreover, we found that acute stress almost doubled blood flow in all WAT studied, favoring the export of free fatty acids.     

Reduced exercise arteriovenous O2 difference in Type 2 diabetes.

Maximal O(2) consumption (Vo(2 max)) is lower in individuals with Type 2 diabetes than in sedentary nondiabetic individuals. This study aimed to determine whether the lower Vo(2 max) in diabetic patients was due to a reduction in maximal cardiac output (Q(max)) and/or peripheral O(2) extraction. After 11 Type 2 diabetic patients and 12 nondiabetic subjects, matched for age and body composition, who had not exercised for 2 yr, performed a bicycle ergometer exercise test to determine Vo(2 max), submaximal cardiac output, Q(max), and arterial-mixed venous O(2) (a-v O(2)) difference were assessed. Maximal workload, Vo(2 max), and maximal a-v O(2) difference were lower in Type 2 diabetic patients (P < 0.05). Q(max) was low in both groups but not significantly different: 11.2 and 10.0 l/min for controls and diabetic patients, respectively (P > 0.05). Submaximal O(2) uptake and heart rate were lower at several workloads in diabetic patients; respiratory exchange ratio was similar between groups at all workloads. Vo(2 max) was linearly correlated with a-v O(2) difference, but not Q(max) in diabetic patients. These data suggest that a reduction in maximal a-v O(2) difference contributes to a decreased Vo(2 max) in Type 2 diabetic patients.     

Energy metabolism in the digestive tract and liver of cattle: influence of physiological state and nutrition

Major functions of portal-drained viscera (PDV) and liver of cattle include absorption of digestion products and modification of the body's supply of intermediary metabolites. The disproportionately high metabolic rate of PDV and liver (7-13% of body tissues) is exemplified by their oxygen uptake (40-50% of whole body). Extensive metabolism of glucose, volatile fatty acids and amino acids by PDV modulates nutrient supply from the diet such that most responses to diet or physiological state are a function of level of diet intake. Similarly, blood flow through PDV is highly correlated with energy intake across a range of body weight, physiological state or diet composition. Most common dietary responses in metabolite uptake by PDV are changes in uptake of ammonia and volatile fatty acids, which emphasize the strong energy: nitrogen interrelationship in the rumen and subsequently the rest of the body. The liver (tissue in series with PDV) removes glucose precursors and ammonia from its blood supply as part of its functions in gluconeogenesis, ammonia detoxification and urea synthesis. The liver also alters amounts and proportions of amino acids supplied by PDV. Accountable percentages of metabolizable energy from net PDV supply include: organic acids, 41-59%; amino acids, 5-13%; and heat energy (from oxygen uptake), 11-22%.     

Brown adipose tissue, liver, and diet-induced thermogenesis in cafeteria diet-fed rats

Diet-induced thermogenesis (DIT) in young rats overeating a "cafeteria" (CAF) diet of palatable human foods is characterized by a chronic, propranolol-inhibitable elevation in resting metabolic rate (VO2) and is associated with various changes in brown adipose tissue (BAT) that have been taken as evidence for BAT as the effector of DIT. But direct evidence for participation of BAT in DIT has been lacking. By employing a nonocclusive cannula to sample the venous effluent of interscapular BAT (IBAT) for analysis of its O2 content and measuring tissue blood flow with microspheres, we accomplished direct determination (Fick principle) of the O2 consumption of BAT in conscious CAF rats. In comparison with normophagic controls fed chow, the CAF rats exhibited a 43% increase in metabolizable energy intake, reduced food efficiency, a 22% elevation in resting VO2 at 28 degrees C (thermoneutrality) or 24 degrees C (housing temperature), and characteristic changes in the properties of their BAT (e.g., increased mass, protein content and mitochondrial GDP binding). They also exhibited the greater metabolic response to exogenous noradrenaline characteristic of CAF rats and the near elimination by propranolol of their elevation in VO2. By the criterion of their elevated VO2, the CAF rats were exhibiting DIT at the time of the measurements of BAT blood flow and blood O2 levels. However, BAT O2 consumption was found to be no greater in the CAF rats than in the controls at either 28 or 24 degrees C. At 28 degrees C it accounted for less than 1% of whole body VO2; at 24 degrees C it increased to about 10% of overall VO2 in both diet groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Type B atrial receptor discharge increases on opening a nonhypotensive arteriovenous shunt in the dog

A vagovagal cardioacceleratory reflex is activated when an arteriovenous (a-v) shunt is opened in the dog. However, the receptors which initiate this reflex have not been localized. Type B atrial receptor excitation was considered to be a major component of this reflex. The effect of opening a femoral nonhypotensive a-v shunt (i.e., shunt open plus infusion of blood to compensate for the resultant fall in mean arterial and pulse pressure) on type B atrial receptor discharge and heart rate was therefore studied in seven anesthetized, artifically ventilated dogs with beta-adrenergic blockade. Right atrial and aortic blood pressures, heart rate, and type B atrial receptor discharge was studied before and after opening a femoral a-v shunt. On opening the a-v shunt there was a significant increase (44%) in the average activity of type B atrial receptors and a small, but significant (6.8%) increase in heart rate. A significant linear positive correlation was observed between the change in activity of type B atrial receptors and the shunt flow. The results suggest that type B atrial receptors may be one of the receptor groups that initiate this vagovagal reflex.     

Gastrointestinal blood flow and postprandial metabolism in swimming sea bass Dicentrarchus labrax

In trout and salmon, the metabolic costs of exercise and feeding are additive, which would suggest that gastrointestinal blood flow during exercise is maintained to preserve digestive and absorptive processes related to the specific dynamic action (SDA) of food. However, in most published studies, gastrointestinal blood flow drops during swimming, hypoxia, and general stress. To test whether gastrointestinal blood flow is spared during exercise after feeding, sea bass were instrumented with flow probes to measure cardiac output and celiacomesenteric blood flow while swimming in a respirometer before and after feeding. Swimming at 2 body lengths per second (bl s(-1)) increased metabolic rate considerably more than did feeding (208% vs. 32% increase, respectively, relative to resting), and a similar pattern was observed for cardiac output. In unfed fish, resting gastrointestinal blood flow was 13.8+/-0.5 mL min(-1) kg(-1). After feeding, resting gastrointestinal blood flow increased by 82% but then decreased progressively with increasing swimming speeds. At 2 bl s(-1), gastrointestinal blood flow in fed fish was not significantly different compared with that in unfed swimming fish, and, therefore, the data do not support the gastrointestinal sparing hypothesis. The magnitude of the SDA was maintained despite the decrease in gastrointestinal blood flow and the consequent reduction in oxygen supply to the gut. An estimate of maximal oxygen flow to the gastrointestinal tract after feeding yielded 2.6 mmol O(2) h(-1) kg(-1), but this amount is not able to cover the oxygen demand of 3.16 mmol O(2) h(-1) kg(-1). Therefore, the SDA must reflect metabolic processes in tissues other than those directly perfused by the celiacomesenteric artery.     

Lower growth hormone and higher cortisol are associated with greater visceral adiposity, intramyocellular lipids, and insulin resistance in overweight girls

Although body composition, insulin sensitivity, and lipids are markedly altered in overweight adolescents, hormonal associations with these parameters have not been well characterized. Growth hormone (GH) deficiency and hypercortisolemia predispose to abdominal adiposity and insulin resistance, and GH secretion is decreased in obese adults. We hypothesized that low-peak GH on the GH-releasing hormone (GHRH)-arginine stimulation test and high cortisol in overweight adolescents would be associated with higher regional fat, insulin resistance, and lipids. We examined the following parameters in 15 overweight and 15 bone age-matched control 12- to 18-yr-old girls: 1) body composition using dual-energy X-ray absorptiometry and MR [visceral and subcutaneous adipose tissue at L(4)-L(5) and soleus intramyocellular lipid ((1)H-MR spectroscopy)], 2) peak GH on the GHRH-arginine stimulation test, 3) mean overnight GH and cortisol, 4) 24-h urinary free cortisol (UFC), 5) fasting lipids, and 6) an oral glucose tolerance test. Stepwise regression was the major tool employed to determine relationships between measured parameters. Log peak GH on the GHRH-arginine test was lower (P = 0.03) and log UFC was higher (P = 0.02) in overweight girls. Log mean cortisol (overnight sampling) was associated positively with subcutaneous adipose tissue and, with body mass index standard deviation score, accounted for 92% of its variability, whereas log peak GH and body mass index standard deviation score accounted for 88% of visceral adipose tissue variability and log peak GH for 34% of the intramyocellular lipid variability. Log mean cortisol was independently associated with log homeostasis model assessment of insulin resistance, LDL, and HDL and explained 49-59% of the variability. Our data indicate that lower peak GH and higher UFC in overweight girls are associated with visceral adiposity, insulin resistance, and lipids.     

禁食及胰岛素水平对大鼠解偶联蛋白-1、2、3基因表达的影响

 为探讨禁食和胰岛素对解偶联蛋白 - 1、2、3基因 (UCP1 ,2 ,3)表达的影响 ,应用 RT- PCR方法观察了在不同禁食时间和应用胰岛素条件下大鼠白色脂肪组织、棕色脂肪组织和骨骼肌中 UCP1 ,2 ,3m RNA水平的变化 .UCP1基因只在大鼠棕色脂肪组织中表达 .UCP2 ,3基因在三种组织中均有表达 ,在白色脂肪组织中以 UCP2表达为主 ;在骨骼肌中以 UCP3表达为主 .过夜禁食使棕色脂肪组织 UCP1 ,3m RNA水平明显下降 (P<0 .0 1 ) ;UCP2 m RNA水平在三种组织中均呈上升反应 ,以白色脂肪组织中表现最为明显 (P<0 .0 5) ;而对白色脂肪组织和骨骼肌中 UCP3基因表达无明显影响 .禁食时间延长至 48h,除棕色脂肪组织中 UCP2 ,3基因有明显下降外 ,各组织中UCPs基因表达基本调节至正常或高于对照组水平 .胰岛素对 UCPs基因表达水平有一定的上调作用 ,这一作用对棕色脂肪组织 UCPs各基因及骨骼肌中 UCP3基因表现得尤为明显 (P<0 .0 5) .大鼠 UCPs基因表达有一定的组织特异性 ;禁食时间对三种组织中 UCPs各成员基因表达的影响有时相上的区别 ;胰岛素可以调 UCPs各成员基因的表达 .结果反映了 UCPs各成员在能量代谢调节上的不同作用 ,这为理解膳食 -产热与体重调节的关系 ,及其能量代谢平衡与疾病关系提供了实验依据     

Exercise, dobutamine, and combined atropine, norepinephrine, and epinephrine compared

We compared the cardiovascular effects evoked in conscious dogs by 1) submaximal exercise; 2) infusion of dobutamine (40 micrograms X kg-1 X min-1); and 3) infusion of a combination of atropine (0.15 mg/kg), norepinephrine (0.19 micrograms X kg-1 X min-1), and epinephrine (0.05 micrograms X kg-1 X min-1). Myocardial O2 demand, as estimated by the double product (heart rate X systolic blood pressure), was similar during all three interventions. Cardiac output and heart rate increased significantly (P less than 0.05) during each of the three interventions. Arteriovenous O2 difference and total body O2 consumption, however, increased only during submaximal exercise. Although myocardial blood flow increased similarly during each of the three interventions, blood flow to skeletal muscle and the tongue increased only during exercise. Exercise and the combined infusion of atropine, norepinephrine, and epinephrine produced similar increases in blood flow to the diaphragm and similar decreases in blood flow to the stomach. These changes in blood flow were associated with appropriate changes in vascular resistance. Additionally, blood flow to the brain, kidney, adrenal glands, liver, and intestine did not change during any of the three interventions. Thus, in dogs, submaximal exercise, infusion of dobutamine, and infusion of a combination of atropine, norepinephrine, and epinephrine to evoke a given level of estimated myocardial O2 consumption produce similar increases in cardiac output, heart rate, and myocardial blood flow. In contrast, the changes in total body O2 consumption, arteriovenous O2 difference, regional blood flow, and regional vascular resistance that occur during each of these three interventions are different.     

Absence of increased oxygen consumption in brown adipose tissue of rats exhibiting "cafeteria" diet-induced thermogenesis

Young male Sprague-Dawley rats were induced to overeat (approximately 45%) by provision of a "cafeteria" (CAF) diet of palatable human foods. Normophagic rats fed a commercial chow or a semisynthetic diet served as controls. The CAF rats exhibited (a) the reduced food efficiency and the propranolol-inhibitable elevation in resting metabolic rate (resting VO2) that are indicative of a facultative diet-induced thermogenesis (DIT) by which excess energy gain is resisted, and (b) certain changes in brown adipose tissue (BAT) that are among those taken as evidence for BAT as the effector of DIT, e.g., increased protein content and increased mitochondrial binding of GDP. To assess directly and quantitatively the contribution by BAT to the elevation in VO2 (apparent DIT) of the CAF rats, BAT O2 consumption was determined (Fick principle) from measurements of tissue blood flow (microsphere method) and the arteriovenous difference in blood O2 across interscapular BAT (IBAT). To obtain the measurements, the animals were fitted under halothane anesthesia with vascular cannulas for intraventricular injection of microspheres and sampling of arterial blood and the venous effluent of IBAT. After recovery from anesthesia and rewarming to normal body temperature the animals were placed singly in a temperature-controlled metabolic chamber and the measurements, which also included determination of resting VO2, were made 1.5-2 h later about 11:30 h. As determined from measurements made at 28 degrees C (thermoneutrality) mean values of resting VO2 for the cannulated rats were unchanged from those of intact (unoperated) CAF or control rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased norepinephrine by medium-chain triglyceride attributable to lipolysis in white and brown adipose tissue of C57BL/6J mice

A further investigation of the lipolysis induced by medium-chain triglyceride (MCT) was conducted on C57BL/6J mice fed with a diet containing 2% MCT or 2% long-chain triglyceride (LCT). Blood norepinephrine, body fat and blood lipid variables, and the protein or mRNA expression of the genes relevant to lipolysis were measured and analyzed in the white and brown adipose tissue (WAT, BAT). Decreased body fat and improved blood lipid profiles attributable to MCT were confirmed. A higher level of blood norepinephrine was observed with the MCT diet. The adipose triglyceride lipase (ATGL) activity and its mRNA expression, the expression of protein and mRNA of the beta 3 adrenergic receptor (β3-AR) in both WAT and BAT, and the hormone-sensitive lipase (HSL) activity and its mRNA expression in BAT were significantly increased in the mice with MCT feeding. The lipolysis induced by MCT might be partially mediated by increasing norepinephrine, thereafter signaling the up-regulation of β3-AR, ATGL, and HSL in WAT and BAT.     

Effect of phentolamine on the relationship between O2 consumption and delivery in sheep.

The oxygen flux challenge test (OFT) has recently been used in critically ill patients as a dynamic test for assessment of the response in oxygen consumption (VO2) to an increase in O2 delivery (QO2). Such a test may indicate whether a patient demonstrates delivery-dependent VO2. However, the increase in whole body VO2 following an increase of QO2 might be due to the agents used for the OFT. In this study, we examined the possibility of obtaining false positive OFT with an alpha-adrenergic antagonist. Five normothermic thiopentone-anaesthetised and mechanically-ventilated (inspired O2 fraction, 0.3; expired CO2 fraction, 0.045-0.055) adult sheep (25-31 kg) were investigated. The QO2 was increased in a stepwise fashion from 200 to 850 ml.min-1 by vasodilatation with intravenous infusion of phentolamine. The VO2 was calculated at each step from the product of arteriovenous. O2 content difference (CO2, a-v) and cardiac output (Qc), the latter being continuously measured with a transit-time ultrasonic flow probe placed around the main pulmonary artery. The VO2 (y) was linearly related to QO2 (x), y = 0.034 (SD 0.024) x + 29.3 (SD 3.9). The relationship between Qc (y) and CO2, a-v (x) was y = 4.6x(-1.12) (n = 69; r2 = 0.75; P = NS compared to the expected relationship for isoconsumption conditions, i.e. where Qc = VO2.(CO2, a-v)(-1). Our data suggested that under stable conditions, an infusion of phentolamine did not sufficiently alter the relationship between Qc and CO2, a-v to invalidate its use for OFT in normal sheep.     

Decreased O2 consumption and cardiac output during normobaric hyperoxia in conscious dogs

Recent reports indicate that under certain restricted conditions hyperoxia may decrease tissue O2 consumption. However, this effect has not been established for whole body O2 consumption in the intact healthy conscious state. The goal of the present study was to document the effect of hyperoxia on resting whole body O2 consumption and hemodynamics under these latter more general physiological conditions. The inspired gas was delivered by mask to six fasted resting conscious dogs and alternated hourly between air and O2-enriched air (hyperoxia) for 5 h, while hemodynamics and blood gas data were obtained every 20 min. Compared with air breathing, hyperoxia increased the mean arterial O2 tension from 95 to 475 Torr and decreased heart rate, cardiac output, pulmonary vascular resistance, and right and left ventricular work rates and thus, presumably, myocardial O2 consumption. Hyperoxia also increased systemic vascular resistance and right atrial pressure but did not change stroke volume or systemic arterial pressure. The increase in arterial O2 content during hyperoxia was counterbalanced by the decrease in cardiac output, so that O2 delivery was unchanged by hyperoxia. Surprisingly, hyperoxia decreased the arterial-to-mixed venous difference in O2 content; this decrease together with the decrease in cardiac output produced a decrease in resting whole body O2 consumption from 5.88 +/- 0.68 to 4.80 +/- 0.62 ml O2.min-1.kg-1 (P = 0.0002). It is concluded that under physiological conditions normobaric hyperoxia may decrease metabolic rate in addition to cardiac output, which may have important implications for the metabolic regulation of O2 utilization as well as for the medical and nonmedical uses of O2.     

Effects of transfusion-induced polycythemia on O2 transport during exercise in the dog

An increased hematocrit could enhance peripheral O2 transport during exercise by improving arterial O2 content. Conversely, it could reduce maximal delivery of O2 by limiting cardiac output during exercise or by limiting the distribution of blood flow to peripheral capillaries with high O2 extractions. We studied O2 transport at rest and during graded treadmill exercise in splenectomized tracheostomized dogs at normal hematocrit (38 +/- 3%), and 48 h after transfusion of type-matched donor cells. This procedure increased hematocrit (60 +/- 3%) but also increased blood volume (P less than 0.05). Following transfusion, resting cardiac output (QT) and heart rate were not different. During exercise, QT was significantly lower at each level of O2 consumption (VO2) at high hematocrit (P less than 0.01). A reduction in QT was also seen during polycythemic exercise with hypoxemia produced by breathing 12 or 10% O2 in N2. Despite the reduction in QT, mixed venous PO2 was not lower at high hematocrit, and the increase in base deficit with VO2 was not different from control measurements. O2 delivery (QT X arterial content) was similar at each level of VO2 at both levels of hematocrit, during both normoxic and hypoxic studies. Both systemic and pulmonary arterial pressures were increased at rest after transfusion (P less than 0.05). However, pulmonary and systemic pressures were not higher than control during exercise at high hematocrit. We conclude that a hematocrit of 60% with increased blood volume is not associated with a cardiac limitation of O2 delivery, nor does it interfere with peripheral O2 extraction during exercise in the dog.     

Cerebral metabolic response to submaximal exercise.

We studied cerebral oxygenation and metabolism during submaximal cycling in 12 subjects. At two work rates, middle cerebral artery blood velocity increased from 62 +/- 3 to 63 +/- 3 and 70 +/- 5 cm/s as did cerebral oxygenation determined by near-infrared spectroscopy. Oxyhemoglobin increased by 10 +/- 3 and 25 +/- 3 micromol/l (P < 0. 01), and there was no significant change in brain norepinephrine spillover. The arterial-to-internal-jugular-venous (a-v) difference for O(2) decreased at low-intensity exercise (from 3.1 +/- 0.1 to 2. 9 +/- 0.1 mmol/l; P < 0.05) and recovered at moderate exercise (to 3. 3 +/- 0.1 mmol/l). The profile for glucose was similar: its a-v difference tended to decrease at low-intensity exercise (from 0.55 +/- 0.05 to 0.50 +/- 0.02 mmol/l) and increased during moderate exercise (to 0.64 +/- 0.04 mmol/l; P < 0.05). Thus the molar ratio (a-v difference, O(2) to glucose) did not change significantly. However, when the a-v difference for lactate (0.02 +/- 0.03 to 0.18 +/- 0.04 mmol/l) was taken into account, the O(2)-to-carbohydrate ratio decreased (from 6.1 +/- 0.4 to 4.7 +/- 0.3; P < 0.05). The enhanced cerebral oxygenation suggests that, during exercise, cerebral blood flow increases in excess of the O(2) demand. Yet it seems that during exercise not all carbohydrate taken up by the brain is oxidized, as brain lactate metabolism appears to lower the balance of O(2)-to-carbohydrate uptake.     

Lung mechanics, cellularity, and surfactant after prenatal starvation in guinea pigs

Prenatal starvation in the guinea pig causes reduced pulmonary diffusing capacity and retarded alveolarization among neonates. To study the impact of such starvation on biochemical and mechanical properties of the neonatal lung, pregnant guinea pigs were fed ad libitum throughout gestation or starved with 50% rations during their last trimester. Neonatal body weight was 35% less due to starvation, and dry lung weight, DNA, and protein contents were decreased 26, 36, and 31%, respectively (P less than 0.001 for all). Hematological data indicated no anemia, hypoproteinemia, or altered glucocorticoid levels due to starvation. Total surfactant phospholipids in these neonates were reduced 61% in lavage and 35% in the neonatal lung tissue, although surfactant compositions were similar to controls. Specific lung compliance in the air-filled lungs was not altered, but the saline-filled lungs were more distensible over deflation pressures of 9-18 cmH2O (transpulmonary). Although starvation retarded both lung cellularity and surfactant, only that portion of lung elastic recoil attributable to tissue forces was affected.     

Influence of prolonged fasting on monoamine oxidase and semicarbazide-sensitive amine oxidase activities in rat white adipose tissue

Monoamine oxidase (MAO) and semicarbazide-sensitive amine oxidase (SSAO) activities are very high in white adipose tissue (WAT). SSAO, also known as Vascular Adhesion Protein-1 in vessels, is present at the surface of fat cells and independent approaches have evidenced its impressive increase during adipogenesis. However, the factors that might regulate the expression SSAO and MAO in adipose tissue are still poorly defined. Here, we report the influence of fasting on MAO and SSAO activities in adipose depots. A decrease of MAO activity occurred after three days of starvation in the intra-abdominal adipose tissue (INWAT) of male Wistar rats, regardless of their initial adiposity or fat loss. The reduced fat stores of seven-week old rats, loosing 59% of INWAT mass during fasting, contained only one half of the MAO activity found in fed control. The same reduction of MAO was observed after prolonged fasting in older rats which lose only 26% of their INWAT during the same starvation duration, leading to a fat mass comparable to that of younger fed control rats. It was therefore the endocrine and metabolic changes occurring during fasting that were responsible for the reduced MAO activity and not the amount of INWAT. Surprisingly, SSAO activity remained unchanged during starvation. In subcutaneous WAT, the changes in MAO and SSAO activities exhibited the same tendencies than those found in INWAT. Taken together, these data show that both MAO and SSAO activities increase in INWAT with age-dependent fattening, and indicate that only MAO diminishes during fasting.