Net Flux Of Glucose Research Articles

A Mix of Dietary Fibres Changes Interorgan Nutrients Exchanges and Muscle-Adipose Energy Handling in Overfed Mini-Pigs.

This study evaluates the capacity of a bread enriched with fermentable dietary fibres to modulate the metabolism and nutrients handling between tissues, gut and peripheral, in a context of overfeeding. Net fluxes of glucose, lactate, urea, short chain fatty acids (SCFA), and amino acids were recorded in control and overfed female mini-pigs supplemented or not with fibre-enriched bread. SCFA in fecal water and gene expressions, but not protein levels or metabolic fluxes, were measured in muscle, adipose tissue, and intestine. Fibre supplementation increased the potential for fatty acid oxidation and mitochondrial activity in muscle (acox, ucp2, sdha and cpt1-m, p < 0.05) as well as main regulatory transcription factors of metabolic activity such as pparα, pgc-1α and nrf2. All these features were associated with a reduced muscle fibre cross sectional area, resembling to controls (i.e., lean phenotype). SCFA may be direct inducers of these cross-talk alterations, as their feces content (+52%, p = 0.05) was increased in fibre-supplemented mini-pigs. The SCFA effects could be mediated at the gut level by an increased production of incretins (increased gcg mRNA, p < 0.05) and an up-regulation of SCFA receptors (increased gpr41 mRNA, p < 0.01). Hence, consumption of supplemented bread with fermentable fibres can be an appropriate strategy to activate muscle energy catabolism and limit the establishment of an obese phenotype.

Postprandial portal glucose and lactate fluxes, insulin production, and portal vein-drained viscera oxygen consumption in growing pigs fed a high-fiber diet supplemented with a multi-enzyme cocktail.

Information on effects of supplementing fibrous diets with exogenous enzymes on nutrient absorption and energetic demands of visceral organs is scarce. Therefore, this study investigated the effects of supplementing a high-fiber (HF) diet with a multi-enzyme cocktail (MC) on net glucose and lactate portal fluxes, insulin production, and O consumption by the portal-drained viscera (PDV) and whole animal in growing pigs. The MC supplied (analyzed values) 5,397 U of xylanase, 162 U of β-glucanase, and 2,000 U of protease per kg of diet, and guaranteed minimum activities of 1,000 U of α-amylase and 25 U of pectinase per kg of diet. Three isocaloric-nitrogenous diets based on corn and soybean meal with 0% (control) or 30% distillers' dried grains with solubles (DDGS; 1:1 corn and wheat mixture; HF) and HF supplemented with MC (HF + MC) were used. Five gilts (initial BW = 22.8 ± 1.6 kg) fitted with permanent catheters in the portal vein and carotid artery (for blood sampling), and ileal vein (to infuse para-amino hippuric acid to measure blood flow rate) were fed the 3 diets at 4% BW once daily at 0900 h for 7 d in a replicated 3 × 3 Latin square design. On d 7, pigs were placed in an open-circuit indirect calorimeter to measure whole-animal O consumption and sample blood for 7 h postprandial. Net glucose and insulin production were calculated from portal-arterial differences × portal blood flow, and PDV O consumption was calculated as arterial-portal O differences × portal blood flow. Diet had no effect on postprandial whole-animal O consumption, flow rate, and lactate flux. In addition, diet had no effect on overall mean postprandial PDV O consumption. Pigs fed control had greater ( < 0.05) portal insulin and glucose fluxes, from 90 to 300 min and net glucose flux from 90 to 240 min postprandial. However, pigs fed control and HF + MC had similar net glucose flux, which was greater ( < 0.05) than in pigs fed the HF diet. In conclusion, diets did not affect the energetic demand of the PDV but adding MC to the HF diet improved postprandial net glucose portal flux in growing pigs.

Dietary Oat β-Glucan Reduces Peak Net Glucose Flux and Insulin Production and Modulates Plasma Incretin in Portal-Vein Catheterized Grower Pigs1–3

Net glucose and SCFA flux and insulin secretion into the portal vein might be associated with the incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). Our objectives were to clarify this association and study the impact of 2 doses of dietary oat β-glucan on the variables. Three 35-kg portal vein-catheterized pigs were fed 3 diets containing 0, 3, or 6% oat β-glucan concentrate (BG0, BG3, and BG6) for 7 d in a repeated 3 times 3 Latin square. On d 7, blood was sampled for 12 h postprandially. Net glucose flux and apparent hormone production were calculated from plasma portal-arterial differences times flow. Postprandially, pigs fed BG6 had lower (P lt 0.05) portal glucose at 15, 30, and 45 min and a lower (P lt 0.05) net glucose flux during the first hour. Pigs fed BG6 tended to have lower (P lt 0.10) portal C-peptide without lowering insulin, indicating that pigs fed BG6 had lower actual insulin release combined with a higher prehepatic retention of insulin. Pigs fed BG6 had lower (P lt 0.05) portal GIP and GLP-1, which in turn were correlated (R2 = 0.81 and 0.88, respectively; P lt 0.01) with portal glucose. Pigs fed BG3 and BG6 had a higher (P lt 0.05) net SCFA flux than pigs fed BG0, indicating increased fermentation. In conclusion, dietary supplementation of 6% oat β-glucan concentrate decreased net glucose flux, increased net SCFA flux, and decreased peak apparent insulin production, changes that were associated with GIP and GLP-1 mediation.

A quantitative overview of glucose dynamics in the gliovascular unit

While glucose is constantly being "pulled" into the brain by hexokinase, its flux across the blood brain barrier (BBB) is allowed by facilitative carriers of the GLUT family. Starting from the microscopic properties of GLUT carriers, and within the constraints imposed by the available experimental data, chiefly NMR spectroscopy, we have generated a numerical model that reveals several hidden features of glucose transport and metabolism in the brain. The half-saturation constant of glucose uptake into the brain (K(t)) is close to 8 mM. GLUT carriers at the BBB are symmetric, show accelerated-exchange, and a K(m) of zero-trans flux (K(zt)) close to 5 mM, determining a ratio of 3.6 between maximum transport rate and net glucose flux (T(max)/CMR(glc)). In spite of the low transporter occupancy, the model shows that for a stimulated hexokinase to pull more glucose into the brain, the number or activity of GLUT carriers must also increase, particularly at the BBB. The endothelium is therefore predicted to be a key modulated element for the fast control of energy metabolism. In addition, the simulations help to explain why mild hypoglycemia may be asymptomatic and reveal that [glucose](brain) (as measured by NMR) should be much more sensitive than glucose flux (as measured by PET) as an indicator of GLUT1 deficiency. In summary, available data from various sources has been integrated in a predictive model based on the microscopic properties of GLUT carriers.

Effect of site of starch digestion on portal nutrient net fluxes in steers

Processing of maize grain is known to modulate the site of starch digestion, thus the nature and amount of nutrients delivered for absorption. We assessed the effect of site of starch digestion on nutrient net fluxes across portal-drained viscera (PDV). Three steers, fitted with permanent digestive cannulas and blood catheters, successively received two diets containing 35 % starch as dent maize grain. Diets differed according to maize presentation: dry and cracked (by-pass, BP) v. wet and ground (control, C). Ruminal physicochemical parameters were not significantly affected. Between C and BP, the decrease in ruminal starch digestion was compensated by an increase in starch digestion in the small intestine. The amount of glucose and soluble alpha-glucoside reaching the ileum was not affected. The amount of glucose disappearing in the small intestine increased from 238 to 531 g/d between C and BP, but portal net flux of glucose remained unchanged (-97 g/d). The portal O2 consumption and net energy release were not significantly affected, averaging 16 % and 57 % of metabolizable energy intake, respectively. The whole-body glucose appearance rate, measured by jugular infusion of [6,6-2H2]glucose, averaged 916 g/d. The present study shows that the increase in the amount of glucose disappearing in the small intestine of conventionally fed cattle at a moderate intake level induces no change in portal net flux of glucose, reflecting an increase in glucose utilization by PDV. That could contribute to the low response of whole-body glucose appearance rate observed at this moderate level of intestinal glucose supply.

Hormonal control of metabolism: regulation of plasma glucose

Blood glucose concentration represents the net flux of glucose entering and leaving the blood. Glucose is delivered to the blood from the liver following ingestion of carbohydrate, from the breakdown of glycogen (the storage form of glucose) and from endogenous glucose synthesis. Glucose is removed from the blood by a number of organs and tissues, notably the brain, skeletal muscle, liver and adipose tissue. With this variety of means of entry and exit from the blood, and the complications arising from too high or too low a glucose concentration, the regulation of blood glucose is complex. Many factors affect the delivery of glucose to, and its removal from, the blood. These include dietary carbohydrate and fat, the circulating free fatty acid concentration, exercise, hypoxia and the actions of several hormones. The plasma glucose concentration is regulated by a number of hormones. Some, such as insulin, promote the clearance of glucose from the plasma, while others, including glucagon, growth hormone, and catecholamines, stimulate the production and release of glucose into the blood. A fall in plasma glucose concentration evokes a number of counter-regulatory measures designed to restore plasma glucose levels, and avoid hypoglycaemia. Basically this response involves an increase in the release of glucose into the circulation, and a decrease in tissue glucose uptake.

Glucose transport in the heart.

The heart is a unique organ in many ways. It consists of specialized muscle cells (cardiomyocytes), which are adapted to contract constantly in a coordinated fashion. This is vital to the survival of the organism given the central role of the heart in the maintenance of the cardiovascular system that delivers oxygen, metabolic substrates and hormones to the rest of the body. In order for the heart to maintain its function it must receive a constant supply of metabolic substrates, to generate ATP to maintain contractile function, without fatigue. Thus the heart is capable of utilizing a variety of metabolic substrates and is able to rapidly adapt its substrate utilization in the face of changes in substrate supply. The major metabolic substrate for the heart is fatty acids. However, up to 30% of myocardial ATP is generated by glucose and lactate, with smaller contributions from ketones and amino acids. Although glucose is not the major metabolic substrate in the heart at rest, there are many circumstances in which it assumes greater importance such as during ischemia, increased workload and pressure overload hypertrophy. Like all other cells, glucose is transported into cardiac myocytes by members of the family of facilitative glucose transporters (GLUTs). In this regard, cardiomyocytes bear many similarities to skeletal muscle, but there are also important differences. For example, the most abundant glucose transporter in the heart is the GLUT4 transporter, in which translocation to the plasma membrane represents an important mechanism by which the net flux of glucose into the cell is regulated. Because cardiomyocytes are constantly contracting it is likely that contraction mediated GLUT4 translocation represents an important mechanism that governs the entry of glucose into the heart. While this is also true in skeletal muscle, because many muscles are often at rest, insulin mediated GLUT4 translocation represents a quantitatively more important mechanism regulating skeletal muscle glucose uptake than is the case in the heart. In contrast to skeletal muscle, where most GLUT1 is in perineural sheaths (1), in the heart there is significant expression of GLUT1 (2), which under certain circumstances is responsible for a significant component of basal cardiac glucose uptake. This review will summarize the current state of knowledge regarding the regulation of glucose transporter expression, and the regulation of glucose transport into myocardial cells.

A Flux Model of Glycolysis and the Oxidative Pentosephosphate Pathway in Developing Brassica napus Embryos

Developing oilseeds synthesize large quantities of triacylglycerol from sucrose and hexose. To understand the fluxes involved in this conversion, a quantitative metabolic flux model was developed and tested for the reaction network of glycolysis and the oxidative pentose phosphate pathway (OPPP). Developing Brassica napus embryos were cultured with [U-13C6]glucose, [1-13C]glucose, [6-13C]glucose, [U-13C12]sucrose, and/or [1,2-13C2]glucose and the labeling patterns in amino acids, lipids, sucrose, and starch were measured by gas chromatography/mass spectrometry and NMR. Data were used to verify a reaction network of central carbon metabolism distributed between the cytosol and plastid. Computer simulation of the steady state distribution of isotopomers in intermediates of the glycolysis/OPPP network was used to fit metabolic flux parameters to the experimental data. The observed distribution of label in cytosolic and plastidic metabolites indicated that key intermediates of glycolysis and OPPP have similar labeling in these two compartments, suggesting rapid exchange of metabolites between these compartments compared with net fluxes into end products. Cycling between hexose phosphate and triose phosphate and reversible transketolase velocity were similar to net glycolytic flux, whereas reversible transaldolase velocity was minimal. Flux parameters were overdetermined by analyzing labeling in different metabolites and by using data from different labeling experiments, which increased the reliability of the findings. Net flux of glucose through the OPPP accounts for close to 10% of the total hexose influx into the embryo. Therefore, the reductant produced by the OPPP accounts for at most 44% of the NADPH and 22% of total reductant needed for fatty acid synthesis.

Hormonal Control of Metabolism: Regulation of Plasma Glucose

Blood glucose concentration represents the net flux of glucose entering and leaving the blood. Glucose is delivered to the blood from the liver following ingestion of carbohydrate, from the breakdown of glycogen (the storage form of glucose) and from endogenous glucose synthesis. Glucose is removed from the blood by a number of organs and tissues, notably the brain, skeletal muscle, liver and adipose tissue. With this variety of means of entry and exit from the blood, and the complications arising from too high or too low a glucose concentration, the regulation of blood glucose is complex. Many factors affect the delivery of glucose to, and its removal from, the blood. These include dietary carbohydrate and fat, the circulating free fatty acid concentration, exercise, hypoxia and the actions of several hormones. The postprandial blood glucose concentration is about 4-5.5 mmol/l or 70-100 mg/100 ml, but arterial concentrations vary throughout the day from about 3.5 mmol/l after exercise to 9 mmol/l following a meal. For the purposes of this article, it is the plasma fraction of blood glucose that is of most interest, because the plasma glucose concentration is the driving force behind the diffusion of glucose molecules across the capillary wall into the interstitial space.

Effect of Supply of Metabolizable Protein on Splanchnic Fluxes of Nutrients and Hormones in Lactating Dairy Cows

The effect of the supply of metabolizable protein on splanchnic fluxes of nutrients and hormones was measured in six catheterized late-lactation Holstein cows in a crossover design. Two isonitrogenous diets (16.3% CP), but differing in rumen protein degradability and estimated metabolizable protein (MP) supply (1654g/d, Lo-MP; 1930g/d, Hi-MP) were fed, each over a 35-d experimental period. On d 34 or 35, net fluxes of nutrients and hormones across the portal-drained viscera, the liver, and total splanchnic tissues were determined. Portal absorption of total, essential, nonessential, and branched-chain amino acids (AA) increased with the Hi-MP diet. Approximately 76% of the additional metabolizable protein supply was recovered as extra AA-N absorption in the portal vein. Liver removal of AA was not different between diets, and this resulted in a greater net release across the splanchnic tissues for the Hi-MP diet. This extra AA supply provided substrates for the observed increased milk protein yield for the Hi-MP diet. Fractional efficiencies of conversion of absorbed individual essential AA into milk protein ranged from 0.42 to 0.68. The corresponding efficiencies for utilization of postsplanchnic AA supply were 0.42 to 1.80. Provision of methionine, phenylalanine, and histidine beyond the liver were similar to outputs in milk protein but the other essential AA were supplied to peripheral tissues in excess of milk output, indicative of oxidative mechanisms in nonhepatic tissues. Net fluxes of glucose, NH3-N, and urea were not affected by the diets. Neither arterial concentrations of insulin, somatotropin, or IGF-1, nor net transfers across the portal-drained viscera or liver of insulin, were affected by the diets. Although portal release of glucagon was not different between the diets, a smaller proportion was removed by the liver on the Hi-MP diet. Metabolism of AA across the splanchnic tissue bed is a major determinant of the quantity and the profile of AA delivered to peripheral tissues.

Relationship of portal-drained viscera and liver net flux of glucose, lactate, volatile fatty acids, and nitrogen metabolites to milk production in the ewe.

The objectives of this study were, first, to determine the relationship between hepatic glucose release and milk production and, second, to determine the relationship between net hepatic uptake of gluconeogenic precursors and milk production. Nine multiparous ewes were individually penned and fed an alfalfa hay-based diet for ad libitum intake. Catheters were surgically placed in the portal vein, a branch of the hepatic vein, a mesenteric vein, and the abdominal aorta. Metabolite fluxes across the portal-drained viscera and liver were subsequently measured at 1, 3, 6, and 10 wk after parturition. Net hepatic glucose release, net hepatic lactate uptake, and net hepatic propionate uptake increased with increased milk production. Hepatic oxygen consumption increased with increased net hepatic glucose release. Net hepatic glucose release increased with increased hepatic propionate uptake and tended to increase with increases in metabolized amino acid and lactate uptakes. The observed increases in oxygen consumption by the portal-drained viscera with increased milk production were probably the result of increased nutrient flux. Increased hepatic oxygen consumption with increased milk production was probably due to increased glucose and urea synthesis.

Net flux of glucose, lactate, volatile fatty acids, and nitrogen metabolites across the portal-drained viscera and liver of pregnant ewes.

Our objective for this study was to determine the pattern of nutrient flux across the portal-drained viscera (PDV) and liver in ewes with varying numbers of fetuses. Catheters were placed in the hepatic portal vein, a branch of the hepatic vein, a mesenteric vein, and the abdominal aorta of ewes. Blood flow and net nutrient release across the PDV and liver were determined before exposure to rams. Ewes were then mated, which resulted in two ewes not pregnant and in six ewes with single and 11 ewes with twin lambs. Additional measurements were taken 103, 82, 61, 39, 19, and 6 d before parturition. Net PDV glucose release did not differ from zero (-.4 +/- 8.4 mmol/h; P = .58). In ewes with singles, premating net hepatic glucose release was 34.4 +/- 2.4 mmol/h, and 19 d before parturition it was 46.2 +/- 3.8 mmol/h. In ewes with twins, premating net hepatic glucose release was 36.8 +/- 2.7 mmol/h, and 19 d before parturition it was 47.4 +/- 2.8 mmol/h. Net PDV lactate release did not differ with litter size (P = .58) or days from parturition (P = .14; 9.7 +/- 4.6 mmol/h). Net lactate uptake by the liver increased in pregnant ewes as the pregnancy progressed (P < .001). The hepatic extraction ratio for lactate increased in late pregnancy (P = .02). Net PDV and hepatic release of acetate and propionate were not different with litter size or days from parturition. Hepatic extraction ratios of VFA did not differ with litter size or day from parturition. The patterns of change in hepatic metabolite fluxes are similar to the patterns of change in gravid uterus metabolite uptake. Hepatic lactate uptake seems to be regulated during pregnancy.

Effects of dietary maize level on net flux across splanchnic tissues of oxygen and nutrients in wethers consuming ad libitum different forages

AbstractCrossbred wethers (34 (s.e. 0·9) kg), with catheters in a hepatic vein, the portal vein and a mesenteric vein and artery, were offered ad libitum alfalfa (A), bermudagrass (B) or ryegrass-wheat (RW) hay and approximately 0, 200 or 400 g/kg maize (dry matter) to determine influences of maize level on net flux of oxygen and nutrients across the portal-drained viscera (PDV) and liver with different forage sources. Digestible energy intake (MJ/day) was 8·5, 12·0 and 12·8 (s.e. VIS) for A; 4·5, 5·5 and 9·0 (s.e. 0·93) for B; and 9·4, 8·8 and 12·2 (s.e. 0·93) for RW with 0, 200 and 400 g/kg maize, respectively. Splanchnic bed oxygen consumption (mmol/h) was 301, 304 and 322 (s.e. 27·2) for A; 178, 187 and 217 (s.e. 30·0) for B; and 226, 133 and 233 (s.e. 19·0) for RW with 0, 200 and 400 g/kg maize, respectively. Increasing dietary maize level linearly increased (P &lt; 0·05) PDV release of alpha-amino nitrogen with B (5, 9 and 14 mmol/h) but not with A or RW. Dietary maize level did not consistently alter PDV or hepatic net flux of urea or ammonia nitrogen, suggesting that changes in ruminally fermentable organic matter from diets offered ad libitum, presumably induced by varying dietary concentrate level, may not alter nitrogen recycling when forage is 86 g/kg or greater in crude protein. Propionate release by the PDV and hepatic uptake increased linearly (P &lt; 0·08) as maize level in A and B diets increased, although increasing dietary maize level did not significantly alter PDV, hepatic or splanchnic bed net flux of glucose regardless of forage source. Nevertheless, glucose concentration in arterial blood with A and RW increased linearly fP &lt; 0·05) with increasing maize level, suggesting increased peripheral glucose availability. In conclusion, the potential to decrease energy consumption by splanchnic tissues relative to digestible energy intake by dietary inclusion of maize, thereby increasing the proportion of absorbed energy available to extra-splanchnic tissues, may be greater for low-quality forage than for forage of moderate or high quality and for moderate v. low dietary levels of maize with low-quality forage.

Effects of different supplements on splanchnic oxygen consumption and net fluxes of nutrients in sheep consuming bromegrass (Bromus inermis) hay ad libitum

Fifteen sheep (53 kg), with catheters in a hepatic vein, the portal vein and a mesenteric vein and artery, were offered a bromegrass (Bromus inermis) hay (104 g crude protein (CP), 700 g neutral-detergent fibre and 65 g acid-detergent lignin/kg dry matter (DM) ad lib. with different supplements to determine the effects on net flux of oxygen and nutrients across the portal-drained viscera (PDV) and liver. The sheep were unsupplemented (Control) or received 5 g DM/kg body weight (BW) of ground maize (M), 7 g DM/kg BW of soya-bean hulls (H) or 0.73 g DM/kg BW of a mix of feedstuffs high in rumenundegradable protein (P). Apparent digestible energy (DE) intakes were 5.3, 10.4, 10.6 and 6.7 (SE 0.74) MJ/d and apparent digestible CP intakes were 37, 50, 79 and 68 (SE 4.3) g/d for Control, M, H and P treatments respectively. Splanchnic tissue oxygen consumption rates were 0.23, 0.32, 0.30 and 0.27 (SE 0.054) mol/h, and oxidative metabolism accounted for 0.46, 0.31, 0.33 and 0.47 (SE 0.051) of DE intakes for Control, M, H and P treatments respectively. Supplements increased (P < 0.05) release of alpha-amino nitrogen (AAN) by the PDV (4.2, 17.5, 19.6 and 18.1 mmol/h for Control, M, H and P treatments respectively). Splanchnic net flux of AAN was not affected by supplement treatments. Hepatic release of urea-N was increased (P < 0.05) by supplement treatments (27, 40, 46 and 44 mmol/h for Control, M, H and P respectively); the P treatment increased (P < 0.05) and the H treatment tended (P = 0.10) to increase splanchnic release of urea-N (7, 10, 20 and 27 mmol/h for Control, M, H and P treatments respectively). Net flux of glucose across the PDV was -4.6, 1.4, -5.6 and -7.2 (SE 1.65) mmol/h for Control, M, H and P treatments respectively. Hepatic glucose released averaged 23 (SE 2.0) mmol/h and was not affected by treatment. Treatments M and H increased (P < 0.05) PDV release of propionate compared with the Control treatment (4.5, 15.5, 16.8 and 7.7 mmol/h for Control, M, H and P treatments respectively). Release of acetate by the PDV was 43, 97, 118 and 67 (SE 23.9) mmol/h for Control, M, H and P treatments respectively. In summary, different supplements of low-quality grass did not increase the efficiency of N metabolism by splanchnic tissues. Treatment P had little effect on net flux across splanchnic tissues of glucose, L-lactate, beta-hydroxybutyrate and volatile fatty acids (VFA).(ABSTRACT TRUNCATED AT 400 WORDS)

Glucose transport across the intestinal wall of the freshwater snail Biomphalaria glabrata

1. 1. Isolated midguts of the freshwater snail Biomphalaria glabrata were mounted in an incubation chamber in saline containing 2 mM glucose and perfused with the same solution. External and internal media were continuously gassed with carbogen gas (95% O 2, 5% CO 2). In order to measure the flux rates of glucose [ 14C]glucose was applied in the perfusion medium or in the incubation medium. Net fluxes of glucose were calculated as the differences between unidirectional in- and effluxes. 2. 2. A directed net flux from the mucosal to the serosal side of the intestine was demonstrated (mucosal to serosal = 50 ± 10 nmol cm −2hr −1( N = 6) serosal to mucosal 7 ± 1 nmol cm −2hr −1 ( N = 6), net flux = 43 nmol cm −2hr −1).r 3. 3. The active transport of glucose was reduced by the presence of metabolic inhibitors, cyanide (1 mM) and dinitrophenol (1 mM) on the mucosal as well as on the serosal side. Ouabain (1 mM) inhibited the transport rate only when it was added on the serosal side. Amiloride (1 mM) had no effect on the transport rate whether added on the mucosal or on the serosal side. 4. 4. Inhibition of glucose transport by oubain, a specific inhibitor of Na +/K +-ATPase, suggests that glucose transport is secondary active and coupled to Na +-transport.

Protein, acetate and propionate for roughage-fed lambs. 2. Nutrient kinetics

AbstractThirty-six wether lambs were given food hourly consisting of mature chopped oaten hay, sprayed with 10 g urea per kg hay. A pelleted supplement was given containing 0 or 75 g/day fish meal and 0 or ca. 1·5 MJ/day gross energy as acetate or propionate in a 2 × 3 factorial design. Dry matter (DM) digestibility, nitrogen retention and urinary allantoin excretion were determined over 7 days. Tissue protein kinetics were estimated using15N-glycine. Net fluxes of acetate, bicarbonate and glucose were estimated with continuous infusion of14C-acetate,14C-bicarbonate and3H-glucose respectively.Intake of oaten hay (g DM per kg live weight per day) was reduced by supplementation. Live-weight gain was lower in lambs supplemented with propionate than in lambs given the basal diet only. Supplementation with fish meal increased DM digestibility, live-weight gain and wool growth. Daily excretion of urinary allantoin did not differ between groups of lambs. Nitrogen retention and protein flux were reduced in lambs supplemented with acetate or propionate and were increased in lambs given fish meal. Plasma acetate concentrations were higher for lambs supplemented with acetate. However, net flux of acetate did not differ between groups of lambs. The net flux of glucose was increased by supplementation with propionate and with fish meal. Plasma levels of β-hydroxybutyrate were reduced in lambs supplemented with propionate.Availability of propionate and glucose were not limiting live-weight gain in these lambs. Also, a high ratio of acetate to propionate did not reduce the apparent efficiency of nutrient use.

Role of the glucose cycle in control of net glucose flux in exercising humans

The hepatic glucose cycle involves the production of plasma glucose from glucose 6-phosphate and the simultaneous conversion of glucose back to glucose 6-phosphate. We have evaluated the role of the glucose cycle in the regulation of plasma glucose concentration during exercise at 70% of maximal O2 uptake and during recovery in five normal volunteers. Total glucose flux was measured by use of [2-2H]glucose (Ra2), net glucose flux through the glucose cycle was determined with [6,6-2H2]glucose (Ra6), and the rate of glucose cycling was determined by Ra2 - Ra6. Gas chromatography-mass spectrometry was used for analysis of isotopic enrichment. At rest, 33% of total glucose flux was recycled. In exercise, total flux increased 300%, but so did glucose cycling, which means that there was no change in the percentage of flux recycled. In recovery, both total flux and the rate of recycling returned rapidly to the resting value. We therefore conclude that whereas total glucose production can respond extremely quickly to large changes in energy requirements caused by exercise, thereby enabling maintenance of a constant blood glucose concentration, glucose cycling does not have an important role in amplifying the control of net hepatic glucose flux through the glucose cycle.

Site of action of putative lipostatic factor: hypothalamic metabolism of parabiotic rats

Studies were conducted to determine whether metabolic adaptation occurred in the hypothalamus of overfed parabiotic rats and their partners to distinguish between the adaptations caused by increased caloric intake and those caused by the production of a "lipostatic factor." The induction of overfed obesity in one parabiotic partner was employed to test the hypothesis that a putative lipostatic factor produced in the obese parabiotic elicited the hypophagic-lipid-mobilizing effect observed in the lean parabiotic via alterations in hypothalamic fatty acid and glucose metabolism. Fatty acid oxidation in the ventrolateral hypothalamus (VLH) of overfed parabiotic rats and their partners was lower than in ad libitum parabiotic rats. Net flux of glucose through the VLH gamma-aminobutyric acid (GABA) shunt was elevated in overfed parabiotic rats compared with the net flux observed in their partners and ad libitum parabiotic rats, the levels being similar in these last two groups. Net flux of glucose through the ventromedial hypothalamic (VMH) pentose shunt in overfed parabiotic rats and their partners was elevated relative to ad libitum parabiotic rats. The putative lipostatic factor may act to regulate energy balance through modification of VLH fatty acid oxidation and/or glucose flux via the VMH pentose shunt.

Effects of gastric fundic stimulation on glucose absorption and water and electrolyte fluxes from rabbit small bowel.

A single-pass perfusion model was developed to measure net fluxes of glucose, water, sodium, and potassium across upper jejunal and duodenal mucosa in vivo in the anaesthetised rabbit. Irrigation of the gastric fundic mucosa with Michaelis' buffer (pH 8) reduced jejunal mean glucose absorption by 21.3% (P less than 0.04) and duodenal glucose absorption by 27.2%. Irrigation of gastric fundic mucosa with 0.1 M glycine at pH 2 increased mean jejunal glucose absorption by 25%. Jejunal net secretion of water and sodium were reduced by gastric fundic alkali. Potassium net fluxes in jejunum and duodenum were not significantly affected. These results support the hypothesis that the gastric fundic mucosa is sensitive to chemical stimulation, responding by a humoral mechanism that modified the rate of glucose absorption from the small bowel mucosa.

Net portal nutrient flux in steers fed diets containing wheat and sorghum grain alone or in combination.

Three Holstein steers (280 to 353 kg during the experiment) fitted with hepatic portal, mesenteric venous and arterial catheters were fed 90% concentrate diets containing wheat, dry-rolled sorghum grain or a 50:50 mixture of the two to determine the effect of dietary grain source on net portal nutrient flux. Steers were allotted to a six-period crossover design with treatments lasting 2 wk. Diets were fed in 12 portions daily to equal intakes across treatments. Simultaneous arterial and portal blood samples were taken four times per day for the final 3 d of the treatment period. Portal blood flow was determined by continuous infusion of p-aminohippuric acid, and net portal nutrient absorption was calculated by venous-arterial difference X blood flow. Dry matter intakes averaged 6.2, 6.1 and 6.0 kg/d for wheat, 50:50 mixture and sorghum grain, respectively. Net fluxes of glucose, lactate, NH3, urea-N or alpha-amino-N were not affected by diet. Net fluxes increased for propionate and decreased for 2-methylbutyrate as the level of wheat increased (P less than .10). Overall, acetate and propionate net fluxes contributed 57% to 66% of the absorbed energy on these diets, with glucose contributing a maximum of 4% on the sorghum grain diet.