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Small primary sensory neurons innervating epidermis and viscera display differential phenotype in the adult rat.

Target tissues contribute to the phenotype and function of sensory neurons. Due to lack of appropriate markers for trkA expressing sensory axons and terminals, the detailed peripheral projection of these neurons is unclear. In this study, the peripheral projections of trkA immunoreactive neurons are characterized using the combined techniques of immunohistochemistry and retrograde tracing. We found approximately 65% of all neurons projecting to the adrenal gland and kidney are trkA immunoreactive, whereas 6, 14 and 37% of neurons innervating whisker follicle, epidermis and footpad, respectively, are immunoreactive for trkA. A low proportion of trkA immunoreactive neurons innervating epidermis indicates that the majority of sensory neurons innervating epidermis are independent of trkA signalling for their normal function. We further investigated whether these epidermal projecting neurons can bind isolectin IB4. We found approximately 70% of all neurons innervating epidermis are IB4 binding neurons, but they did not express trkA. Thus, NGF sensitive neurons primarily project to viscera but not epidermis or other skin structures, whereas IB-4 positive neurons primarily project to epidermis in the adult rat.

Adrenal Glands↗

Substance P, calcitonin gene related peptide and PGE2 co-released from the mouse colon: a new model to study nociceptive and inflammatory responses in viscera, in vitro.

Visceral inflammation is thought to play an important role in the sensitization of low and high threshold mechanosensory and polymodal afferents and to recruit silent nociceptors. Yet, little is known about the potential role of the mediators involved in nociceptor sensitization to mechanical stimulation as compared to heat sensitization in the skin. In the present study we developed a new isolated preparation of the mouse colon which allowed to apply controlled mechanical distensions. Excised segments of colon from CD mice were immersed in synthetic interstitial fluid (SIF) exposing the serosal surface during 5 min to different types of noxious stimuli; the increase in neuropeptide and PGE(2) release were analyzed (by EIA technique). Capsaicin, heat and pH 5.2 were able to induce significant increases in calcitonin gene related peptide (CGRP) release (14.6-, 5.1-, and 2.3-fold over baseline), however, only capsaicin induced a significant increase in substance P (SP) levels (1.8-fold over baseline). When pH 3.4 was used, a massive liberation of both CGRP and SP was obtained (14- and 15-fold from baseline) which was Ca(2+)-independent and not recovering, suggesting unphysiological release. Mechanical distensions in the noxious range (45, 60 and 90 mmHg) evoked a long-linear graded release of CGRP (1.3-, 1.6- and 2.6-fold over baseline) and of PGE(2) (1.9- 3.8-, 12.3-fold over baseline). Only the 90 mmHg distension evoked a significant increase of SP (1.9-fold over baseline). We conclude that the mouse colon preparation is a suitable model to study inflammatory and nociceptive mechanisms in viscera. Furthermore, a potentially important and yet unexplored role of PGE(2) in noxious visceral distension has been revealed.

Animals↗

Linkage mapping of a mouse gene, iv, that controls left-right asymmetry of the heart and viscera.

Inherited single gene defects have been identified in both humans and mice that lead to loss of developmental control over the left-right asymmetry of the heart and viscera. In mice the recessively inherited mutation iv leads to such apparent loss of control over situs: 50% of iv/iv mice exhibit situs inversus and 50% exhibit normal situs. The affected gene product has not been identified in these animals. To study the normal function of iv, we have taken an approach directed to the gene itself. As a first step, we have mapped iv genetically, by examining its segregation in backcrosses with respect to markers defined by restriction fragment length polymorphisms. The iv locus lies 3 centimorgans (cM) from the immunoglobulin heavy-chain constant-region gene complex (Igh-C) on chromosome 12. A multilocus map of the region suggests the gene order centromere-Aat (alpha 1-antitrypsin gene complex)-(11 cM)-iv-(3 cM)-Igh-C-(1 cM)-Igh-V (immunoglobulin heavy-chain variable-region gene complex).

Animals↗

Glucose and [13C]leucine metabolism by the portal-drained viscera of sheep fed on dried grass with acute intravenous and intraduodenal infusions of glucose.

The effect of exogenous glucose supply by either intrajugular (IJG) or intraduodenal (IDG) infusion at 2.0 mg glucose/kg body weight per min was investigated in four wether sheep (average weight 44 (SD 4) kg) chronically catheterized in the carotid artery and portal veins. Sheep were fed on a dried grass pellet diet hourly using continuous belt feeders. Whole-body glucose irreversible loss (IL) rate, measured with [6-3H]glucose, was increased by 0.5 and 0.8 of exogenous supply for IJG and IDG infusions respectively. Portal glucose utilization, measured by isotope dilution across the portal-drained viscera, was unaffected by additional glucose regardless of the route of glucose supply (P = 0.76 for control v. glucose infusions) and was a constant proportion of glucose IL (0.28) for all treatments. Portal plasma flow was higher during IDG infusions compared with IJG infusions (1.65 v. 1.44 litres/min, P = 0.055). Circulating total free amino acid concentrations fell during glucose infusions (2146, 1808 and 1683 mumol/l for control, IJG and IDG treatments respectively, P = 0.067 for treatment effect) but net portal absorption was not affected by increased glucose supply. Recovery in the portal vein of [1-13C]leucine infused into the duodenum averaged 0.65 and was not affected by increasing glucose supply to the gut tissues. The results show that glucose utilization by gut tissues is responsive to changes in both vascular and luminal glucose supply. The effects of changing gut tissue use of glucose and increased whole body glucose IL on metabolism of nutrients is discussed.

Amino Acids↗

Dietary arginine deficiency and gut ammonium infusion alter flux of urea cycle intermediates across the portal-drained viscera of pigs.

The objective of these experiments in pigs were to test the hypotheses that 1) gut synthetic processes could adapt to additional dietary glutamate or ornithine to meet tissue needs for arginine with feeding arginine-deficient diets and 2) acute elevation of ammonium in the hepatic-portal blood leads to increased glutamine production. Arterial [117 +/- 5.3 (arginine-deficient) vs. 78 +/- 5 (arginine-adequate) mumol/L] and portal ammonium concentrations were elevated in pigs fed arginine-deficient diets. Dietary ornithine, which elevated portal-drained visceral flux of ornithine, corrected the urinary orotic aciduria, but not the hyperammonemia seen with feeding arginine-deficient diets. Concentrations or portal drained viscera fluxes of arginine, ornithine, glutamate and glutamine were not altered even though portal and arterial ammonium concentrations were increased 8- and 3.5-fold with mesenteric infusion of ammonium. It was concluded that 1) substitution of glutamate for glycine or alanine does not alter gut production of ornithine, citrulline or arginine; 2) gut citrulline production is not altered by levels of dietary arginine, ornithine or glutamate; 3) increased ammonium challenge does not lead to increased glutamine production even though peripheral ammonium levels increased over threefold; and 4) provision of arginine for tissue needs will have to be met from dietary sources, as adaptations in gut synthetic processes seem to be refractory to dietary arginine status.

Alanine↗

Relationship between feed withdrawal and viscera condition of broilers.

This study was conducted to investigate the effects of feed withdrawal on the viscera of commercial broilers. Birds were withdrawn from feed 0, 3, 9, 12, 14, 16, or 18 h before slaughter. Crop and gizzard contents were determined after dissection, and intestinal shape and villi were subjectively scored. Raw liver color was measured colorimetrically. Length of feed withdrawal (time) and its interaction with grower (time by grower) and replication (time by replication) had a significant effect (P < 0.05) on gizzard contents, intestinal shape, and villi; however, time by grower and time by replication did not affect the crop contents or the incidence of bile contamination in the digestive tract. Results also suggested that the integrity of the intestines declined after 12 to 14 h feed withdrawal, as indicated by heavy intestinal sloughing. Color analyses of livers showed that length of feed withdrawal did not affect lightness (L* values), but livers became less red (lower positive a*) as feed withdrawal time increased. It was concluded that length of feed withdrawal significantly affected the gastrointestinal tract; however, variation in the appearance of the liver could not be attributed solely to broiler feed withdrawal time.

Abattoirs↗

Transcutaneous ultrasonography of the coelomic viscera of the ostrich (Struthio camelus).

Ultrasonographic examinations were performed on clinically healthy growing and adult nonbreeding female ostriches. Multiple acoustic windows and the normal ultrasonographic appearance of the coelomic viscera were described. Good images of the heart and its major vessels, proventriculus, ventriculus, intestines, liver, and kidneys could be obtained. Additionally, an anechoic structure, believed to function as an urinary bladder, could be imaged in the cloacal region. The pancreas, spleen, thyroid glands, ovary, and adrenals could not be seen in this study. General limitations were the size of the ostriches, massive leg and dorsal muscles, large sternum, the extensive air sac system, compact convoluted intestines, and varying amounts of gastrointestinal gas. Ostriches do not posses a gall bladder, and thus it could not be used as a landmark or acoustic window. The extensive air sac system and feathers did not limit the use of ultrasonography as much as anticipated. Imaging of air sacs should, however, be considered to detect pathology such as air sacculitis, which may result in consolidation. Veterinary

Animals↗

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.

Animals↗

Substrate oxidation by the portal drained viscera of fed piglets.

Fully fed piglets (28 days old, 7-8 kg) bearing portal, arterial, and gastric catheters and a portal flow probe were infused with enteral [U-(13)C]glutamate (n = 4), enteral [U-(13)C]glucose (n = 4), intravenous [U-(13)C]glucose (n = 4), or intravenous [U-(13)C]glutamine (n = 3). A total of 94% of the enteral [U-(13)C]glutamate but only 6% of the enteral [U- (13)C]glucose was utilized in first pass by the portal-drained viscera (PDV). The PDV extracted 6.5% of the arterial flux of [U-(13)C]glucose and 20.4% of the arterial flux of [U-(13)C]glutamine. The production of (13)CO(2) (percentage of dose) by the PDV from enteral glucose (3%), arterial glucose (27%), enteral glutamate (52%), and arterial glutamine (70%) varied widely. The substrates contributed 15% (enteral glucose), 19% (arterial glutamine), 29% (arterial glucose), and 36% (enteral glutamate) of the total production of CO(2) by the PDV. Enteral glucose accounted for 18% of the portal alanine and 31% of the portal lactate carbon outflow. We conclude that, in vivo, three-fourths of the energy needs of the PDV are satisfied by the oxidation of glucose, glutamate, and glutamine, and that dietary glutamate is the most important single contributor to mucosal oxidative energy generation.

Alanine↗

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.

Amino Acids↗

Glucagon-like peptide 1 excites hypocretin/orexin neurons by direct and indirect mechanisms: implications for viscera-mediated arousal.

Glucagon-like peptide 1 (GLP-1) is produced by neurons in the caudal brainstem that receive sensory information from the gut and project to several hypothalamic regions involved in arousal, interoceptive stress, and energy homeostasis. GLP-1 axons and receptors have been detected in the lateral hypothalamus, where hypocretin neurons are found. The electrophysiological actions of GLP-1 in the CNS have not been studied. Here, we explored the GLP-1 effects on GFP (green fluorescent protein)-expressing hypocretin neurons in mouse hypothalamic slices. GLP-1 receptor agonists depolarized hypocretin neurons and increased their spike frequency; the antagonist exendin (9-39) blocked this depolarization. Direct GLP-1 agonist actions on membrane potential were abolished by choline substitution for extracellular Na+, and dependent on intracellular GDP, suggesting that they were mediated by sodium-dependent conductances in a G-protein-dependent manner. In voltage clamp, the GLP-1 agonist Exn4 (exendin-4) induced an inward current that reversed near -28 mV and persisted in nominally Ca2+-free extracellular solution, consistent with a nonselective cationic conductance. GLP-1 decreased afterhyperpolarization currents. GLP-1 agonists enhanced the frequency of miniature and spontaneous EPSCs with no effect on their amplitude, suggesting presynaptic modulation of glutamate axons innervating hypocretin neurons. Paraventricular hypothalamic neurons were also directly excited by GLP-1 agonists. In contrast, GLP-1 agonists had no detectable effect on neurons that synthesize melanin-concentrating hormone (MCH). Together, our results show that GLP-1 agonists modulate the activity of hypocretin, but not MCH, neurons in the lateral hypothalamus, suggesting a role for GLP-1 in the excitation of the hypothalamic arousal system possibly initiated by activation by viscera sensory input.

Action Potentials↗

Net uptakes of oestradiol-17 beta and progesterone across the portal-drained viscera and the liver of ewes.

The objective of this study was to determine whether circulating concentrations or prior exposure to estradiol-17 beta (OE2) and progesterone affected their uptake by splanchnic tissues. Catheters were surgically placed in the portal vein, a branch of the hepatic vein, a mesenteric vein and the abdominal aorta of three multiparous ovariectomized Dorset ewes. Blood and plasma flow across the portal-drained viscera (PDV) and the liver, and net uptake of OE2 and O2 consumption in these same tissues were determined in ovariectomized ewes (control), during OE2 infusion into the jugular vein, 7 days after an OE2 implant had been given, and during OE2 infusion into the jugular vein 7 days after an OE2 implant. The above treatments were repeated for progesterone. Plasma flows across visceral organs were determined by marker dilution (para-aminohippuric acid), and OE2 and progesterone concentrations were determined by radioimmunoassay. During the infusion with OE2, OE2 arterial concentration (mean +/- S.D.) was 346 +/- 199 pg/ml, PDV net uptake was 9.7 +/- 5.6 micrograms OE2/h and hepatic net uptake was 15.5 +/- 9.5 micrograms OE2/h. Hepatic uptake was 82% of the jugular OE2 infusion rate. Blood flow and oxygen consumption by hepatic tissue increased when ewes were exposed to an OE2 implant for 7 days. During the infusion with progesterone, progesterone arterial concentration (mean +/- S.D.) was 8.8 +/- 3.4 ng/ml, PDV net uptake was 220 +/- 118 micrograms progesterone/h and hepatic net uptake was 238 +/- 52 micrograms progesterone/h. Hepatic net uptake was 23% of the progesterone jugular infusion rate.

Animals↗

Effect of topical administration of glucose on neurons innervating abdominal viscera in dorsal motor nucleus of vagus in rats.

Neural responses in the dorsal motor nucleus of the vagus (DMV) to topical administration of glucose were investigated electrophysiologically using multibarrel electrodes in anesthetized rats. Of 52 neurons that showed the antidromic response to the ventral gastric vagus, 4 neurons increased and 14 neurons decreased their discharge rates in response to topical administration of glucose from the multibarrel pipette. Thirty-four neurons did not respond to this administration. Of 4 neurons that showed the antidromic response to the accessory celiac vagus, 1 neuron increased and 1 neuron decreased their discharge rates in response to topical administration of glucose. Two neurons did not respond to this administration. These results suggest that some DMV neurons innervating the abdominal viscera may have an enteroceptor function detecting the change in glucose concentration of their environment.

Administration, Topical↗

Effects of growth hormone-releasing factor and feed intake on energy metabolism in growing beef steers: net hormone metabolism by portal-drained viscera and liver.

Effects of growth hormone-releasing factor (GRF) and intake on arterial concentrations and net visceral metabolism of hormones were measured in six growing Hereford x Angus steers using a split-plot design with 4-wk injection periods within 8-wk intake periods. Steers were fed a 75% concentrate diet at two intakes and were injected s.c. twice daily with saline or GRF (10 micrograms/kg of BW). Arterial concentrations of growth hormone (GH) were measured on d 1 and d 8 to 10 of injections. Eleven measurements, obtained at 30-min intervals, of arterial concentration and net flux of hormones across portal-drained viscera (PDV) and liver were obtained on d 8 to 10 of injections (six hourly measurements were used for insulin-like growth factor-I [IGF-I] and somatostatin). The area under the GH curve and average and peak GH concentrations were increased (P less than .01) by GRF and were greater (P less than .10) at low than at high intake. Liver removal of GH was not affected by GRF or intake. Arterial IGF-I concentration was increased (P less than .05) by GRF and not affected by intake. Treatments did not affect IGF-I flux across the liver. Arterial insulin concentration was greater (P less than .05) at high than at low intake, in part because of greater (P less than .01) PDV release. Increased (P less than .10) arterial insulin concentration in GRF-treated steers was not attributable to significant changes in PDV or liver net flux. Arterial glucagon concentration was greater (P less than .01) at high than at low intake, in part because of greater (P less than .05) PDV glucagon release and decreased (P less than .10) liver extraction ratio. Effects of intake on arterial concentration of insulin and glucagon were in part due to changes in visceral metabolism, but GRF did not affect PDV or liver hormone metabolism.

Animals↗

Effects of growth hormone-releasing factor and feed intake on energy metabolism in growing beef steers: net nutrient metabolism by portal-drained viscera and liver.

Effects of growth hormone-releasing factor (GRF) and intake on net nutrient metabolism by portal-drained viscera (PDV) and liver were measured in six growing Hereford x Angus steers fed a 75% concentrate diet at two intakes in a split-plot design with 4-wk saline or GRF injection periods within 8-wk intake periods. Daily rations were fed as 12 equal meals delivered every 2 h. Steers were injected s.c. for 21 d with either saline or 10 micrograms/kg of (1-29)NH2 human GRF at 12-h intervals. Six hourly measurements of net nutrient flux (venous-arterial concentration different [VA] x blood flow) across PDV and liver were obtained 8 to 10 d after injections began. Energy and N balances were measured using respiration calorimetry during the last week of injections. Greater intake increased blood flow (P less than .01) and net visceral release or removal of most nutrients (P less than .10). Exceptions included a decrease (P less than .10) in net PDV glucose release with greater intake in saline-treated steers and a decrease (P less than .01) in net liver removal of lactate with greater intake. Treatment of steers with GRF decreased net liver removal of alpha-amino N (AAN; P less than .05) and ammonia N (NH3N; P less than .10) and release of urea N (UN; P less than .05), increased liver release of glutamate (P less than .05), and decreased net PDV release of NH3 N (P less than .10). Decreased liver extraction ratio for AAN in GRF-treated steers (P less than .01) implies a direct effect of GRF treatment on liver metabolism separate from changes in liver AAN supply. Proportions of body N retention not accounted for by net total splanchnic AAN release increased with GRF treatment. This suggests a change in peripheral utilization of dietary AAN supply or an increase in total splanchnic N retention.

Amino Acids↗

Metabolite flux across portal-drained viscera, liver, and hindquarters of hyperinsulinemic, euglycemic beef steers.

Metabolic response to i.v., exogenous insulin was characterized in three younger (355 d old, 340 kg BW) and four older (480 d old, 456 kg BW) beef steers. The steers had chronic indwelling catheters to allow measurement of blood flow and net flux of metabolites across portal-drained viscera (PDV), liver, and hindquarters (HQ). Daily N and ME intakes provided at least 1.8 times maintenance requirements. Net flux was measured before and after each steer received intramesenteric infusions of insulin, which ranged from 5 to 80 mU.h-1.kg BW-1, and intrajugular infusion of glucose to maintain euglycemia. Nonlinear fits of data provided predictions of maximal glucose entry (Rmax) for glucose infused, liver glucose release, HQ glucose uptake, and total glucose entry (TGE, sum of glucose infused plus liver release). Differences in BW could account for differences (P < .05) in Rmax for TGE between older steers (688 mmol/h) and younger steers (493 mmol/h). Plasma insulin needed to elicit half-maximal response (ED50) for TGE tended (P < .17) to be greater for older (82 mU/L) than for younger steers (49 mU/L). The decrease in liver glucose release in response to infusion of insulin was greater (P < .01) for older (-170 mmol/h) than younger (-106 mmol/h) steers. The ED50 for liver production of glucose tended (P = .13) to be greater for older (45 mU/L) than for younger (5 mU/L) steers. At 80 mU.h-1.kg BW-1, liver extraction of insulin decreased to approximately 50% of control extraction, and arterial insulin concentration was at least 9.4 times control concentrations. The PDV release and liver removal of L-lactate and propionate were not reduced by insulin infusion, although liver glucose release was 51 and 76% of control for younger and older steers, respectively. We concluded that older steers tended to be less sensitive than younger steers to the effects of insulin on glucose metabolism.

Aging↗

Effect of intraruminal propionic acid infusion on metabolism of mesenteric- and portal-drained viscera in growing steers fed a forage diet: I. Volatile fatty acids, glucose, and lactate.

This experiment investigated the effect of intraruminal infusion of propionic acid on ruminal VFA metabolism and the absorption of nutrients by the mesenteric- and portal-drained viscera of seven Friesian steers, average BW 127 kg, fed a dried grass-pellet diet. Each received by random allocation 0 (control), .5, or 1.0 mol of propionic acid/d for 7 d. Ruminal acetate and propionate irreversible loss rates and carbon exchange between VFA and CO2 were measured during continuous intraruminal infusions of 2-14C-acetic acid and 2-14C-propionic acid. Ruminal acetate irreversible loss rate was not affected by propionic acid infusion (overall mean 8.09, error mean square [EMS] 2.68 mol/d), whereas propionate irreversible loss increased incrementally with PA supply (3.22 vs 4.16, EMS .61 mol/d, for control and 1.0 mol of propionic acid/d, respectively, P = .09). Glucose irreversible loss rate was increased at the highest level of PA infusion (2.84, 2.83, and 3.22, EMS .06 mol/d, for control, .5, and 1.0 mol of propionic acid/d, respectively; P = .02 for control vs .5 + 1.0), although the proportion of glucose irreversible loss derived from propionate remained constant (.6). Net absorption into venous blood showed that propionate was extensively metabolized in the rumen wall and that the tissues of the small intestine utilized acetate. Utilization of glucose was reduced in portal tissues as a result of intraruminal infusion, and the data were used to derive a model of glucose and lactate interrelationships in gut tissues.

Absorption↗

Effect of intravenous glucose infusion on metabolism of portal-drained viscera in sheep fed a cereal/straw-based diet.

This experiment investigated the effect of intrajugular infusion of glucose on whole-body glucose metabolism and the absorption of nutrients by the portal-drained viscera of four Suffolk-cross sheep, average BW 46 +/- 7 kg, fed a cereal/straw-based pelleted diet. Each sheep received by random allocation 0 (control), 1.0, or 2.0 mg of glucose.kg BW-1.min-1 for 8 h infused into the jugular vein. Glucose irreversible loss rate, measured by simultaneous infusion of 6-[3H]-glucose, increased approximately stoichiometrically during glucose infusion (.51, .75, and 1.09 error mean square [EMS] .032 mmol/min for control, 1.0, and 2.0 mg of glucose infused.kg BW-1.min-1, respectively). Utilization of glucose increased in portal tissues (P = .089) as a result of glucose infusion (.17, .18, and .33 EMS .008 mmol/min) and was a constant proportion of glucose irreversible loss (.28). Portal blood flow was not affected by glucose infusion (overall mean 1.13 L/min EMS .034). Net portal absorption of acetate increased during glucose infusion although ruminal VFA concentrations were not affected. In contrast, net free amino acid absorption by portal-drained tissues was reduced during glucose infusion (291, 115, and 4 EMS 33,816 mumol/min, P = .054). These results show that metabolism of nutrients across the gut wall is influenced by glucose availability to gastrointestinal tissues and affects the pattern of nutrients available to the liver and peripheral tissues.

Absorption↗