| 1. |
- McNurlan, Margaret A., et al.
(författare)
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Response of protein synthesis in human skeletal muscle to insulin : an investigation with L[2H5]phenylalanine
- 1994
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Ingår i: American Journal of Physiology. - : American Physiological Society. - 0002-9513 .- 2163-5773. ; 67:Part 1, s. E102-E108
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Tidskriftsartikel (refereegranskat)abstract
- The role of insulin in the regulation of muscle protein synthesis in adult humans has been investigated with intravenous infusion of insulin at levels comparable with those observed after normal feeding. Glucose was also infused to maintain euglycemia. Muscle protein synthesis was measured in six healthy subjects before and during insulin and glucose infusion from the incorporation of L-[H-2(5)]phenylalanine into the protein of vastus lateralis sampled by percutaneous biopsy. L-[H-2(5)]phenylalanine was given as a single injection of a flooding amount (45 mg/kg). The relatively low levels of enrichment of phenylalanine in protein (0.005 atom%) were measured by modified gas chromatography-mass spectrometry and verified by comparison with incorporation of L-[2,6-H-3]phenylalanine. Similarity of enrichment in tissue-free and plasma pools (flooding) and linear incorporation over the period of measurement were also verified. The fractional rate of muscle protein synthesis in the group of postabsorptive subjects was 1.65 +/- 0.11% (SE)/day. The rate was unaltered by insulin and glucose infusion, 1.66 +/- 0.16%/day.
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| 2. |
- Alibegovic, A., et al.
(författare)
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Pretreatment with glucose infusion prevents fatal outcome after hemorrhage in food deprived rats
- 1993
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Ingår i: Circulatory Shock. - Hoboken, NJ, USA : John Wiley & Sons. - 0092-6213. ; 39:1, s. 1-6
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Tidskriftsartikel (refereegranskat)abstract
- Twenty-four hour food deprivation increases mortality after experimental hemorrhage. Survival after hemorrhage is closely related to the capacity of the animal to develop hyperglycemia. In this study, 24 hr food deprived rats were given a 3-hr infusion of either 0.3 ml/100 g b.wt./h 30% glucose iv (n = 10) or the same volume of 0.9% NaCl (n = 10) prior to 60 min of standardized hemorrhage. Glucose infusion resulted in a transient hyperglycemia, and 600% greater hepatic glycogen content compared to saline (P < 0.001). During hemorrhage, glucose-treated rats developed substantial hyperglycemia while glucose levels fell in saline treated (P < 0.001). Concomitant developments in hematocrits indicated improved plasma refill in glucose treated animals (P < 0.01). While saline treated rats developed irreversible shock and died within 3 hr of bleeding, glucose treated rats had a MAP of 52 ± 2 (mean ± SEM) mm Hg by the end of hemorrhage (P < 0.01). All glucose-treated rats recovered and survived the seven-day observation period. It is concluded that glucose infusion leading to hepatic glycogen repletion alters outcome after experimental hemorrhage in food deprived animals. These experimental results may be of clinical relevance, since elective surgery is generally performed after overnight fasting, which substantially reduces the hepatic glycogen reserve.
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| 3. |
- Esahili, A. H., et al.
(författare)
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Twenty-four hour fasting increases endotoxin lethality in the rat
- 1991
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Ingår i: European Journal of Surgery. - 1102-4151 .- 1741-9271. ; 157:2, s. 89-95
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Tidskriftsartikel (refereegranskat)abstract
- The effect of 24 h food deprivation on endotoxin (ET) lethality in SpD rats was studied. Fed and fasted animals received either 6 h i.v. infusions or i.p. boluses of ET at low, intermediate and high doses, and survival for seven days observed. Fasting was associated with 208-240% greater mortality when ET was infused i.v., and 87-200% when given i.p. ET doses LD10-LD80 gave a linear relationship with mortality. In non-fasted control rats liver glycogen content reduced by 1.28 mumols/min/g dry liver wt over the first post-prandial six hours, and increased by 65-99% in a dose dependent manner after ET (p less than 0.01). Evidence was also obtained relating both liver damage (assessed blind by histopathological scoring) and leucopenia with endotoxin dose, results which were modified by nutritional status. The evidence supports the role of liver glycogen as a protective substrate resource in endotoxic shock.
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| 4. |
- Ljungqvist, Olle, 1954-, et al.
(författare)
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Food deprivation alters liver glycogen metabolism and endocrine responses to hemorrhage
- 1990
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Ingår i: American Journal of Physiology. - : American Physiological Society. - 0002-9513 .- 2163-5773. ; 259:5 Part 1, s. E692-E698
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Tidskriftsartikel (refereegranskat)abstract
- Liver glycogen content, blood glucose, insulin, glucagon, and epinephrine were determined during 1 h hemorrhagic hypotension at 60 mmHg and 23 h thereafter in fed and two groups of 24-h food-deprived rats receiving either no infusion or 30% glucose intravenously during hemorrhage. Liver glycogen content was reduced by greater than 90% after 24-h food deprivation. Fed and food-deprived rats given glucose developed similar and substantial elevations of blood glucose during hemorrhage, whereas changes in blood glucose were modest in food-deprived rats given no infusion. In fed rats, liver glycogen was reduced by 60% during the 1-h bleed, but within 2 h after hemorrhage repletion of liver glycogen content commenced. By 6 h, approximately 75% of the glycogen lost during hemorrhage had been restored, and 23 h after hemorrhage liver glycogen content was six times greater compared with nonbled controls. Although glycogen levels increased after hemorrhage in food-deprived animals, the increase was negligible compared with that found in fed rats. Infusion of glucose during hemorrhage or adrenergic blockade after hemorrhage did not alter glycogen repletion in food-deprived rats. Posthemorrhage fed animals had high levels of insulin, glucagon, and epinephrine during hemorrhage, whereas insulin levels remained low in food-deprived rats despite exogenously induced hyperglycemia. It is concluded that rapid and substantial glycogen repletion can occur even immediately poststress. The conditions seem to be related to the nutritional state at the time of the insult.
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| 5. |
- Ljungqvist, Olle, 1954-, et al.
(författare)
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Hyperglycemia and survival after haemorrhage
- 1994
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Ingår i: European Journal of Surgery. - : Taylor & Francis. - 1102-4151 .- 1741-9271. ; 160:9, s. 465-469
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To assess the relation between the degree of hyperglycaemia during a standard haemorrhage and survival.Design: Prospective laboratory studySetting: University department of surgery, Sweden.Material: 5 groups of 8-12 adult male Sprague-Dawley rats.Interventions: Different degrees of hyperglycaemia were achieved in the 5 groups of rats (which had been starved for 24 hours) by infusion of the same amount of 0.9% saline, or 5%, 10%, 20% or 30% glucose during a 48% standard haemorrhage over 60 minutes. Blood glucose concentration and packed cell volume were measured every 30 minutes, and mean arterial pressure was monitored constantly.Main Outcome Measure: Survival at 7 days.Results: Increases in blood glucose concentrations during haemorrhage correlated with plasma refill as indicated by reductions in packed cell volume (r = 0.85, p < 0.0001). Both increases in blood glucose concentrations and reductions in packed cell volume were inversely related to blood pressure during haemorrhage (p < 0.0001). The more glucose that was infused, the higher the blood glucose concentration and the better the plasma refill during haemorrhage which correlated with improvement in the rate of survival at 7 days (p < 0.001).Conclusion: The ability to mount a hyperglycaemic response is an important prognostic factor in survival after experimental haemorrhage.
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