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  • American Physiological Society  (4)
  • 2000-2004  (4)
  • 2001  (4)
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  • American Physiological Society  (4)
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  • 2000-2004  (4)
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  • 2001  (4)
  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 281, No. 5 ( 2001-11-01), p. E998-E1004
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 281, No. 5 ( 2001-11-01), p. E998-E1004
    Abstract: To determine the source(s) of blood and very low density lipoprotein (VLDL)-triglyceride glycerol during fasting, four men ingested 2 H 2 O from 14 to 20 h into a 60-h fast to achieve ∼0.5% body water enrichment. At 60 h of fasting, glycerol flux was measured using [2- 14 C]glycerol. Blood was taken for measurement of 2 H enrichment at carbon 6 of glucose and at carbon 3 of free glycerol and VLDL-triglyceride glycerol. 2 H enrichment of the 2 hydrogens bound to carbon 3 of VLDL-triglyceride glycerol was 105 ± 2% of the 2 H enrichment of the 2 hydrogens bound to carbon 6 of glucose, indicating isotopic equilibrium between hepatic glyceraldehyde 3- P and glycerol 3- P. The 2 H enrichment of the 2 hydrogens bound to carbon 3 of free glycerol was 17 ± 3% of VLDL-triglyceride glycerol, indicating that a significant percentage of free glycerol in blood originated from the hydrolysis of circulating VLDL-triglyceride or a pool of glycerol with similar 2 H enrichment. Glycerol flux was 6.3 ± 1.1 μmol · kg −1 · min −1 . Glycerol appearing from nonadipose tissue sources was then ∼1.1 μmol · kg −1 · min −1 . Seven other subjects were fasted for 12, 42, and 60 h. A small percentage of glycerol in the circulation after 12 h of fasting was enriched with 2 H. The enrichment of the 2 hydrogens bound to carbon 3 of free glycerol in the longer periods of fasting was ∼16% of the enrichment of the 2 hydrogens bound to carbon 6 of glucose. Therefore, as much as 15–20% of systemic glycerol turnover during fasting is not from lipolysis of adipose tissue triglyceride.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 281, No. 3 ( 2001-09-01), p. E413-E419
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 281, No. 3 ( 2001-09-01), p. E413-E419
    Abstract: Simultaneous synthesis and breakdown of glycogen is called glycogen cycling. The extent of hyperglycemia and decreased glycogen stores in diabetes mellitus may relate in part to the extent cycling occurs. Four methods have been introduced to estimate its extent in liver in humans. 1) In the fasted state, the rate of net hepatic glycogenolysis, i.e., glycogen breakdown minus synthesis, is estimated using NMR, and the rate of glycogenolysis is estimated from deuterium labeling of blood glucose on 2 H 2 O ingestion. 2) The rate of glycogen synthesis is estimated from the rate of labeling of carbon 1 of glycogen on [1- 13 C]glucose infusion, monitored by NMR, and the rate of breakdown from the rate of disappearance of that labeling on unlabeled glucose infusion. 3) The rate of synthesis from glucose-1- P, formed by glycogenolysis, is measured by the decrease in the 3 H/ 14 C ratio in acetaminophen glucuronide on acetaminophen and [2- 3 H,6- 14 C]galactose administration. 4) The rate of synthesis is estimated from the dilution of label from labeled galactose in its conversion to the acetaminophen glucuronide, and the rate of glycogenolysis is estimated from the amount of label in blood glucose. In the first method, the fate of glucose-6- P is assumed to be only to glycogen and glucose. In the second, only glucose-6- P molecules formed by breakdown that are not cycled back to glycogen are measured. In the third, 3 H is assumed to be removed completely during cycling, and only the molecules cycled back to glycogen are measured. In the fourth, galactose conversion to glucose is assumed to be via glycogen. Quantitations in all four methods depend on assuming the order in which the molecules deposited in glycogen are released.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477331-4
    SSG: 12
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 281, No. 4 ( 2001-10-01), p. E789-E793
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 281, No. 4 ( 2001-10-01), p. E789-E793
    Abstract: These studies were conducted to understand the relationship between measures of systemic free fatty acid (FFA) reesterification and regional FFA, glycerol, and triglyceride metabolism during fasting. Indirect calorimetry was used to measure fatty acid oxidation in six men after a 60-h fast. Systemic and regional (splanchnic, renal, and leg) FFA ([ 3 H]palmitate) and glycerol ([ 3 H]glycerol) kinetics, as well as splanchnic triglyceride release, were measured. The rate of systemic FFA reesterification was 366 ± 93 μmol/min, which was greater ( P 〈 0.05) than splanchnic triglyceride fatty acid output (64 ± 6 μmol/min), a measure of VLDL triglyceride fatty acid export. The majority of glycerol uptake occurred in the splanchnic and renal beds, although some leg glycerol uptake was detected. Systemic FFA release was approximately double that usually present in overnight postabsorptive men, yet the regional FFA release rates were of the same proportions previously observed in overnight postabsorptive men. In conclusion, FFA reesterification at rest during fasting far exceeds splanchnic triglyceride fatty acid output. This indicates that nonhepatic sites of FFA reesterification are important, and that peripheral reesterification of FFA exceeds the rate of simultaneous intracellular triglyceride fatty acid oxidation.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477331-4
    SSG: 12
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 280, No. 4 ( 2001-04-01), p. R1037-R1044
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 280, No. 4 ( 2001-04-01), p. R1037-R1044
    Abstract: The phagocytosis of IgG-coated erythrocytes (EIgG) has been shown to augment the bacterial lipopolysaccharide (LPS)-stimulated increase in serum tumor necrosis factor-α (TNF-α) levels. The present study evaluated the role of Fcγ-receptor (FcγR) signaling and complement activation in the effect of EIgG on the TNF-α response to LPS. The role of FcγR was determined using FcR γ-chain knockout mice that lack functional FcγRI and FcγRIII. In wild-type animals, EIgG caused a 16-fold augmentation of the serum TNF-α response to LPS, whereas there was no augmentation in the FcγR-deficient animals. Heat-damaged erythrocytes also augmented the TNF-α response to LPS. This effect was absent in FcγR-deficient animals. An IgG antibody against heated erythrocytes was detected in mouse serum. The complement activation caused by EIgG had little effect on the LPS-stimulated increase in serum TNF-α levels as indicated by activation of complement with cobra venom factor or IgM-coated erythrocytes as well as studies with C5-deficient mice. These results indicate that FcγR signaling primarily mediates the augmented serum TNF-α response to LPS caused by EIgG.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Location Call Number Limitation Availability
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