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Tissue uptake of fatty acids plays an important role in the regulation of plasma triglyceride elimination
lipid clearances in the short term. To avoid lipid accumulation, we suggest that patients would beneffi from the use of lipid emulsions with a low PUG ratio, i.e. 0.06 or perhaps even less.
0.36 Intravenous amino acids and long-chain glycerols induces gallbladder contraction
K. Vagenaq A. Michael, P. Vasiiakos, S. Markou and f. Kalfarentzos School of Medicine, University of Patras. Greece Oral amino acids and long-chain triacylgfycerols are known to release cholecystokinin (CCK) and to cause gallbladder (GE) contraction. It is unknown if intravenous amino acids (MA) and long-chain triacylglycerols (IVLCT) do so. This study was undertaken to examine the possible physiologic effects of IVAA and IVLCT on GB motility and release of CCK in humans. Twelve fasted normal volunteers were studied. The GB contractilty was observed by ultrasound. CCK-8 and CCK-33/39 were measured by RIA. In six volunteers a commercial preparation of 10% IVAA (1OOmgIKg BW/h) was infused. In the other six a commercial preparation of 10% IVLCT (75mg/Kg BW/h) was infused. Serial plasma samples CCK and GB volume measurements were obtained. Data on GB volume and release of CCK are summarized in table. Basal GB volume is taken as 100% and subsequent contraction given as per cent of basal volume. Values are expressed as mean i SD and student t-test was used to establish significant change from basal conditions.
0.35 Tissue uptake of fatty acids plays an important role in the regulation of plasma triglyceride elimination YA. carpentier, T. Olivecrona, V. Crabbe, C. R6ssle, M. Richelle and R.J. Deckelbaum Univ. Libre de Bruxelles, Univ. of Umea and Columbia Univ. The elimination of plasma triglycerides is usually considered to depend on the activity of endothelial bound lipoprotein (LPL) and hepatic lipases. Fatty acids (FA) resulting from TG hydrolysis at the endothelial sites are largely assimilated by adjacent tissues, the remainder being spilled into the circulation and accounting for the rise in plasma non-esterified fatty acid (nefas). Recently, it was shown that a high local production of FA could have a feedback inhibition on LPL activiiy but also release substantial amounts of LPL into the circulation (1). In the present study, 2 groups of 4 dogs have been daily infused (0.5 g TG/Kg.h over 8 h) with LCT emulsions for a period of 10 days. Both emulsions contain 1OOg TG/L, but emulsion A and B contain 129 and 6g phospholipids/L respectively. Plasma lipids (mmol/I) and LPL activity (U/L) were measured before and at the end of lipid infusion on each day: A TG N&S LPL PL
Oh 0.3 0.5 11 3.9
owl 6h 132 23 407 10.0
B Oh 04 0.9 08 4.5
A 8h 88 3 71.0 8.0
1
Oh 0.5 0.4 30 8.6
oa13 6h 5.8 15 25.5 13.4
Oh 0.3 0.8 2.6 5.4
Basal
6h 4.6 16 588 78
Oh 6h 0.4 22 0.8 09 14.4 37 10.7 14.5
B Oh 0.3 08 17 6.3
5 min
15 min 35 min 55 min 90 min 180 min Gaabladdef wium 93.8z146 ffit20.9 63.6?191 686-117.9 9uM+14 99.1f15 lCQ.6~32 78?2&4t 635i209* 635?15.8+ 63.8?19t 97fi3 CCK - 8 Ipplml) lb/AA 231t16.4 31fit178 413t224 56.6t29.6t53.6?343 47.66+3005 22.2_+11.2 IVLCT 223t11.8 41.3?280450.3+29.7+61.5?41.M+595?364+ 56.6t32.6'23.1r9.3 CCK-33AW(Wlm# IVM 69.4?232 67.5i-23.1 66.2ri6.8 666t128 75.iti6.9 791+22 67.3+11 IVLCT 68.9i18 649f165 625115.5 684'155 68SiI8 72.8?16 691?-18
MAP, 100% IVLCT loDei
DUflO A
B
triacyl-
8h 29 10 9.3 87
The rise in plasma TG, Nefas and LPL activity in response to lipid infusion markedly decreased during the study period, with both emulsions in spite of a marked accumulation of PL observed with emulsion A. These data suggest a primary role for an increased tissue assimilation of FA, reducing the local production at the endothelial site and allowing for higher lipolytic rate by LPL. (1) Proc. Nat. Acad. Sci., 1990.
11
tp<005.#p<0.01
We conclude that IVAA and IVLCT can result in human GB contraction and induce the release only of CCK-8. Postprandial GB contraction may depend in part on circulating amino acids and triacylglycerols. The mechanism of IVAA and IVLCT stimulation appears to be through release of CCK-8. It appears that amino acid and triacylglycerols receptors are present on the basal membranes of the CCK-d-containing gut endocrine cells, in addition to conventionally accepted luminal surface receptors in small bowel mucosa.
0.36 Intravenous amino acids and long-chain glycerols induces gallbladder contraction
K. Vagenaq A. Michael, P. Vasiiakos, S. Markou and f. Kalfarentzos School of Medicine, University of Patras. Greece Oral amino acids and long-chain triacylgfycerols are known to release cholecystokinin (CCK) and to cause gallbladder (GE) contraction. It is unknown if intravenous amino acids (MA) and long-chain triacylglycerols (IVLCT) do so. This study was undertaken to examine the possible physiologic effects of IVAA and IVLCT on GB motility and release of CCK in humans. Twelve fasted normal volunteers were studied. The GB contractilty was observed by ultrasound. CCK-8 and CCK-33/39 were measured by RIA. In six volunteers a commercial preparation of 10% IVAA (1OOmgIKg BW/h) was infused. In the other six a commercial preparation of 10% IVLCT (75mg/Kg BW/h) was infused. Serial plasma samples CCK and GB volume measurements were obtained. Data on GB volume and release of CCK are summarized in table. Basal GB volume is taken as 100% and subsequent contraction given as per cent of basal volume. Values are expressed as mean i SD and student t-test was used to establish significant change from basal conditions.
0.35 Tissue uptake of fatty acids plays an important role in the regulation of plasma triglyceride elimination YA. carpentier, T. Olivecrona, V. Crabbe, C. R6ssle, M. Richelle and R.J. Deckelbaum Univ. Libre de Bruxelles, Univ. of Umea and Columbia Univ. The elimination of plasma triglycerides is usually considered to depend on the activity of endothelial bound lipoprotein (LPL) and hepatic lipases. Fatty acids (FA) resulting from TG hydrolysis at the endothelial sites are largely assimilated by adjacent tissues, the remainder being spilled into the circulation and accounting for the rise in plasma non-esterified fatty acid (nefas). Recently, it was shown that a high local production of FA could have a feedback inhibition on LPL activiiy but also release substantial amounts of LPL into the circulation (1). In the present study, 2 groups of 4 dogs have been daily infused (0.5 g TG/Kg.h over 8 h) with LCT emulsions for a period of 10 days. Both emulsions contain 1OOg TG/L, but emulsion A and B contain 129 and 6g phospholipids/L respectively. Plasma lipids (mmol/I) and LPL activity (U/L) were measured before and at the end of lipid infusion on each day: A TG N&S LPL PL
Oh 0.3 0.5 11 3.9
owl 6h 132 23 407 10.0
B Oh 04 0.9 08 4.5
A 8h 88 3 71.0 8.0
1
Oh 0.5 0.4 30 8.6
oa13 6h 5.8 15 25.5 13.4
Oh 0.3 0.8 2.6 5.4
Basal
6h 4.6 16 588 78
Oh 6h 0.4 22 0.8 09 14.4 37 10.7 14.5
B Oh 0.3 08 17 6.3
5 min
15 min 35 min 55 min 90 min 180 min Gaabladdef wium 93.8z146 ffit20.9 63.6?191 686-117.9 9uM+14 99.1f15 lCQ.6~32 78?2&4t 635i209* 635?15.8+ 63.8?19t 97fi3 CCK - 8 Ipplml) lb/AA 231t16.4 31fit178 413t224 56.6t29.6t53.6?343 47.66+3005 22.2_+11.2 IVLCT 223t11.8 41.3?280450.3+29.7+61.5?41.M+595?364+ 56.6t32.6'23.1r9.3 CCK-33AW(Wlm# IVM 69.4?232 67.5i-23.1 66.2ri6.8 666t128 75.iti6.9 791+22 67.3+11 IVLCT 68.9i18 649f165 625115.5 684'155 68SiI8 72.8?16 691?-18
MAP, 100% IVLCT loDei
DUflO A
B
triacyl-
8h 29 10 9.3 87
The rise in plasma TG, Nefas and LPL activity in response to lipid infusion markedly decreased during the study period, with both emulsions in spite of a marked accumulation of PL observed with emulsion A. These data suggest a primary role for an increased tissue assimilation of FA, reducing the local production at the endothelial site and allowing for higher lipolytic rate by LPL. (1) Proc. Nat. Acad. Sci., 1990.
11
tp<005.#p<0.01
We conclude that IVAA and IVLCT can result in human GB contraction and induce the release only of CCK-8. Postprandial GB contraction may depend in part on circulating amino acids and triacylglycerols. The mechanism of IVAA and IVLCT stimulation appears to be through release of CCK-8. It appears that amino acid and triacylglycerols receptors are present on the basal membranes of the CCK-d-containing gut endocrine cells, in addition to conventionally accepted luminal surface receptors in small bowel mucosa.