In Vivo Effects of Insulin and Free Fatty Acids on Matrix Metalloproteinases in Rat Aorta

Diabetes ◽  
2007 ◽  
Vol 57 (2) ◽  
pp. 476-483 ◽  
Author(s):  
G. Boden ◽  
W. Song ◽  
L. Pashko ◽  
K. Kresge
1990 ◽  
Vol 36 (4) ◽  
pp. 611-613 ◽  
Author(s):  
R Sapin ◽  
J L Schlienger ◽  
F Grunenberger ◽  
F Gasser ◽  
J Chambron

Abstract To compare in vitro and in vivo effects of increased concentrations of free fatty acids (FFA) on free thyroxin (FT4) values, we measured FT4 in three pooled sera supplemented with oleate and in serum from 18 euthyroid patients before and after an infusion of fat emulsion (Intralipid). We used five FT4 RIA kits: two two-step methods [Gammacoat, Baxter (GC); Ria-gnost, Behring (RG)], two analog RIAs [Amerlex-M, Amersham (AM); Coat-Ria, BioMérieux (CR)], and one kit with labeled antibodies [Amerlex-MAB*, Amersham (AA)]. In vitro, at the maximum oleate addition of 5 mmol/L, FT4 increased when measured by the GC and RG kits, decreased by the AM kit, and showed no significant change by the CR and AA kits. In vivo, post-Intralipid, FFA concentrations rose significantly and the FT4 changes agreed with the results of the in vitro experiments, except for the RG kit, for which FT4 increased in only nine patients. We conclude that in vitro oleate addition is useful to predict the in vivo effect of increased FFA on FT4 values; moreover, in serum from euthyroid subjects with high concentrations of FFA, FT4 analyzed with the CR or AA kits should better agree with normal results for thyrotropin than FT4 values measured with the other kits.


1984 ◽  
Vol 100 (3) ◽  
pp. 345-352 ◽  
Author(s):  
J. Knudtzon

ABSTRACT Intravenous injection of 8·5 nmol (1–24)ACTH increased the plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits. The (1–24)ACTH-induced hyperglucagonaemia and hyperinsulinaemia started 3 and 20 min after the injection respectively. Similar increases in the plasma levels of glucagon, insulin and free fatty acids were found with 5·3 nmol (1–39)ACTH, whereas (1–4)ACTH, (4–10)ACTH, (1–10)ACTH, (11–24)ACTH, (7–38)ACTH and (18–39)ACTH (corticotrophin-like intermediate lobe peptide) injected at doses of approximately 8 nmol were inactive. Infusions with the alpha-adrenergic blocking drug, phentolamine, reduced the (1–24) ACTH-induced hyperglucagonaemia and hypergly-caemia, and augmented the (1–24)ACTH-induced hyperinsulinaemia, which now became significant after 5 min. Infusions with the beta-adrenergic blocking drug, propranolol, did not diminish the (1–24)ACTH-induced effects, but killed the rabbits after 2–4 h. It is concluded that the acute in-vivo effects of ACTH in rabbits are modulated by the involvement of alpha-adrenergic receptors, which increased the plasma levels of glucagon and glucose, and delayed and diminished the ACTH-induced increases in the plasma levels of insulin. The (1–24)ACTH-induced increases in the plasma levels of free fatty acids were not influenced by the adrenergic blocking drugs. J. Endocr. (1984) 100, 345–352


1997 ◽  
Vol 273 (1) ◽  
pp. G184-G190 ◽  
Author(s):  
M. Saghir ◽  
J. Werner ◽  
M. Laposata

Fatty acid ethyl esters (FAEE), esterification products of fatty acids and ethanol, are in use as fatty acid supplements, but they also have been implicated as toxic mediators of ethanol ingestion. We hypothesized that hydrolysis of orally ingested FAEE occurs in the gastrointestinal (GI) tract and in the blood to explain their apparent lack of toxicity. To study the in vivo inactivation of FAEE by hydrolysis to free fatty acids and ethanol, we assessed the hydrolysis of FAEE administered as an oil directly into the rat stomach and when injected within the core of low-density lipoprotein particles into the circulation of rats. Our studies demonstrate that FAEE are rapidly degraded to free fatty acids and ethanol in the GI tract at the level of the duodenum with limited hydrolysis in the stomach. In addition, FAEE are rapidly degraded in the circulation, with a half-life of only 58 s. Thus the degradation of FAEE in the GI tract and in the blood provides an explanation for the apparent lack of toxicity of orally ingested FAEE.


1975 ◽  
Vol 229 (4) ◽  
pp. 885-889 ◽  
Author(s):  
Crass MF ◽  
GM Pieper

The metabolism of cardiac lipids and glycogen in hypoxic and well-oxygenated perfused rat hearts was studied in the presence or absence of epinephrine. Heart lipids were pre-labeled in vivo with [1-14C]palmitate. Triglyceride disappearance (measured chemically and radiochemically) was observed in well-oxygenated hearts and was stimulated by epinephrine (4.1 X 10(-7)M). Utilization of tissue triglycerides was inhibited in hypoxic hearts in the presence or absence of added epinephrine. Hypoxia resulted in a small increase in tissue 14C-free fatty acids and inhibition of 14C-labeled triglyceride fatty acid oxidation. Epinephrine had no stimulatory effect on fatty acid oxidation in hypoxic hearts. Utilization of 14C-labeled phospholipids (and total phospholipids) was similar in well-oxygenated and hypoxic hearts with or without added epinephrine. These results suggested that the antilipolytic effects of hypoxia were predominant over the lipolytic effects of epinephrine. Glycogenolysis was stimulated threefold by epinephrine in well-oxygenated hearts. Hypoxia alone was a potent stimulus to glycogenolysis. Addition of epinephrine to perfusates of hypoxic hearts resulted in a slight enhancement of glycogenolysis.


1981 ◽  
Vol 36 (1-2) ◽  
pp. 62-70 ◽  
Author(s):  
Margrit Bertrams ◽  
Käthe Wrage ◽  
Ernst Heinz

Abstract De novo-synthesis of glycerolipids in chloroplasts is initiated by a stroma enzyme which catalyzes the formation of lyso-phosphatidic acid from glycerophosphate and acyl-CoA. When these substrates are added to isolated, intact chloroplasts, only glycerophosphate can readily pass through the chloroplast envelope which represents a permeation barrier for acyl-CoA, although higher thioester concentrations destroy this membrane system. At low concentrations of acyl-CoA, which do not impair the envelope, intact chloroplasts metabolize exogenous acyl-CoA in two ways to give free fatty acids and labelled phosphatidyl choline. This indicates that the envelope thioesterase can use exogenous substrates. Isolated, intact chloroplasts fixing radioactive CO2 label free fatty acids and acylglycerols but not galactolipids, since they cannot convert 3-phosphoglycerate into UDP-galactose which in vivo is supplied by the cytoplasm. This cooperation was simulated in vitro by adding all enzymes and cofactors necessary for conversion of 3-phosphoglycerate into UDP-galactose to intact chloro­plasts which then formed labelled monogalactosyl diacylglycerol from labelled CO2. The time required to transfer envelope-made galactolipids from the envelope into thylakoids was studied by incubating intact chloroplasts with radioactive UDP-galactose, subsequent osmotic disruption of organelles with concomitant enzymatic degradation of UDP-galactose followed by separation of envelopes and thylakoids. Only after short times (< 1min) appreciable proportions 920-30%) of radioactive galactolipid export from envelopes into thylakoids.


1971 ◽  
Vol 33 (3) ◽  
pp. 662-666 ◽  
Author(s):  
J. J. O'Connor ◽  
G. S. Meyers ◽  
D. C. Maplesden ◽  
G. W. Vander Noot

1984 ◽  
Vol 18 ◽  
pp. 353A-353A
Author(s):  
Timos Valaes ◽  
Kevin Murphy ◽  
Richard Wennberg ◽  
Boris Senior
Keyword(s):  

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