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Biomedical subjects

A Ulvestad

Publications and source records attributed to A Ulvestad.

5 recordsLinked to original sources
PubMed2006

Vildagliptin therapy reduces postprandial intestinal triglyceride-rich lipoprotein particles in patients with type 2 diabetes.

AIMS/HYPOTHESIS: We assessed the effects of vildagliptin, a novel dipeptidyl peptidase IV inhibitor, on postprandial lipid and lipoprotein metabolism in patients with type 2 diabetes. SUBJECTS, MATERIALS AND METHODS: This was a single-centre, randomised, double-blind study in drug-naive patients with type 2 diabetes. Patients received vildagliptin (50 mg twice daily, n=15) or placebo (n=16) for 4 weeks. Triglyceride, cholesterol, lipoprotein, glucose, insulin, glucagon and glucagon-like peptide-1 (GLP-1) responses to a fat-rich mixed meal were determined for 8 h postprandially before and after 4 weeks of treatment. RESULTS: Relative to placebo, 4 weeks of treatment with vildagliptin decreased the AUC(0-8h) for total trigyceride by 22+/-11% (p=0.037), the incremental AUC(0-8h) (IAUC(0-8h)) for total triglyceride by 85+/-47% (p=0.065), the AUC(0-8h) for chylomicron triglyceride by 65+/-19% (p=0.001) and the IAUC(0-8h) for chylomicron triglyceride by 91+/-28% (p=0.002). This was associated with a decrease in chylomicron apolipoprotein B-48 (AUC(0-8h), -1.0+/-0.5 mg l(-1) h, p=0.037) and chylomicron cholesterol (AUC(0-8h), -0.14+/-0.07 mmol l(-1) h, p=0.046). Consistent with previous studies, 4 weeks of treatment with vildagliptin also increased intact GLP-1, suppressed inappropriate glucagon secretion, decreased fasting and postprandial glucose, and decreased HbA(1c) from a baseline of 6.7% (change, -0.4+/-0.1%, p<0.001), all relative to placebo. CONCLUSIONS/INTERPRETATION: Treatment with vildagliptin for 4 weeks improves postprandial plasma triglyceride and apolipoprotein B-48-containing triglyceride-rich lipoprotein particle metabolism after a fat-rich meal. The mechanisms underlying the effects of this dipeptidyl peptidase IV inhibitor on postprandial lipid metabolism remain to be explored.

Adamantane↗
PubMed2000

Subcellular organization of bile acid amidation in human liver: a key issue in regulating the biosynthesis of bile salts.

To extend our knowledge of how the synthesis of free bile acids and bile salts is regulated within the hepatocyte, bile acid-CoA:amino acid N-acyltransferase and bile acid-CoA thioesterase activities were measured in subcellular fractions of human liver homogenates. Some bile acids, both conjugated and unconjugated, have been reported to be natural ligands for the farnesoid X receptor (FXR), an orphan nuclear receptor. The conversion of [(14)C]choloyl-CoA and [(14)C]chenodeoxycholoyl-CoA into the corresponding tauro- and glyco-bile acids or the free bile acids was measured after high-pressure liquid radiochromatography. There was an enrichment of the N-acyltransferase in the cytosolic and the peroxisomal fraction. Bile acid-CoA thioesterase activities were enriched in the cytosolic, peroxisomal, and mitochondrial fractions. The highest amidation activities of both choloyl-CoA and chenodeoxycholoyl-CoA were found in the peroxisomal fraction (15-58 nmol/mg protein/min). The K(m) was higher for glycine than taurine both in cytosol and the peroxisomal fraction.These results show that the peroxisomal de novo synthesis of bile acids is rate limiting for peroxisomal amidation, and the microsomal bile acid-CoA synthetase is rate limiting for the cytosolic amidation. The peroxisomal location may explain the predominance of glyco-bile acids in human bile. Both a cytosolic and a peroxisomal bile acid-CoA thioesterase may influence the intracellular levels of free and conjugated bile acids.

Acyltransferases↗
PubMed1985

Inhibitory effects of dopamine and isoprenaline on antral motor activity stimulated by acetylcholine or physostigmine in vitro.

Continuous pressure recordings were made in guinea-pig antral pouches in vitro. The antral phasic activity was stimulated by acetylcholine and by the cholinesterase inhibitory agent physostigmine. Dopamine and isoprenaline both significantly impaired antral pressure responses to physostigmine, whereas the acetylcholine-induced response was not significantly reduced. This suggests that both dopamine and isoprenaline to some extent act by reducing the spontaneously released acetylcholine, suggesting that both drugs act on intramural cholinergic neural pathways.

Acetylcholine↗
PubMed1984

Effects of alpha- and beta-adrenergic agents and dopamine on gastric motor activity stimulated by acetylcholine or physostigmine.

The inhibitory actions of phenylephrine, adrenaline, isoprenaline and dopamine on the antral and fundic pressure responses to exogenous acetylcholine or physostigmine were tested on isolated whole guinea-pig stomachs. Phenylephrine, adrenaline and dopamine markedly inhibited pressure responses to physostigmine, while the responses to acetylcholine were impaired to a less extent. The antral inhibition was more pronounced than the fundic. Isoprenaline was significantly less potent, but like the former inhibited physostigmine more than acetylcholine in the antrum. It may be concluded that adrenergic agents and dopamine exert their inhibition of gastric motor activity partly on intramural cholinergic neural pathways. Dopaminergic as well as alpha-adrenergic influence appear to be more effective than beta-adrenergic. The pronounced effect on phasic antral activity indicates principal inhibitory actions on propulsive motility and gastric emptying.

Acetylcholine↗