Gastric emptying: the validity of the paracetamol absorption test adjusted for individual pharmacokinetics

Medhus, Asle W.; Lofthus, C. M.; Bredesen, J. E.; Husebye, Einar

doi:10.1046/j.1365-2982.2001.00249.x

Cited by 89 publications

(75 citation statements)

References 23 publications

(44 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The glucagon assay was directed against the COOH-terminal of the glucagon molecule and, therefore, measures glucagon of pancreatic origin (32). Serum acetaminophen was measured by the Vitros ACET slide method based on an aryl acyl amidase reaction linked to a color shift reaction using liquid chromatography for quantification as described elsewhere (29,30). Total serum bile acids were measured using the enzymatic colorimetric method in which the enzyme 3-␣-hydroxysteroid-dehydrogenase in the presence of nicotinamide adenine dinucleotide transforms bile acids to 3-ketosteroids and NADH.…”

Section: Aucmentioning

confidence: 99%

Postprandial gut hormone responses and glucose metabolism in cholecystectomized patients

Sonne

Hare

Martens

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

Sonne DP, Hare KJ, Martens P, Rehfeld JF, Holst JJ, Vilsbøll T, Knop FK. Postprandial gut hormone responses and glucose metabolism in cholecystectomized patients. Am J Physiol Gastrointest Liver Physiol 304: G413-G419, 2013. First published December 28, 2012 doi:10.1152/ajpgi.00435.2012.-Preclinical studies suggest that gallbladder emptying, via bile acid-induced activation of the G protein-coupled receptor TGR5 in intestinal L cells, may play a significant role in the secretion of the incretin hormone glucagon-like peptide-1 (GLP-1) and, hence, postprandial glucose homeostasis. We examined the secretion of gut hormones in cholecystectomized subjects to test the hypothesis that gallbladder emptying potentiates postprandial release of GLP-1. Ten cholecystectomized subjects and 10 healthy, age-, gender-, and body mass index-matched control subjects received a standardized fat-rich liquid meal (2,200 kJ). Basal and postprandial plasma concentrations of glucose, insulin, C-peptide, glucagon, GLP-1, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-2 (GLP-2), cholecystokinin (CCK), and gastrin were measured. Furthermore, gastric emptying and duodenal and serum bile acids were measured. We found similar basal glucose concentrations in the two groups, whereas cholecystectomized subjects had elevated postprandial glucose excursions. Cholecystectomized subjects had reduced postprandial concentrations of duodenal bile acids, but preserved postprandial plasma GLP-1 responses, compared with control subjects. Also, cholecystectomized patients exhibited augmented fasting glucagon. Basal plasma CCK concentrations were lower and peak concentrations were higher in cholecystectomized patients. The concentrations of GIP, GLP-2, and gastrin were similar in the two groups. In conclusion, cholecystectomized subjects had preserved postprandial GLP-1 responses in spite of decreased duodenal bile delivery, suggesting that gallbladder emptying is not a prerequisite for GLP-1 release. Cholecystectomized patients demonstrated a slight deterioration of postprandial glycemic control, probably because of metabolic changes unrelated to incretin secretion. bile acids; gallbladder; incretins; TGR5 BESIDES THEIR ESTABLISHED roles in dietary lipid absorption and cholesterol homeostasis, bile acids are now being recognized as metabolic regulators. Preclinical studies suggest that gallbladder emptying, via bile acid-induced activation of the G protein-coupled receptor TGR5 in intestinal L cells, plays a significant role in the secretion of the incretin hormone glucagon-like peptide-1 (GLP-1) and postprandial glucose homeostasis (40). GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) are the main incretin hormones and act in concert to generate the so-called incretin effect (12). The incretin effect has been defined as the augmentation of insulin secretion after oral glucose compared with insulin secretion after isoglycemic intravenous glucose. The incretin effect accounts for up to 70% of the insulin secreted afte...

show abstract

Section: Aucmentioning

confidence: 99%

Postprandial gut hormone responses and glucose metabolism in cholecystectomized patients

Sonne

Hare

Martens

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

show abstract

“…At 0 min, subjects ingested the standardized liquid meal within 5 min. Since atropine was shown to affect gastrointestinal motility, we estimated the rate of gastric emptying by use of the acetaminophen absorption test (24,25). For this…”

Section: Methodsmentioning

confidence: 99%

Parasympathetic Blockade Attenuates Augmented Pancreatic Polypeptide But Not Insulin Secretion in Pima Indians

et al. 2004

View full text Add to dashboard Cite

There is evidence from animal models of obesity and type 2 diabetes that increased parasympathetic vagal input to the pancreas contributes to hyperinsulinemia. Compared with Caucasians, Pima Indians have a high risk of type 2 diabetes and exhibit marked hyperinsulinemia and elevated plasma levels of pancreatic polypeptide (PP), an islet hormone considered a surrogate marker of parasympathetic nervous system (PNS) drive to the pancreas. To test if hyperinsulinemia in Pima Indians is due to increased vagal input to the ␤-cell, we examined the effect of PNS blockade in 17 Caucasian (aged 35 ؎ 8 years, body fat 23 ؎ 7% [mean ؎ SD]) and 17 Pima Indian males (aged 28 ؎ 8 years, body fat 29 ؎ 5%) with normal glucose tolerance. Each participant underwent four consecutive standardized liquid meal tests (64% carbohydrate, 22% fat, and 14% protein) during which a primed infusion of atropine was administered for 120 min at the following doses: 0, 2.5, 5, and 10 g ⅐ kg fat-free mass (FFM) ؊1 ⅐ h ؊1 . Areas under the curve for early (AUC 0 -30 min ) and total (AUC 0 -120 min ) postprandial insulin and PP secretory responses were calculated. Early postprandial insulin and PP secretory responses were higher in Pima Indians compared with those of Caucasians (both P ‫؍‬ 0.01). Secretion of insulin and PP was inhibited by atropine (both P < 0.001). Increasing doses of atropine attenuated the ethnic difference in PP (P ‫؍‬ 0.01) but not in early insulin secretory responses (P ‫؍‬ 0.6), an effect that was not due to differences in gastric emptying rate (acetaminophen test) and/or circulating glucose. Similar results were observed for total secretory responses. These results confirm that compared with Caucasians, Pima Indians have an exaggerated PNS drive to pancreatic F-cells that secrete PP. However, the hyperinsulinemia of this population does not appear to be due to increased vagal input to pancreatic ␤-cells.

show abstract

“…One and a half grams of paracetamol (Panodil, GlaxoSmithKline A/S) dissolved in 50 ml water was added to the test meal for the evaluation of gastric emptying (20,21).…”

Section: Experimental Protocolmentioning

confidence: 99%

Postprandial incretin and islet hormone responses and dipeptidyl-peptidase 4 enzymatic activity in patients with maturity onset diabetes of the young

Østoft

Hansen

Hartmann

et al. 2015

European Journal of Endocrinology

View full text Add to dashboard Cite

Objective: The role of the incretin hormones in the pathophysiology of maturity onset diabetes of the young (MODY) is unclear. Design: We studied the postprandial plasma responses of glucagon, incretin hormones (glucagon-like peptide 1 (GLP1) and glucose-dependent insulinotropic polypeptide (GIP)) and dipeptidyl-peptidase 4 (DPP4) enzymatic activity in patients with glucokinase (GCK) diabetes (MODY2) and hepatocyte nuclear factor 1a (HNF1A) Results: All of the groups exhibited similar baseline values of glucagon (MODY2: 7G1 pmol/l; MODY3: 6G1 pmol/l; CTRLs: 8G 2 pmol/l, PZ0.787), but patients with MODY3 exhibited postprandial hyperglucagonaemia (area under the curve (AUC) 838G108 min!pmol/l) as compared to CTRLs (182G176 min!pmol/l, PZ0.005) and tended to have a greater response than did patients with MODY2 (410G154 min!pmol/l, PZ0.063). Similar peak concentrations and AUCs for plasma GIP and plasma GLP1 were observed across the groups. Increased fasting DPP4 activity was seen in patients with MODY3 (17.7G 1.2 mU/ml) vs CTRLs (13.6G0.8 mU/ml, PZ0.011), but the amount of activity was similar to that in patients with MODY2 (15.0G0.7 mU/ml, PZ0.133). Conclusion: The pathophysiology of MODY3 includes exaggerated postprandial glucagon responses and increased fasting DPP4 enzymatic activity but normal postprandial incretin responses both in patients with MODY2 and in patients with MODY3.

show abstract

Gastric emptying: the validity of the paracetamol absorption test adjusted for individual pharmacokinetics

Cited by 89 publications

References 23 publications

Postprandial gut hormone responses and glucose metabolism in cholecystectomized patients

Postprandial gut hormone responses and glucose metabolism in cholecystectomized patients

Parasympathetic Blockade Attenuates Augmented Pancreatic Polypeptide But Not Insulin Secretion in Pima Indians

Postprandial incretin and islet hormone responses and dipeptidyl-peptidase 4 enzymatic activity in patients with maturity onset diabetes of the young

Contact Info

Product

Resources

About