Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Alteration of the plasma peptidome of gastrectomised patients during an OGTT

ABSTRACT: Performing gastric bypass surgery on patients severely changes their gut hormone response to glucose. The plasma concentrations of Insulin and a number of associated incretin peptides are significantly raised shortly after ingestion of glucose. Typically the plasma concentrations of these peptides are monitored using immunoassays. A simple and high throughput plasma peptidomics approach was used to simulatneously monitor a large number of these peptides. Comparison of gastresctomised and control individuals showed significant increases of insulin, glucagon gene products, PYY and neurotensin.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Plasma

DISEASE(S): Postgastrectomy Syndrome

SUBMITTER: Richard Kay

LAB HEAD: Fiona Gribble, Frank Reimann

PROVIDER: PXD016690 | Pride | 2020-06-05

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	17060107.mgf	Mgf
	17060107.pride.mgf.gz	Mgf
	17060107.raw	Raw
	17060108.mgf	Mgf
	17060108.pride.mgf.gz	Mgf

Items per page:

1 - 5 of 168

Publications

Mass spectrometric characterisation of the circulating peptidome following oral glucose ingestion in control and gastrectomised patients.

Kay Richard G RG Foreman Rachel E RE Roberts Geoff P GP Hardwick Richard R Reimann Frank F Gribble Fiona M FM

Rapid communications in mass spectrometry : RCM 20200901 18

<h4>Rationale</h4>Meal ingestion triggers secretion of a variety of gut and endocrine peptides important in diabetes research which are routinely measured by immunoassays. However, similarities between some peptides (glucagon, oxyntomodulin and glicentin) can cause specificity issues with immunoassays. We used a liquid chromatography/tandem mass spectrometry (LC/MS/MS) methodology to unambiguously monitor multiple gut peptides in human plasma.<h4>Methods</h4>A simple acetonitrile-based protein p ...[more]

PMID: 32492232

Similar Datasets

A Trial of Preoperative CHO Drinks on Postoperative Walking Capacity in Colorectal Surgery

Project description:This prospective randomized controlled study is designed to investigate whether preoperative oral carbohydrate loading improves postoperative walking performance, a surrogate indicator for overall functional recovery, in patients undergoing colorectal surgery as measured by 2-minute and 6-minute walk test. The secondary outcomes are postoperative insulin resistance measured with plasma insulin and glucose concentrations. The tertiary outcomes are duration of hospital stay, patients satisfaction during staying in the hospital and morbidity measured as postoperative complications.

| 2144105 | ecrin-mdr-crc

Single cell transcriptome profiling of kidney cell populations and the effect of liraglutide in diabetes

Project description:While incretin-based therapies are known to improve glucose control in diabetes, growing evidence suggests a glucose-independent mechanism in protection against kidney disease. To further investigate incretin effects in kidney, we examined long-term therapy with liraglutide, a Glucagon-like peptide 1 receptor (GLP1R) agonist, in diabetic (Ins2Akita) and control mice and profiled renal cell transcriptomes using single-cell sequencing.

2024-05-02 | GSE220045 | GEO

Topp2000_BetaCellMass_Diabetes

Project description:This model is from the article: A model of beta-cell mass, insulin, and glucose kinetics: pathways to diabetes. Topp B, Promislow K, deVries G, Miura RM, Finegood DT. J Theor Biol.2000 Oct 21;206(4):605-19. 11013117, Abstract: Diabetes is a disease of the glucose regulatory system that is associated with increased morbidity and early mortality. The primary variables of this system are beta-cell mass, plasma insulin concentrations, and plasma glucose concentrations. Existing mathematical models of glucose regulation incorporate only glucose and/or insulin dynamics. Here we develop a novel model of beta -cell mass, insulin, and glucose dynamics, which consists of a system of three nonlinear ordinary differential equations, where glucose and insulin dynamics are fast relative to beta-cell mass dynamics. For normal parameter values, the model has two stable fixed points (representing physiological and pathological steady states), separated on a slow manifold by a saddle point. Mild hyperglycemia leads to the growth of the beta -cell mass (negative feedback) while extreme hyperglycemia leads to the reduction of the beta-cell mass (positive feedback). The model predicts that there are three pathways in prolonged hyperglycemia: (1) the physiological fixed point can be shifted to a hyperglycemic level (regulated hyperglycemia), (2) the physiological and saddle points can be eliminated (bifurcation), and (3) progressive defects in glucose and/or insulin dynamics can drive glucose levels up at a rate faster than the adaptation of the beta -cell mass which can drive glucose levels down (dynamical hyperglycemia).

2024-09-02 | BIOMD0000000341 | BioModels

Feedback Inhibition of CREB Signaling Promotes Beta Cell Dysfunction in Insulin Resistance.

Project description:Although persistent elevations in circulating glucose concentrations promote compensatory increases in pancreatic islet mass, unremitting insulin resistance causes a deterioration in beta cell function that disrupts glucose balance and signals the progression to diabetes 1. Glucagon like Peptide 1 (GLP1) agonists improve glucose tolerance in insulin resistance, although some individuals are unresponsive to treatment. Here we show that increases in GLP1 during feeding promote beta cell function in part through the PKA-mediated activation of CREB and its coactivator CRTC2 2. Mice with a knockout of CRTC2 in beta cells have impaired oral glucose tolerance due to decreases in circulating insulin concentrations. CRTC2 was found to promote beta cell function in part by stimulating the expression of the transcription factor MafA. Chronic hyperglycemia associated with high fat or high carbohydrate diet feeding disrupted cAMP signaling in pancreatic islets. Indeed, prolonged elevations in circulating glucose concentrations interfered with CREB signaling by activating the mTOR pathway and triggering the hypoxia inducible factor (HIF1)-dependent induction of the Protein Kinase A Inhibitor beta (PKIB), a potent inhibitor of PKA catalytic activity 3. As disruption of the PKIB gene restored glucose tolerance and insulin secretion in obesity, our results demonstrate how cross-talk between nutrient and hormonal pathways contributes to loss of pancreatic islet function in insulin resistance.

2015-02-23 | GSE60158 | GEO

Decreased adipose tissue oxygenation is associated with insulin resistance in people with obesity

Project description:We evaluated the potential importance of adipose tissue (AT) oxygenation on AT biology and insulin sensitivity in people. AT oxygen partial pressure (pO2), branched chain amino acid (BCAA) catabolism and marker of inflammation were determined in three groups stratified by adiposity and insulin sensitivity: 1) metabolically-healthy lean (MHL); 2) metabolically-healthy obese (MHO); and 3) metabolically-unhealthy obese (MUO). AT pO2 progressively declined from the MHL to the MHO to the MUO group, and was positively associated with hepatic and whole-body insulin sensitivity. AT pO2 was positively associated with AT expression of genes involved in BCAA catabolism and negatively associated with plasma BCAA concentrations. Although AT pO2 was negatively associated with AT markers of inflammation, it was not associated with plasma adipokine concentrations. These results support the notion that reduced AT pO2 in people with obesity contributes to insulin resistance by decreasing AT BCAA catabolism and thereby increasing plasma BCAA concentrations.

2020-12-07 | GSE152991 | GEO

Effect of insulin infusion on human skeletal muscle

Project description:To identify insulin responsive genes in humans, in the first protocol, skeletal muscle biopsies from six non-diabetic subjects were obtained before and after a two-hour of hyperinsulinaemic (infusion rate 40 mU/m2/min) euglycemic clamp. A variable infusion of glucose (180 g/l) enriched with tritiated glucose (100 μCi/500 ml) maintained euglycemia during insulin infusion, with monitoring of plasma glucose concentration every 5 to 10 min during the basal and clamp periods using an automated glucose oxidation method (Glucose Analyzer 2, Beckman Instruments, Fullerton, CA). In the second protocol, skeletal muscle biopsies from six non-diabetic subjects were obtained before and after a 3-hour hyperinsulinemic (infusion rate 40 mU/m2/min) euglycemic clamp in order to increase the effects of insulin on gene expression. A variable infusion of glucose (180 g/l) was used to maintain euglycemia during insulin infusion with monitoring of plasma glucose concentration every 5 to 10 min using an automated glucose oxidation method (Glucose Analyzer 2, Beckman Instruments, Fullerton, CA). Keywords: dose response The muscle biopsies were obtained from the vastus lateralis muscle under local anesthesia before and after hyperinsulinaemic (infusion rate 40 mU/m2/min) euglycemic clamp

2007-03-01 | E-GEOD-7146 | biostudies-arrayexpress

Topp200 - Model of b-Cell Mass, Insulin, and Glucose Kinetics:Pathways to Diabetes

Project description:A Model of β -Cell Mass, Insulin, and Glucose Kinetics: Pathways to Diabetes BRIANTOPP, KEITHPROMISLOW, GERDADEVRIES, ROBERT MMIURA, DIANE TFINEGOOD Diabetes is a disease of the glucose regulatory system that is associated with increasedmorbidity and early mortality. The primary variables of this system areb-cell mass, plasmainsulin concentrations, and plasma glucose concentrations. Existing mathematical models ofglucose regulation incorporate only glucose and/or insulin dynamics. Here we develop a novelmodel ofb-cell mass, insulin, and glucose dynamics, which consists of a system of threenonlinear ordinary di!erential equations, where glucose and insulin dynamics are fast relativetob-cell mass dynamics. For normal parameter values, the model has two stable"xed points(representing physiological and pathological steady states), separated on a slow manifold bya saddle point. Mild hyperglycemia leads to the growth of theb-cell mass (negative feedback)while extreme hyperglycemia leads to the reduction of theb-cell mass (positive feedback). Themodel predicts that there are three pathways in prolonged hyperglycemia: (1) the physiological"xed point can be shifted to a hyperglycemic level (regulated hyperglycemia), (2) the physio-logical and saddle points can be eliminated (bifurcation), and (3) progressive defects in glucoseand/or insulin dynamics can drive glucose levels up at a rate faster than the adaptation of theb-cell mass which can drive glucose levels down (dynamical hyperglycemi

2020-01-08 | MODEL2001080002 | BioModels

Effect of insulin infusion on human skeletal muscle

2007-03-01 | GSE7146 | GEO

Adipose tissue immunology, inflammation and exosomes in regulating insulin sensitivity in people with obesity and nonalcoholic fatty liver disease

Project description:Background and Aims: Insulin resistance is a key factor in the pathogenesis of NAFLD. We evaluated the importance of subcutaneous abdominal adipose tissue (SAAT) inflammation and both plasma and SAAT-derived exosomes in regulating insulin sensitivity in people with obesity and NAFLD. Methods: Adipose tissue inflammation (macrophage and T cell content and gene expression of proinflammatory cytokines), liver and whole-body insulin sensitivity (assessed by a hyperinsulinemic-euglycemic clamp and glucose tracer infusion), and 24-hour serial plasma cytokine concentrations were evaluated in three groups stratified by adiposity, insulin sensitivity and intrahepatic triglyceride (IHTG) content: 1) metabolically-healthy lean (LEAN; n=14); 2) metabolically-healthy obese with normal IHTG content (OB-NL; n=28); and 3) metabolically-unhealthy obese with NAFLD (OB-NAFLD; n=28). The effect of plasma and SAAT-derived exosomes on insulin action (insulin-stimulated Akt phosphorylation) in human skeletal muscle myotubes was assessed in a subset of participants. Results: Proinflammatory macrophages, proinflammatory CD4 and CD8 T cell populations, and gene expression of several cytokines in SAAT were greater in the OB-NAFLD than the OB-NL and LEAN groups. However, with the exception of PAI-1, which was greater in the OB-NAFLD than the LEAN and OB-NL groups, 24-hour plasma cytokine concentration areas-under-the-curve (AUC) were not different between groups. The percentage of proinflammatory macrophages and plasma PAI-1 concentration AUC were inversely correlated with both hepatic and whole-body insulin sensitivity. Compared with exosomes from OB-NL participants, plasma and SAAT-derived exosomes obtained from the OB-NAFLD group impaired insulin action in myotubes. Conclusion: These results suggest SAAT-derived exosomes and PAI-1 are involved in the pathogenesis of systemic insulin resistance in people with obesity and NAFLD. ClinicalTrials.gov number: NCT02706262.

2021-10-01 | GSE156906 | GEO

Feedback Inhibition of CREB Signaling Promotes Beta Cell Dysfunction in Insulin Resistance.

2015-02-23 | E-GEOD-60158 | biostudies-arrayexpress