Defective response to insulin secretagogues may arise from A) decreased concentrations of a given secretagogue, B) loss of β-cell responsiveness to that.

Slides:



Advertisements
Similar presentations
Body Temperature and Blood Glucose Sun Hwa Dong. Control of Body temperature Hypothalamus monitors temp. and compares it with a set point (around 37°C.
Advertisements

Diabetes and Aging MCB 135K Laura Epstein 4/14/06.
Glucose in the Blood By: Paul.B, Carl.B, Joseph.G, Ace.C, Joshua.C.
The control of blood sugar 1. Blood sugar levels are higher than normal after a meal is digested. 2.
By, Shakree Gibson. Location The pancreas is located deep in the abdomen, between the stomach and the spine. It lies partially behind the stomach. The.
Diabetes. PANCREAS Regulates blood sugar levels and glucose metabolism Secretes 2 hormones Insulin-allows blood sugar (glucose) to be taken out of the.
Endocrine Society Annual Meeting
Plasma insulin concentrations (A) and insulin secretion rates (B) in response to molar increments of plasma glucose concentration during the graded glucose.
Pushback What about ‘pure’ Insulin Resistance Syndromes?
Volume 15, Issue 7, Pages (May 2016)
Ghrelin—a new player in glucose homeostasis?
IL-1β differentially regulates CXCL5 and CXCL8 protein secretion in NHTBE and NSCLC cells. IL-1β differentially regulates CXCL5 and CXCL8 protein secretion.
IL-1β stimulates CXCL5 and CXCL8 gene expression and protein secretion in A549 cells in a time- and dose-dependent manner. IL-1β stimulates CXCL5 and CXCL8.
Insulin By: Joanna C and Lucy D.
Regenerative Medicine in Diabetes
Insulin Release: Shedding Light on a Complex Matter
6.5 Notes Homeostasis.
Insulin and glucagon secretion: nondiabetic and diabetic subjects.
A Clock Ticks in Pancreatic β Cells
GLP-1 Agonists and DPP-4 Inhibitors How do they work?
The Role of Obesity and Related Metabolic Disturbances in Cancers of the Colon, Prostate, and Pancreas  Edward Giovannucci, Dominique Michaud  Gastroenterology 
cardiovascular and renal systems
Xianzhong Ding, Peter R. Flatt, Johan Permert, Thomas E. Adrian 
Selective versus Total Insulin Resistance: A Pathogenic Paradox
The Stunned β Cell: A Brief History
Volume 11, Issue 3, Pages (March 2010)
Suppression of β Cell Energy Metabolism and Insulin Release by PGC-1α
What is type 2 diabetes? Medicine
Hormonal Regulation of Carbohydrates
ADA/EASD general recommendations for type 2 diabetes management (1).
Representative images of human islets infected with strains of CVB
Cyp8b1−/− mice have improved islet insulin secretion and increased islet insulin content but unchanged β-cell mass. Cyp8b1−/− mice have improved islet.
Effect of metformin on glycemic control, insulin secretion, and insulin sensitivity in T2D. Effect of metformin on glycemic control, insulin secretion,
Effect of insulin on hepcidin expression in HepG2 cells.
Comparison of the protective effects of R and S isomers of LA on insulin-stimulated 2-DG uptake. Comparison of the protective effects of R and S isomers.
1018-NT-β-cell clusters protect mice from STZ-induced diabetes.
Model for the regulation of insulin secretion in the β-cell stimulated by glucose and amino acids. Model for the regulation of insulin secretion in the.
Compensatory hyperinsulinemia maintains euglycemia in HFHC-fed guinea pigs but is lost with STZ treatment. Compensatory hyperinsulinemia maintains euglycemia.
α-Cells mainly express SSTR2 and SSTR3
Glycemia and glucose tolerance of RIP-N mice.
AGE stimulation increases MMP2 and MMP9 secretion and activation in cultured retinal endothelial cells. AGE stimulation increases MMP2 and MMP9 secretion.
Mean ± SEM concentration of insulin in plasma and CSF and glucose in plasma 30 min after the intraperitoneal administration of DET or NPH insulin at different.
Grg3 works with Pdx1 to repress α-cell genes and induce glucose-stimulated insulin secretion. Grg3 works with Pdx1 to repress α-cell genes and induce glucose-stimulated.
Zn2+ and NAD(P)H content in Mafa∆panc and Mafa∆panc;Mafb+/− β-cells.
Comparison of women carrying a male fetus and those carrying a female fetus, with respect to mean adjusted blood glucose levels during the OGTT (A), mean.
The underlying physiological basis of the HOMA model.
Grg3 is expressed in most β-cells but less frequently in α-cells.
Somatostatin released by δ-cells exerts a tonic inhibition on glucagon and insulin secretion but is not required for the glucagonostatic effect of glucose.
GLP-1 and gastrin combination therapy increases pancreatic insulin content (A) and β-cell mass (B) in NOD mice. GLP-1 and gastrin combination therapy increases.
Total plasma BCAA (A) and C3 and C5 acylcarnitine (AC) (B) concentrations in the basal state and during insulin infusion in obese subjects before and after.
Hashimoto et al. Hashimoto et al. (10) provide the data that insulin produced by β-cells is important for the maintenance of islet blood perfusion, and.
ChREBPα increases β-cell mitochondrial activity and ATP production in human islets. ChREBPα increases β-cell mitochondrial activity and ATP production.
Glucose stimulates GLP-1 secretion from the perfused rat intestine by a dose- and absorption-dependent manner. Glucose stimulates GLP-1 secretion from.
The lack of effect of denatonium to stimulate insulin release in the absence of extracellular Ca2+ or in the presence of 10 μmol/l nitrendipine. The lack.
Mean (±SE) plasma glucose concentrations before, during, and after infusions of octreotide (with growth hormone) with saline (•), with insulin replacement.
Glucose-stimulated insulin secretion, plasma glucagon levels, and pancreatic hormone contents. Glucose-stimulated insulin secretion, plasma glucagon levels,
Plasma glucose, GIR, rates of EGP and glucose utilization, and plasma concentrations of free fatty acids (FFAs) and β-hydroxy-butyrate after a subcutaneous.
Sulphonylureas and Glitazones In spite of the big number of anti-diabetic factors obtainable.
Loss of Phb2 in β-cells induces development of diabetes over a 3-week period in β-Phb2−/− mice. Loss of Phb2 in β-cells induces development of diabetes.
Summary of the new mechanistic findings of the present study.
Chronic rapamycin treatment impairs β-cell mass and insulin clearance in rats. Chronic rapamycin treatment impairs β-cell mass and insulin clearance in.
Metabolic parameters in the three groups of patients during l-arginine infusion. Metabolic parameters in the three groups of patients during l-arginine.
The hyperbolic relationship between fasting insulin and Si (A) and AIRg and Si (B) for NFG (FPG
Results supporting the validity of TEF as a descriptor of posttransplant β-cell secretion. Results supporting the validity of TEF as a descriptor of posttransplant.
Should I Stay or Should I Go: A Clash of α-Cell Identity
Pathophysiology and drug targets.
Schematic model illustrating how paracrine signaling drives LPS-stimulated cytokine secretion. Schematic model illustrating how paracrine signaling drives.
Liver fat content and impairment of insulin sensitivity and β-cell function in obese children and adolescents. Liver fat content and impairment of insulin.
The Stomach in Diabetes: From Villain to Ally
(A) Twenty-four-hour plasma profiles of insulin and amylin in healthy subjects. (A) Twenty-four-hour plasma profiles of insulin and amylin in healthy subjects.
Presentation transcript:

Defective response to insulin secretagogues may arise from A) decreased concentrations of a given secretagogue, B) loss of β-cell responsiveness to that secretagogue (defective sensing), or C) a partial inability of β-cells to secrete insulin in response to stimulation. Defective response to insulin secretagogues may arise from A) decreased concentrations of a given secretagogue, B) loss of β-cell responsiveness to that secretagogue (defective sensing), or C) a partial inability of β-cells to secrete insulin in response to stimulation. Adrian Vella, and Claudio Cobelli Diabetes 2015;64:2324-2325 ©2015 by American Diabetes Association