ΑGLP-1R−/− mice show glucose intolerance and disturbed glucagon secretion in response to i.p. glucose administration. αGLP-1R−/− mice show glucose intolerance.

Slides:



Advertisements
Similar presentations
Volume 4, Issue 12, Pages (December 2015)
Advertisements

Insulin and glucagon secretion: nondiabetic and diabetic subjects.
Glucose homeostasis: roles of insulin, glucagon, amylin, and GLP-1.
Impaired glucose tolerance in adult S1/3 KO mice on a normal chow
Change in random blood glucose level, body weight, and intraperitoneal glucose tolerance test (IPGTT) in streptozotocin (STZ)-induced diabetic mice. Change.
Volume 18, Issue 13, Pages (March 2017)
Volume 19, Issue 6, Pages (June 2014)
Treatment with AAV8‐hAAT‐FGF21 improves insulin sensitivity and glucose tolerance Treatment with AAV8‐hAAT‐FGF21 improves insulin sensitivity and glucose.
Volume 1, Issue 4, Pages (April 2005)
Volume 96, Issue 3, Pages (February 1999)
Comparison of triglycerides AUC 480’ between IGT+reduced FPIS group, IGT+preserved FPIS group, and IGT+reduced FPIS+reduced FPIS and FPIS restitution with.
Exosomes transfected with obesity-associated miRNAs induce glucose intolerance dissociated from obesity. Exosomes transfected with obesity-associated miRNAs.
Cyp8b1−/− mice have improved islet insulin secretion and increased islet insulin content but unchanged β-cell mass. Cyp8b1−/− mice have improved islet.
VAN GLP-1R kd disturbed postmeal glycemia and insulinemia but did not impair tolerance of an oral glucose bolus. VAN GLP-1R kd disturbed postmeal glycemia.
Overexpression of BTG2 resulted in an increase in hepatic gluconeogenesis. Overexpression of BTG2 resulted in an increase in hepatic gluconeogenesis. A:
Deletion of neuronal insulin receptor signaling reduces TG secretion, while the targeted knockout of insulin receptors restricted to the periphery increases.
Changes (mean +SEM) in glucose, insulin, glucagon-like peptide (GLP)-1 and ghrelin from the baseline values after administration of placebo (broken lines.
Exogenous CRP administration causes fasting hyperglycemia and hyperinsulinemia without altering body composition. Exogenous CRP administration causes fasting.
1018-NT-β-cell clusters protect mice from STZ-induced diabetes.
WASH cKO mice display a normal pancreatic development.
TG-CRP mice display fasting hyperglycemia, hyperinsulinemia, and insulin resistance. TG-CRP mice display fasting hyperglycemia, hyperinsulinemia, and insulin.
Transplantation of the ω3-modified microbiome as a relevant way to preserve a lean phenotype in mice fed the HFHS diet. Transplantation of the ω3-modified.
GSIS. GSIS. In vivo: serum insulin levels at fasting state and 30 min after glucose injection (A) and the fold change in serum insulin after glucose loading.
Activation of β-adrenoceptors improves glucose tolerance in diabetic animals and increases glucose uptake in vivo, ex vivo, and in vitro. Activation of.
Volume 27, Issue 11, Pages e3 (June 2019)
Glycemia and glucose tolerance of RIP-N mice.
Nrf2−/− mice suffered greater renal damage by STZ compared with Nrf2+/+ mice. Nrf2−/− mice suffered greater renal damage by STZ compared with Nrf2+/+ mice.
Modulation of insulin sensitivity by IL-6 in mice: A lack of PTP1B prevents chronic effects of IL-6. Modulation of insulin sensitivity by IL-6 in mice:
TXNIP and caspase-1 protein levels are increased in the adipose tissue of ob/ob mice. TXNIP and caspase-1 protein levels are increased in the adipose tissue.
Measurement of insulin release from islets evoked by glucose, diazoxide, and high K+. Measurement of insulin release from islets evoked by glucose, diazoxide,
Glucose tolerance in WT and TRPM2-KO mice.
Transgenic restoration of long-chain n-3 PUFA protects against obesity-linked insulin resistance and glucose intolerance. Transgenic restoration of long-chain.
Grg3 is expressed in most β-cells but less frequently in α-cells.
BAFF-deficient (BAFFnull) and anti-BAFF antibody (Ab)–treated obese mice exhibit superior glucose metabolic control compared with WT and Bnull mice. BAFF-deficient.
The figure shows the mean±SD of glucose and insulin for the 2-hour OGTTs and MTTs for the 12 HP diet subjects and the 12 HC diets subjects. The figure.
GLP-1 and gastrin combination therapy restores normoglycemia in NOD mice. GLP-1 and gastrin combination therapy restores normoglycemia in NOD mice. Beginning.
A: Chemical structure of pterosin A
Fig. 2 HHKO mice exhibit improved glucose tolerance by increasing plasma incretin levels and insulin secretion. HHKO mice exhibit improved glucose tolerance.
Fig. 4 Deletion of hepatocyte HIF-2α does not affect obesity-induced glucose, glucagon, and insulin intolerance. Deletion of hepatocyte HIF-2α does not.
Chop deletion preserves β-cell function in P58IPK−/− mice.
Rapid improvement of glucose tolerance induced by PP
Adoptive transfer of purified activated G9Cα−/−
Effect of anandamide on blood glucose clearance and insulin sensitivity. Effect of anandamide on blood glucose clearance and insulin sensitivity. A: Intraperitoneal.
Mean (±SE) plasma glucose concentrations before, during, and after infusions of octreotide (with growth hormone) with saline (•), with insulin replacement.
Joan Goulley, Ulf Dahl, Nathalie Baeza, Yuji Mishina, Helena Edlund 
HFD feeding induced insulin resistance in TRIB3 MOE mice.
High-glucose–induced insulin resistance in TRIB3 MOE mice.
Absence of OcaB protects against age-induced insulin resistance.
Liver fibrosis after CCl4 injury in 5αR1-KO and WT mice.
Insulin resistance and hepatic steatosis in ASKO mice.
MϕRIP140KD mice exhibit improved metabolic phenotypes.
Effects of Rosi treatment on ASKO mice.
Effects of berberine on in vivo metabolism in two animal models of insulin resistance. Effects of berberine on in vivo metabolism in two animal models.
Metabolic effects of VSG in GLP-1r KO mice.
Glucose-stimulated insulin secretion, plasma glucagon levels, and pancreatic hormone contents. Glucose-stimulated insulin secretion, plasma glucagon levels,
Estimated glucose delta values (mmol/L) after glucagon injection (5 µg/kg) in octreotide-treated rats. Estimated glucose delta values (mmol/L) after glucagon.
GTTs and ITTs. A: GTTs of WT (◇), LepTg (♦), Akita (open circles), and LepTg:Akita (closed circles) mice at 8 and 16 weeks of age. GTTs and ITTs. A: GTTs.
High-fat diet–induced glucose intolerance is prevented in ghrelin knockout (Ghr-KO) mice. High-fat diet–induced glucose intolerance is prevented in ghrelin.
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.
Lack of OcaB impairs age-associated B-lymphocyte accumulation in WAT
Mice lacking Y1 receptor in the hematopoietic compartment remain healthy under normal chow feeding conditions. Mice lacking Y1 receptor in the hematopoietic.
Effects of rhein on FBG (A) and glucose intolerance (B) in db/db mice.
Deficiency of adipocyte IKKβ does not affect diet-induced weigh gain but results in an exaggerated diabetic phenotype when challenged with an HFD. A: IKKβ.
Glycemic control and body weight over 52 weeks.
SORCS1 and SORCS3 control energy balance and orexigenic peptide production A, BBlood glucose (A) and insulin (B) levels after overnight fasting in 9‐month‐old.
Median (interquartile range) of sensor glucose (A) and insulin delivery (B) during closed-loop (solid red line and red shaded area) and control period.
Distribution of daily frequency of BGM
Postprandial glucose, insulin and glucagon-like peptide-1 (GLP-1) levels following carbohydrate-first (CF), carbohydrate-last (CL) and sandwich (S) meal.
Fig. 4 In vivo evaluation of insulin complex for type 1 diabetic mice treatment. In vivo evaluation of insulin complex for type 1 diabetic mice treatment.
Receiver operator characteristic (ROC) curve for fasting blood glucose (FBG) predicting posttransplantation diabetes (PTD) using time 0 FBG (a) and screening.
Presentation transcript:

αGLP-1R−/− mice show glucose intolerance and disturbed glucagon secretion in response to i.p. glucose administration. αGLP-1R−/− mice show glucose intolerance and disturbed glucagon secretion in response to i.p. glucose administration. A: Female αGLP-1R−/− KO mice (ko, red) and their WT littermates (wt, gray), 4–5 months old (n = 8–10), were used in these assays. A: ipGTT with glucose at 2 g/kg body weight after overnight fasting. B: Area under the curve (AUC) of the ipGTT. C: Circulating insulin levels of the ko and wt mice during ipGTT. D: First-phase insulin secretion after glucose injection. E: ITT with insulin at 0.5 units/kg body weight after 6 h fasting. F: Glucagon secretion after glucose injection in the same setting as ipGTT. Only two time points were examined because glucagon measurements require a large amount of blood (50 μL), and the Institutional Animal Care and Use Committee guidelines have a limit on live blood collection from each mouse.*P < 0.05; **P < 0.01. Yanqing Zhang et al. Diabetes 2019;68:34-44 ©2019 by American Diabetes Association