1 – 25 of 25
- show: 50
- |
- sort: year (new to old)
Close
Embed this list
<iframe src=" "
width=" "
height=" "
allowtransparency="true"
frameborder="0">
</iframe>
- 2018
-
Mark
DPP-4 is expressed in human pancreatic beta cells and its direct inhibition improves beta cell function and survival in type 2 diabetes
(
- Contribution to journal › Article
- 2016
-
Mark
Mixed meal diminishes glucose excursion compared to glucose by several adaptive mechanisms in man.
(
- Contribution to journal › Article
-
Mark
Beta-Cell Function and Its Underlying Mechanism 2015.
(
- Contribution to journal › Debate/Note/Editorial
-
Mark
Enhanced Insulin Sensitivity by Adipose Tissue Browning Alters Islet Morphology and Hormone Secretion in Response to Autonomic Nervous Activation in Female Mice.
(
- Contribution to journal › Article
-
Mark
Defective insulin secretion by chronic glucagon receptor activation in glucose intolerant mice.
(
- Contribution to journal › Article
-
Mark
Incretin hormone receptors are required for normal beta cell development and function in female mice
(
- Contribution to journal › Article
-
Mark
Evidence for neural contribution to islet effects of DPP-4 inhibition in mice
(
- Contribution to journal › Article
-
Mark
Extrapancreatic contribution to glucose regulation by dipeptidyl peptidase 4 inhibition
(
- Contribution to journal › Scientific review
- 2015
-
Mark
Incretin and islet hormone responses to meals of increasing size in healthy subjects.
(
- Contribution to journal › Article
-
Mark
Fibroblast growth factor 21 prevents glycemic deterioration in insulin deficient mouse models of diabetes.
(
- Contribution to journal › Article
- 2014
-
Mark
Fibroblast Growth Factor 21 (FGF21) and Glucagon Like-Peptide 1 Contribute to Diabetes Resistance in Glucagon Receptor Deficient Mice.
(
- Contribution to journal › Article
-
Mark
Conditional glucagon receptor overexpression has multi-faceted consequences for beta-cell function.
(
- Contribution to journal › Article
-
Mark
Dipeptidyl peptidase 4 (DPP-4) is expressed in mouse and human islets and its activity is decreased in human islets from individuals with type 2 diabetes.
(
- Contribution to journal › Article
-
Mark
Pleiotropic Mechanisms for the Glucose-Lowering Action of DPP-4 Inhibitors.
(
- Contribution to journal › Article
-
Mark
Impact of glucose dosing regimens on modeling of glucose tolerance and β-cell function by intravenous glucose tolerance test in diet-induced obese mice.
(
- Contribution to journal › Article
-
Mark
Dipeptidyl peptidase-4 (DPP-4): Localization and activity in human and rodent islets.
(
- Contribution to journal › Article
- 2013
-
Mark
Methods and Models for Metabolic Assessment in Mice
2013) In Journal of Diabetes Research(
- Contribution to journal › Article
-
Mark
Enhanced beta cell function and anti-inflammatory effect after chronic treatment with the dipeptidyl peptidase-4 inhibitor vildagliptin in an advanced-aged diet-induced obesity mouse model.
(
- Contribution to journal › Article
-
Mark
A link between GIP and osteopontin in adipose tissue and insulin resistance.
(
- Contribution to journal › Article
- 2012
-
Mark
Regulation of the pro-inflammatory cytokine osteopontin by GIP in adipocytes - A role for the transcription factor NFAT and phosphodiesterase 3B.
(
- Contribution to journal › Article
-
Mark
Differential Development of Glucose Intolerance and Pancreatic Islet Adaptation in Multiple Diet Induced Obesity Models
(
- Contribution to journal › Article
- 2011
-
Mark
From PDE3B to the regulation of energy homeostasis.
(
- Contribution to journal › Article
-
Mark
Alterations in Cyclic Nucleotide Phosphodiesterase Activities in Omental and Subcutaneous Adipose Tissues in Human Obesity
(
- Contribution to journal › Article
- 2009
-
Mark
Regulation of AMP-activated protein kinase by cAMP in adipocytes: Roles for phosphodiesterases, protein kinase B, protein kinase A, Epac and lipolysis.
(
- Contribution to journal › Article
-
Mark
Protein kinase B activity is required for the effects of insulin on lipid metabolism in adipocytes.
(
- Contribution to journal › Article