Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.11.17 (
CaMKII
)
4,029
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The incretin hormone glucagon-like peptide-1 (GLP-1) is secreted by enteroendocrine L cells. Stimulating endogenous GLP-1 secretion by dietary factors is a promising strategy to increase GLP-1 action. Several studies have examined the specific physiological function of wheat protein hydrolysate. Some reports suggested that intake of wheat protein ameliorates hyperglycemia. We hypothesized that wheat protein hydrolysate reduces blood glucose concentration via stimulation of GLP-1 secretion. In this study, we investigated whether wheat protein hydrolysate stimulates GLP-1 secretion and its molecular mechanism in an enteroendocrine L cell line (GLUTag cells), and we examined the effect on glucose tolerance via stimulation of GLP-1 secretion followed by induction of insulin secretion in rats. The low-molecular fraction of wheat protein hydrolysate (LWP) significantly increased GLP-1 secretion, whereas the high-molecular fraction did not. This increase was found to involve activation of the Ca
2+
/
calmodulin-dependent kinase II
pathway mediated by G protein-coupled receptor family C group 6 subtype A. Moreover, preadministration of LWP ameliorated hyperglycemia via the stimulation of GLP-1 secretion followed by induction of insulin secretion in rats. Furthermore, this LWP-induced glucose-lowering effect was significantly attenuated by the administration of a
GLP-1 receptor
antagonist. These results demonstrate that LWP significantly increased GLP-1 secretion through activation of the Ca
2+
/
calmodulin-dependent kinase II
pathway mediated by G protein-coupled receptor family C group 6 subtype A in GLUTag cells. Moreover, preadministration of LWP ameliorated hyperglycemia via the stimulation of GLP-1 secretion followed by induction of insulin secretion in rats.
...
PMID:Low-molecular fraction of wheat protein hydrolysate stimulates glucagon-like peptide-1 secretion in an enteroendocrine L cell line and improves glucose tolerance in rats. 2821 13
The
glucagon-like peptide-1 receptor
(
GLP-1R
) agonist exendin-4 is a long-acting analog of GLP-1, which stimulates insulin secretion and is clinically used in the treatment of type 2 diabetes. Previous studies have demonstrated that GLP-1 agonists and analogs serve as cardioprotective factors in various conditions. Disturbances in calcium cycling are characteristic of heart failure (HF); therefore, the aim of this study was to investigate the effect of exendin-4 (a GLP-1 mimetic) on the regulation of calcium handling and to identify the underlying mechanisms in an HF rat model after myocardial infarction (MI). Rats underwent surgical ligation of the left anterior descending coronary artery or sham surgery prior to infusion with vehicle, exendin-4, or exendin-4 and exendin9-39 for 4 weeks. Exendin-4 treatment decreased MI size, suppressed chamber dilation, myocyte hypertrophy, and fibrosis and improved in vivo heart function in the rats subjected to MI. Exendin-4 resulted in an increase in circulating GLP-1 and
GLP-1R
in ventricular tissues. Additionally, exendin-4 activated the eNOS/cGMP/PKG signaling pathway and inhibited the Ca
2+
/
calmodulin-dependent kinase II
(
CaMKII
) pathways. Myocytes isolated from exendin-4-treated hearts displayed higher Ca
2+
transients, higher sarcoplasmic reticulum Ca
2+
content, and higher l-type Ca
2+
current densities than MI hearts. Exendin-4 treatment restored the protein expression of sarcoplasmic reticulum Ca
2+
uptake ATPase (SERCA2a), phosphorylated phospholamban (PLB) and Cav1.2 and decreased the levels of phosphorylated ryanodine receptor (RyR). Moreover, the favorable effects of exendin-4 were significantly inhibited by exendin9-39 (a
GLP-1 receptor
antagonist). Exendin-4 treatment of an HF rat model after MI inhibited cardiac and cardiomyocytes progressive remodeling. In addition, Ca
2+
handling and its molecular modulation were also improved by exendin-4 treatment. The beneficial effects of exendin-4 on cardiac remodeling may be mediated through activation of the eNOS/cGMP/PKG pathway.
...
PMID:Exendin-4 inhibits structural remodeling and improves Ca
2+
homeostasis in rats with heart failure via the GLP-1 receptor through the eNOS/cGMP/PKG pathway. 2824 57
