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Variants in KCNQ1 are associated with susceptibility to type 2 diabetes mellitus
TLDR
The data implicate KCNQ1 as a diabetes susceptibility gene in groups of different ancestries as well as in two independent Japanese populations, and the risk allele of this polymorphism was associated with impairment of insulin secretion according to the homeostasis model assessment of β-cell function or the corrected insulin response.
Inhibition of gastric inhibitory polypeptide signaling prevents obesity
TLDR
GIP directly links overnutrition to obesity and it is a potential target for anti-obesity drugs.
The murine glucagon-like peptide-1 receptor is essential for control of bone resorption.
TLDR
An essential role is established for endogenous GLP-1 receptor signaling in the control of bone resorption, likely through a calcitonin-dependent pathway.
The protective roles of GLP-1R signaling in diabetic nephropathy: possible mechanism and therapeutic potential.
TLDR
GLP-1 has a crucial role in protection against increased renal oxidative stress under chronic hyperglycemia, by inhibition of NAD(P)H oxidase, a major source of superoxide, and by cAMP-PKA pathway activation.
Extrapancreatic incretin receptors modulate glucose homeostasis, body weight, and energy expenditure.
TLDR
The findings extend the understanding of how endogenous incretin circuits regulate glucose homeostasis independent of the beta cell via control of adipokine secretion and energy expenditure through analysis of mice fed a high-fat (HF) diet.
Double incretin receptor knockout (DIRKO) mice reveal an essential role for the enteroinsular axis in transducing the glucoregulatory actions of DPP-IV inhibitors.
TLDR
It is demonstrated that glucose-stimulated insulin secretion is maintained despite complete absence of both incretin receptors, and a critical role for incret in receptors as essential downstream targets for the acute glucoregulatory actions of DPP-IV inhibitors is delineated.
Gastric inhibitory polypeptide as an endogenous factor promoting new bone formation after food ingestion.
TLDR
In vitro examination showed the percentage of osteoblastic cells undergoing apoptosis to be significantly decreased in the presence of GIP, indicating that GIPR(-/-) mice have high-turnover osteoporosis.
The C42R mutation in the Kir6.2 (KCNJ11) gene as a cause of transient neonatal diabetes, childhood diabetes, or later-onset, apparently type 2 diabetes mellitus.
TLDR
These results broaden the spectrum of diabetes phenotypes caused by mutations of KCNJ11 and suggest that mutations in this gene should be taken into consideration for not only permanent neonatal diabetes but also other forms of diabetes with milder phenotypes and later onset.
Roles of 14-3-3 and calmodulin binding in subcellular localization and function of the small G-protein Rem2.
TLDR
It is shown that Rem2 in fact does interact with 14-3-3 and CaM and induces dendrite-like extensions in COS cells and shares many previously unrecognized features with the other RGK family members.
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