Hexosamine pathway but not interstitial changes mediates glucotoxicity in pancreatic β-cells as assessed by cytosolic Ca2+ response to glucose

@article{Yanagida2014HexosaminePB,
  title={Hexosamine pathway but not interstitial changes mediates glucotoxicity in pancreatic $\beta$-cells as assessed by cytosolic Ca2+ response to glucose},
  author={Kazuhiro Yanagida and Yuko Maejima and Putra Santoso and Zesemdorj Otgon-Uul and Yifei Yang and Kazuya Sakuma and Kenju Shimomura and Toshihiko Yada},
  journal={Aging (Albany NY)},
  year={2014},
  volume={6},
  pages={207 - 214}
}
Hyperglycemia impairs insulin secretion as well as insulin action, being recognized as the glucotoxicity that accelerates diabetes. [...] Key Method In this study, to explore direct effects of these alterations on β-cells, single β-cells isolated from rat islets were cultured for 3 days with high (22.3 mM) glucose (HG), compared with control 5.6 mM glucose, followed by their functional assessment by measuring cytosolic Ca2+ concentration ([Ca2+]i). The [Ca2+]i response to a physiological rise in glucose…Expand
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References

SHOWING 1-10 OF 30 REFERENCES
Glucosamine-induced &bgr;-cell Dysfunction: A Possible Involvement of Glucokinase or Glucose-transporter Type 2
TLDR
The data imply that glucosamine impairs glucose-induced insulin release probably through the inhibition of glucose metabolism. Expand
Role of Cytosolic Ca2+ in Impaired Sensitivity to Glucose of Rat Pancreatic Islets Exposed to High Glucose In Vitro
TLDR
Observations confirm that exposure of pancreatic β-cells to high glucose concentrations induces a selective reduction of the GSIR and shows that this impaired response is reversibly restored by an additional culture with normal glucose, and suggest that the inability of glucose to provoke a [Ca2+]i rise, which is observed in the β- cells exposed tohigh glucose, may be responsible for the selective impairment of theGSIR. Expand
Activation of the Hexosamine Pathway by Glucosamine in Vivo Induces Insulin Resistance in Multiple Insulin Sensitive Tissues.
We determined the effect of infusion of glucosamine (GlcN), which bypasses the rate limiting reaction in the hexosamine pathway, on insulin-stimulated rates of glucose uptake and glycogen synthesisExpand
The molecular mechanisms of pancreatic β-cell glucotoxicity: Recent findings and future research directions
TLDR
Deciphering these molecular mechanisms of β- cell glucotoxicity is a mandatory first step toward the development of therapeutic strategies to protect β-cells and improve the functional β-cell mass in type 2 diabetes. Expand
Hexosamines as mediators of nutrient sensing and regulation in diabetes.
  • D. McClain
  • Biology, Medicine
  • Journal of diabetes and its complications
  • 2002
TLDR
Excess hexosamine flux leads to a coordinated response whereby fuel is shunted toward long-term storage, mirroring the "thrifty phenotype" and suggesting a mechanism by which chronic overnutrition leads to the phenotype of Type 2 diabetes. Expand
Coupling of β-Cell Desensitization by Hyperglycemia to Excessive Stimulation and Circulating Insulin in Glucose-Infused Rats
TLDR
It is concluded that excessiveβ-cell stimulation rather than glucotoxicity underlies hyperglycemia-induced β-cell insensitivity and effects of hyperinsulinemia can form part of the mechanisms whereby excessive stimulation affects β- cell secretion. Expand
Single pancreatic beta-cells from normal rats exhibit an initial decrease and subsequent increase in cytosolic free Ca2+ in response to glucose.
TLDR
The results demonstrate that the glucose-induced bimodal change in [Ca2+]i is a physiological response of islet beta-cells, and that the decrease and increase in [ Ca2+)i are generated by mutually-independent mechanisms which are operated through glucose metabolism by islet Beta-cells. Expand
Increased hexosamine biosynthetic pathway flux dedifferentiates INS-1E cells and murine islets by an extracellular signal-regulated kinase (ERK)1/2-mediated signal transmission pathway
TLDR
Glucotoxic ER stress dedifferentiates beta cells, in the absence of apoptosis, through a transcriptional response, and these effects are mediated by the activation of ERK1/2. Expand
The hexosamine biosynthesis pathway regulates insulin secretion via protein glycosylation in mouse islets.
TLDR
It is shown that inhibition of the hexosamine biosynthesis pathway decreases insulin secretion from mouse islets in response to a number of secretagogues, including glucose, which may have implications for the development of type 2 diabetes. Expand
Hexosamines, insulin resistance, and the complications of diabetes: current status.
  • M. Buse
  • Biology, Medicine
  • American journal of physiology. Endocrinology and metabolism
  • 2006
TLDR
Increased flux through HBP is required and sufficient for some of the metabolic effects of sustained, increased glucose flux, which promotes the complications of diabetes, e.g., diminished expression of sarcoplasmic reticulum Ca(2+)-ATPase in cardiomyocytes and induction of TGF-beta and plasminogen activator inhibitor-1 in vascular smooth muscle cells, mesangial cells, and aortic endothelial cells. Expand
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