N. Kaiser

Publications102
h-index42
Citations7,393
Highly Influential Citations171
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Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets.
TLDR
In vitro exposure of islets from nondiabetic organ donors to high glucose levels resulted in increased production and release of IL-1beta, followed by NF-kappaB activation, Fas upregulation, DNA fragmentation, and impaired beta cell function, which implicate an inflammatory process in the pathogenesis of glucotoxicity in type 2 diabetes. Expand
Pancreatic and duodenal homeobox gene 1 induces expression of insulin genes in liver and ameliorates streptozotocin-induced hyperglycemia
TLDR
The capacity of PDX-1 to reprogram extrapancreatic tissue towards a β-cell phenotype, may provide a valuable approach for generating ‘self’ surrogate β cells, suitable for replacing impaired islet-cell function in diabetics. Expand
Distinct effects of saturated and monounsaturated fatty acids on beta-cell turnover and function.
TLDR
The results suggest that the lipotoxic effect of the saturated palmitic acid involves an increased apoptosis rate coupled with reduced proliferation capacity of beta-cells and impaired insulin secretion, and the monounsaturated palmitoleic acid promotes beta-cell proliferation at low glucose concentrations, counteracting the negative effects of palmitoic acid as well as improving beta- cell function. Expand
mTOR Inhibition by Rapamycin Prevents β-Cell Adaptation to Hyperglycemia and Exacerbates the Metabolic State in Type 2 Diabetes
TLDR
The essential role of mTOR/S6K1 in orchestrating β-cell adaptation to hyperglycemia in type 2 diabetes is emphasized and it is likely that treatments based on mTOR inhibition will cause exacerbation of diabetes. Expand
Glucose-induced β cell production of IL-1β contributes to glucotoxicity in human pancreatic islets.
TLDR
In vitro exposure of islets from nondiabetic organ donors to high glucose levels resulted in increased production and release of IL-1beta, followed by NF-kappaB activation, Fas upregulation, DNA fragmentation, and impaired beta cell function, which implicate an inflammatory process in the pathogenesis of glucotoxicity in type 2 diabetes. Expand
Glucose induces beta-cell apoptosis via upregulation of the Fas receptor in human islets.
TLDR
A new role for glucose in regulating Fas expression in human beta-cells is supported and may contribute to beta-cell destruction by the constitutively expressed FasL independent of an autoimmune reaction, thus providing a link between type 1 and type 2 diabetes. Expand
Beta-cell protein kinases and the dynamics of the insulin response to glucose.
TLDR
It is suggested that three families of PKs function as distal amplifiers for stimulus-secretion coupling signals originating from fuel metabolism, as well as from incretins acting through membrane receptors, adenylate cyclase, and phospholipase C. Expand
Monolayer culture of adult rat pancreatic islets on extracellular matrix: modulation of B-cell function by chronic exposure to high glucose.
TLDR
These studies suggest that generation of the reduced insulin response may be related to the prolonged high insulin secretion rate; expression of the functional change is specific to the nutrient stimulus-secretion coupling; and modifications in intercellular contacts may be involved in B-cell desensitization. Expand
Differential Regulation of Glucose Transport and Transporters by Glucose in Vascular Endothelial and Smooth Muscle Cells
TLDR
The ability of vascular smooth muscle cells to down-regulate glucose transport in response to chronic hyperglycemia may serve as a protective mechanism against possible adverse effects of increased intracellular glucose. Expand
Radiocontrast agents induce endothelin release in vivo and in vitro.
TLDR
The intravascular administration of the ionic radiocontrast agent sodium iothalamate and iohexol stimulated endothelin release from cultured bovine endothelial cells, suggesting a direct effect of ionic and nonionic agents on vascular endothelium. Expand
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