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Establishment of new clonal pancreatic ?-cell lines (MIN6-K) useful for study of incretin/cyclic adenosine monophosphate signaling.

ABSTRACT: Incretin/cyclic adenosine monophosphate (cAMP) signaling is critical for potentiation of insulin secretion. Although several cell lines of pancreatic ?-cells are currently available, there are no cell lines suitable for investigation of incretin/cAMP signaling. In the present study, we have newly established pancreatic ?-cell lines (named MIN6-K) from the IT6 mouse, which develops insulinoma. MIN6-K8 cells respond to both glucose and incretins, such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), as is the case in pancreatic islets, whereas MIN6-K20 cells respond to glucose, but not to incretins. Despite the difference in incretin-potentiated insulin secretion between these two cell lines, the accumulation of cAMP after stimulation of GLP-1 is comparable in these cells. Interestingly, we also found that incretin responsiveness is drastically induced by the formation of pseudoislets from MIN6-K20 cells to a level comparable to that of pancreatic islets. Thus, these cell lines are useful for studying incretin/cAMP signaling in ?-cells. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2010.00026.x, 2010).

SUBMITTER: Iwasaki M

PROVIDER: S-EPMC4008005 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature

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Establishment of new clonal pancreatic β-cell lines (MIN6-K) useful for study of incretin/cyclic adenosine monophosphate signaling.

Iwasaki Masahiro M Minami Kohtaro K Shibasaki Tadao T Miki Takashi T Miyazaki Jun-Ichi J Seino Susumu S

Journal of diabetes investigation 20100801 4

Incretin/cyclic adenosine monophosphate (cAMP) signaling is critical for potentiation of insulin secretion. Although several cell lines of pancreatic β-cells are currently available, there are no cell lines suitable for investigation of incretin/cAMP signaling. In the present study, we have newly established pancreatic β-cell lines (named MIN6-K) from the IT6 mouse, which develops insulinoma. MIN6-K8 cells respond to both glucose and incretins, such as glucagon-like peptide-1 (GLP-1) and glucose ...[more]

PMID: 24843422

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Project description:An antagonistic communication exists between adenosinergic and dopaminergic signaling in the basal ganglia, which suggests that the suppression of adenosine A2A receptors-cyclic adenosine monophosphate pathway may be able to restore the disrupted dopamine transmission that results in motor symptoms in Parkinson's disease (PD). Arbutin is a natural glycoside that possesses antioxidant, anti-inflammatory, and neuroprotective properties. The purpose of this study was to investigate whether arbutin could ameliorate the symptoms of PD and to examine the underlying mechanism. In this study, Swiss albino mouse models of PD were established by the intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine for 4 successive days, with the concurrent intraperitoneal administration of arbutin (50 and 100 mg/kg) for 7 days. The results showed that arbutin significantly reduced lipid peroxidation, total nitrite levels, and inflammation in the substantia nigra and striatum of PD mouse models. In addition, arbutin decreased the activity of endogenous antioxidants, reduced the levels of dopamine, 3,4-dihydroxyphenylacetic acid, homovanillic acid, and γ-aminobutyric acid, and minimized neurodegeneration in the striatum. Arbutin also reduced the abnormal performance of PD mouse models in the open field test, bar test, pole test, and rotarod test. The therapeutic efficacy of arbutin was similar to that of madopar. The intraperitoneal injection of the A2AR agonist CGS21680 (0.5 mg/kg) attenuated the therapeutic effects of arbutin, whereas the intraperitoneal injection of forskolin (3 mg/kg) enhanced arbutin-mediated improvements. These findings suggest that arbutin can improve the performance of PD mouse models by inhibiting the function of the A2AR and enhancing the effects of cyclic adenosine monophosphate. This study was approved by the Institutional Animal Ethics Committee (1616/PO/Re/S/12/CPCSEA) on November 17, 2019 (approval No. IAEC/2019/010).

Dataset Information

Establishment of new clonal pancreatic ?-cell lines (MIN6-K) useful for study of incretin/cyclic adenosine monophosphate signaling.

Publications

Establishment of new clonal pancreatic β-cell lines (MIN6-K) useful for study of incretin/cyclic adenosine monophosphate signaling.

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