Regulation of GAD expression in rat pancreatic islets and brain by γ-vinyl-GABA and glucose

Petersen, Jacob Sten; Rimvall, Karin; Jørgensen, P. N.; Hasselager, E.; Moody, A. J.; Hejnæs, Kim R.; Clausen, Jes Thorn; Dyrberg, Thomas

doi:10.1007/s001250050942

Cited by 11 publications

(8 citation statements)

References 38 publications

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“…V52 levels, however, increased in response to higher glucose levels. Consistent with previous published results (Hao et al 1994, Petersen et al 1998, levels of GAD67 -the form of GAD present, along with VIAAT, in the islet mantle -were also observed to increase (data not shown).…”

Section: Differential Regulation Of V52 and V57 Expressionsupporting

confidence: 93%

“…Levels of GAD65 and GAD67 expression and of GABA release vary in response to glycemic conditions (Hao et al 1994, Smismans et al 1997, Petersen et al 1998. This suggests that GABA signaling may play a role in co-ordinating islet function to maintain euglycemia.…”

Section: Discussionmentioning

confidence: 99%

“…Since, in the pancreatic islets, GAD65 and GAD67 expression and GABA release are subject to metabolic regulation, we hypothesized that islet VIAAT content may be similarly regulated (Hao et al 1994, Smismans et al 1997, Petersen et al 1998. We therefore investigated VIAAT expression after islet exposure to different glycemic conditions.…”

Section: Differential Regulation Of V52 and V57 Expressionmentioning

confidence: 99%

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Identification and characterization of a novel isoform of the vesicular γ-aminobutyric acid transporter with glucose-regulated expression in rat islets

Suckow

Sweet

Yserloo

et al. 2006

Journal of Molecular Endocrinology

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Pancreatic islets are unique outside the nervous system in that they contain high levels of the inhibitory neurotransmitter -aminobutyric acid (GABA), synthesized by the enzyme glutamic acid decarboxylase (GAD). Since the role that GABA plays in the islet and the mechanisms whereby the two major GAD isoforms (GAD65 and GAD67) function as diabetes-associated autoantigens are unknown, continued characterization of the islet GAD-GABA system is important. We previously demonstrated that the GABA and glycine transporter vesicular inhibitory amino acid transporter (VIAAT also known as VGAT) is present in rat islets. Here we identify a novel 52 kDa variant of VIAAT in rat islets: VIAAT-52 (V52). V52 is an amino-terminally truncated form of VIAAT (V57) that likely results from utilization of a downstream start site of translation. V57 and V52 display different patterns of post-translational modification and cellular expression. Our results have indicated that islet content of V52, but not V57, is responsive to changes in glucose concentration and other extracellular conditions. VIAAT is expressed in the islet cells, but there have been conflicting findings regarding the presence of VIAAT in the cells. Here we have also provided additional evidence for the presence of VIAAT in islet cells and show that the cell line INS-1 expresses V57. V52 may be better adapted than V57 to the unique rat cell GAD-GABA system, which lacks GAD65 and in which VIAAT traffics to secretory granules rather than just to synaptic microvesicles.

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Section: Differential Regulation Of V52 and V57 Expressionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Differential Regulation Of V52 and V57 Expressionmentioning

confidence: 99%

See 1 more Smart Citation

Identification and characterization of a novel isoform of the vesicular γ-aminobutyric acid transporter with glucose-regulated expression in rat islets

Suckow

Sweet

Yserloo

et al. 2006

Journal of Molecular Endocrinology

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show abstract

“…Degli et al suggested that accumulation of glutamate upon perturbation of GABA network, produced by nutrient or environmental stress, could up-regulate expression of GAD [17]. High glucose concentrations were also shown to increase GAD expression in cultured islets [18][19][20]. GAD expression varies also during ontogeny.…”

Section: Introductionmentioning

confidence: 99%

Streptozotocin Upregulates GAD67 Expression in MIN6N8a Mouse Beta Cells

Choi

Noh

Kim

et al. 2002

Journal of Autoimmunity

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“…Along these lines, several viral infections are known to target ,%cells, and viruses, for example Coxsackie virus, have been isolated from islets of individuals with IDDM [15,21]. In humans it is difficult to directly establish an association between viral infection and initiation of a-cell destruction, because pancreatic material cannot easily be recovered during the course of disease and frequently there is a long lag period between a viral infection and clinically manifested IDDM [22,23]. For these reasons, there is a need to establish animal models that allow the dissection of the kinetics of pathogenesis leading to IDDM.…”

mentioning

confidence: 99%

Pathogenesis and treatment of virus-induced autoimmune diabetes: novel insights gained from the RIP-LCMV transgenic mouse model

Herrath¹,

Homann

Gairin

et al. 1997

Biochemical Society Transactions

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Regulation of GAD expression in rat pancreatic islets and brain by γ-vinyl-GABA and glucose

Cited by 11 publications

References 38 publications

Identification and characterization of a novel isoform of the vesicular γ-aminobutyric acid transporter with glucose-regulated expression in rat islets

Identification and characterization of a novel isoform of the vesicular γ-aminobutyric acid transporter with glucose-regulated expression in rat islets

Streptozotocin Upregulates GAD67 Expression in MIN6N8a Mouse Beta Cells

Pathogenesis and treatment of virus-induced autoimmune diabetes: novel insights gained from the RIP-LCMV transgenic mouse model

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