Mika Kimura

Gifu University Hospital, Gihu, Gifu, Japan

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Publications (4)5.53 Total impact

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    ABSTRACT: This study examined the effect of glucose and 12-O-tetradecanoylphorbol-13-acetate (TPA) on insulin secretion in isolated human insulinoma cells. In addition, we analyzed conventional PKCα and β activation in the membrane fractions, respectively. Treatment with 5 mM and 20 mM glucose for 5 min and 20 min resulted in 6∼7-fold increases in insulin secretion, and treatment with 1 μM TPA for 5 min also resulted in 3-fold increases in insulin secretion from the basal level. Immunoblot analysis of membrane fractions showed increases in PKCα and β immunoreactivities after treatment with 5 mM, 20 mM glucose and 1 μM TPA. Translocations of PKCα after treatment with glucose and TPA were greater than those of PKCβ in membrane fractions. These results suggest that TPA independently provokes insulin secretion via PKC activation and that PKCα and β activation may be involved in insulin secretion in human insulinoma cells.
    International Union of Biochemistry and Molecular Biology Life 01/2008; 46(4):739 - 745. · 2.79 Impact Factor
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    ABSTRACT: Vitamin E, an antioxidant, improves insulin sensitivity through the suppression of conventional PKC in vascular smooth muscle cells. It has been reported that vitamin E reduces platelet aggregation through the suppression of PKC alpha and beta (Diabetes 47 (1998) 1494). On the other hand, 1 alpha,25-dihydroxy vitamin D3 (1,25D3) activates conventional PKC and may subsequently cause insulin resistance. Against this background, we examined the effect of vitamin E and 1,25D3 on PKC beta and PKC zeta/lambda activities in vitro and 10 nM insulin-induced glucose uptake in rat adipocytes. In vitro PKC beta activity of adipocytes was slightly decreased by the addition of 1 microM vitamin E, but not PKC zeta/lambda activity. In contrast, a 10-1000 nM 1,25D3 dose responsively activated PKC beta activity of adipocytes (ED 50%, 10 nM), but not PKC zeta/lambda activity. Pretreatment with 1 microM vitamin E for 60 min did not improve the insulin-induced glucose uptake. On the other hand, pretreatment with a 10-1000 nM 1,25D3 dose responsively suppressed insulin-induced glucose uptake. Moreover, 1,25D3 increased membrane-associated PKC beta immunoreactivity for 60 min, but no additional increase in membrane-associated PKC beta immunoreactivity during treatment with insulin was observed. These results suggest that 1,25D3 reduces insulin-induced glucose uptake via activation of PKC beta, but not vitamin E in rat adipocytes.
    Diabetes Research and Clinical Practice 04/2002; 55(3):175-83. · 2.74 Impact Factor
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    ABSTRACT: Vitamin E, an antioxidant, improves insulin sensitivity through the suppression of conventional PKC in vascular smooth muscle cells. It has been reported that vitamin E reduces platelet aggregation through the suppression of PKCα and β (Diabetes 47 (1998) 1494). On the other hand, 1α,25-dihydroxy vitamin D3 (1,25D3) activates conventional PKC and may subsequently cause insulin resistance. Against this background, we examined the effect of vitamin E and 1,25D3 on PKCβ and PKC ζ/λ activities in vitro and 10 nM insulin-induced glucose uptake in rat adipocytes. In vitro PKCβ activity of adipocytes was slightly decreased by the addition of 1 μM vitamin E, but not PKC ζ/λ activity. In contrast, a 10–1000 nM 1,25D3 dose responsively activated PKCβ activity of adipocytes (ED 50%, 10 nM), but not PKC ζ/λ activity. Pretreatment with 1 μM vitamin E for 60 min did not improve the insulin-induced glucose uptake. On the other hand, pretreatment with a 10–1000 nM 1,25D3 dose responsively suppressed insulin-induced glucose uptake. Moreover, 1,25D3 increased membrane-associated PKCβ immunoreactivity for 60 min, but no additional increase in membrane-associated PKCβ immunoreactivity during treatment with insulin was observed. These results suggest that 1,25D3 reduces insulin-induced glucose uptake via activation of PKCβ, but not vitamin E in rat adipocytes.
    Diabetes Research and Clinical Practice - DIABETES RES CLIN PRACT. 01/2002; 55(3):175-183.
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    ABSTRACT: Although much evidence has been accumulated suggesting that tumor necrosis factor-α (TNF-α) is an important mediator of insulin resistance, the precise mechanism involved is still unclear. Recently, it has been reported that insulin-induced glucose uptake is mediated by activation of second messengers such as insulin receptor substrate 1 (IRS-1), phosphatidylinositol 3-kinase (PI3K), and diacylglycerol (DG)-protein kinase C (PKC). We have examined the effect of TNF-α on insulin-induced glucose uptake and activations of tyrosine kinase, IRS-1, PI3K and PKC in rat adipocytes. Pretreatment with 0.1–100 nM TNF-α for 60 min resulted in a significant decrease in 10 nM insulin- or 1 μM 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced [3H]2-deoxyglucose uptake without affecting basal glucose uptake. 10 nM insulin-stimulated activation of tyrosine kinase, IRS-1 and PI3K was suppressed by preincubation with 0.1–10 nM TNF-α for 60 min. 10 nM TNF-α pretreatment also suppressed 10 nM insulin- and 1 μM TPA-induced increases in membrane-associated PKCβ and PKCζ. Furthermore, 10 nM TNF-α, by itself, altered PKCβ translocation from the membrane to cytosol. These results suggest that TNF-α inhibits insulin-stimulated activation of both the tyrosine kinase-IRS-1-PI3K-PKCζ pathway and DG-PKC pathway. Finally, TNF-α contributes to insulin resistance in rat adipocytes.
    Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 04/1999;