Rat Pancreatic Islet and RINm5F Cell Responses to Epiandrosterone, Dehydroepiandrosterone and Interleukin-1β

Laychock, Suzanne G.

doi:10.1016/s0006-2952(97)00666-7

Cited by 15 publications

(14 citation statements)

References 42 publications

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“…In RINm5F cells treated with DHEAS, 16.7 mM glucose-induced insulin secretion was preserved but not enhanced (Laychock 1998). Conversely, INS-1 cells showed a better insulin response to 10 mM glucose and L-pyruvate following DHEAS treatment (Dillon et al 2000).…”

Section: Discussionmentioning

confidence: 88%

“…This suggests that other factors or metabolites produced in the gut may contribute to their glucose-lowering effects. Enhanced glucose-induced insulin release in DHEAS-treated RINm5F-cells, derived from rat insulinoma, has been reported (Laychock 1998). Although DHEA has been shown to counteract the cytotoxic effects of interleukin 1-b, it has detrimental effects on glucose transport, oxidation, and responsiveness in RIN cells or rat islets (Laychock and Bauer 1996;Giroix et al 1997).…”

Section: Introductionmentioning

confidence: 95%

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Deleterious Effects of Supplementation with Dehydroepiandrosterone Sulphate or Dexamethasone on Rat Insulin-Secreting Cells Under In Vitro Culture Condition

et al. 2006

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Dehydroepiandrosterone (DHEA) and glucocorticoids are steroid hormones synthesised in the adrenal cortex. Administration of DHEA, its sulphate derivative, DHEAS, and more controversially dexamethasone (DEX), a synthetic glucocorticoid, have beneficial effects in diabetic animals. Cultivating BRIN-BD11 cells for 3 days with either DHEAS (30 muM) or DEX (100 nM), reduced total cell number and reduced cell viability and cellular insulin content. DHEAS-treated cells had poor glucose responsiveness and regulated insulin release, coupled with reduced basal insulin release. In contrast, DEX-treated cells lacked responsiveness to glucose and membrane depolarisation, and both protein kinase A (PKA) and protein kinase C (PKC) secretory pathways were desensitised. Therefore, we conclude that this steroid hormone and synthetic glucocorticoid are not beneficial to pancreatic beta-cells in vitro.

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Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 95%

Deleterious Effects of Supplementation with Dehydroepiandrosterone Sulphate or Dexamethasone on Rat Insulin-Secreting Cells Under In Vitro Culture Condition

et al. 2006

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“…Administration of DHEA to rats and mice reduces visceral adipose tissue accumulation, and has a protective effect against insulin resistance that occurs with aging. DHEA also has been described to enhance insulin release and protect pancreatic islets from the cytotoxicity effects of interleukin1b and streptozotocin [9][10][11][12][13][14][15][16][17][18][19][20]. However, the mechanisms underlying the effects of DHEA on insulin release and pancreatic islet survival are not completed understood.…”

Section: Introductionmentioning

confidence: 99%

Dehydroepiandrosterone increases β‐cell mass and improves the glucose‐induced insulin secretion by pancreatic islets from aged rats

et al. 2005

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The effect of dehydroepiandrosterone (DHEA) on pancreatic islet function of aged rats, an animal model with impaired glucose-induced insulin secretion, was investigated. The following parameters were examined: morphological analysis of endocrine pancreata by immunohistochemistry; protein levels of insulin receptor, IRS-1, IRS-2, PI 3-kinase, Akt-1, and Akt-2; and static insulin secretion in isolated pancreatic islets. Pancreatic islets from DHEA-treated rats showed an increased b-cell mass accompanied by increased Akt-1 protein level but reduced IR, IRS-1, and IRS-2 protein levels and enhanced glucose-stimulated insulin secretion. The present results suggest that DHEA may be a promising drug to prevent diabetes during aging.

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“…Interleukin-1 (IL-1 ) exposure did not affect the activity of catalase in RINm5F cells (Laychock 1998); however, IL-1 treatment of rat islets (Borg et al 1992) and more recently of purified rat -cells (Cardozo et al 2001b) has been shown to up-regulate the expression of the antioxidant enzyme manganese-superoxide dismutase. De novo synthesis of catalase has been demonstrated to be up-regulated following IL-1 treatment of islets from diabetes-prone BB rats (Sparre et al 2002).…”

Section: Introductionmentioning

confidence: 99%

Cytokines and nitric oxide inhibit the enzyme activity of catalase but not its protein or mRNA expression in insulin-producing cells

Sigfrid¹,

Cunningham²,

Beeharry³

et al. 2003

Journal of Molecular Endocrinology

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Pancreatic -cells have low activities of the antioxidant enzyme catalase. Nitric oxide interacts with the haem group of catalase inhibiting its activity. We have studied the activity of catalase in -cells under conditions mimicking prediabetes and in which nitric oxide is generated from cytokine treatment in vitro. We also studied whether there is regulation of catalase enzyme activity by nitric oxide at the protein or gene expression level. RINm5F insulin-producing cells, treated for 24 h with cytokines, showed increased medium nitrite production (17±2·2 vs 0·3±0·2 pmol/µg protein) and significantly decreased cellular catalase activity (42·4±4·5%) compared with control cells. A similar reduction was seen in catalase-overexpressing RIN-CAT cells and in rat or human pancreatic islets of Langerhans. Catalase activity was also suppressed by the long-acting nitric oxide donor diethylenetriamine/nitric oxide adduct (Deta-NO) and this inhibition was reversible. The inhibition of catalase activity by cytokines in RINm5F cells was significantly reversed by the addition of the nitric oxide synthase 2 (NOS2) inhibitors nitro monomethylarginine or N-(3-(aminomethyl)benzyl)acetamidine (1400W). Protein expression was found to be unchanged in cytokine-or Deta-NO-treated RINm5F cells, while mRNA expression was marginally increased. We have shown that inhibition of catalase activity by cytokines is nitric oxide dependent and propose that this inhibition may confer increased susceptibility to cytokine-or nitric oxide-induced cell killing.

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Rat Pancreatic Islet and RINm5F Cell Responses to Epiandrosterone, Dehydroepiandrosterone and Interleukin-1β

Cited by 15 publications

References 42 publications

Deleterious Effects of Supplementation with Dehydroepiandrosterone Sulphate or Dexamethasone on Rat Insulin-Secreting Cells Under In Vitro Culture Condition

Deleterious Effects of Supplementation with Dehydroepiandrosterone Sulphate or Dexamethasone on Rat Insulin-Secreting Cells Under In Vitro Culture Condition

Dehydroepiandrosterone increases β‐cell mass and improves the glucose‐induced insulin secretion by pancreatic islets from aged rats

Cytokines and nitric oxide inhibit the enzyme activity of catalase but not its protein or mRNA expression in insulin-producing cells

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