Troglitazone can prevent development of type 1 diabetes induced by multiple low-dose streptozotocin in mice

Ogawa, Jun; Takahashi, Sayaka; Fujiwara, Toshihiko; Fukushige, Junichiro; Hosokawa, Tsunemichi; Izumi, Tohru; Kurakata, Shinichi; Horikoshi, Hiroyoshi

doi:10.1016/s0024-3205(99)00364-1

Cited by 24 publications

(22 citation statements)

References 30 publications

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“…These findings were further confirmed by other groups (9,10) and another thiazolidinedione was also reported to prevent the type 1 diabetes (11,12). It was proposed that thiazolidinediones might be considered for β cell protection in LADA patients (12).…”

Section: Recently Maruyama Et Al Showed That a Low Dose Of Insulin Asupporting

confidence: 70%

Pioglitazone Might Prevent the Progression of Slowly Progressive Type 1 Diabetes

et al. 2009

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Section: Recently Maruyama Et Al Showed That a Low Dose Of Insulin Asupporting

confidence: 70%

Pioglitazone Might Prevent the Progression of Slowly Progressive Type 1 Diabetes

et al. 2009

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“…Cytokine signaling or nitric oxide generation cannot stimulate insulin secretion within 10 min under our experimental conditions, because intracellular complexes including cytokines are replaced by a pipette solution during the whole-cell mode. In addition, Ogawa et al (1999) reported that application of a low concentration of troglitazone (3 M) does not induce insulin secretion in HIT-T15 cells. Our results showed that troglitazone inhibited K ATP channel and stimulated acute-phase insulin secretion with a comparatively high concentration.…”

Section: Discussionmentioning

confidence: 99%

Fenofibrate, Troglitazone, and 15-Deoxy-Δ^12,14-prostaglandin J₂Close K_ATPChannels and Induce Insulin Secretion

Shimomura

Shimizu²,

Ikeda³

et al. 2004

J Pharmacol Exp Ther

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It is known that peroxisome proliferator-activated receptor-␥ (PPAR-␥) ligands stimulate acute-phase insulin secretion with a rapid Ca 2ϩ influx into pancreatic ␤-cells, but the precise mechanisms are not clear. The effects of PPAR-␣ ligands on pancreatic ␤-cells also remain unclear. We investigated the effects of PPAR-␣ ligands (fenofibrate and fenofibric acid), a PPAR-␥ ligand (troglitazone), and an endogenous ligand of PPAR-␥ [15-deoxy-⌬ 12,14 -prostaglandin J 2 (15-deoxy-⌬ 12,14 -PGJ 2 )] on K ATP channel activity in clonal hamster insulinoma cell line, HIT-T15 cells. As assessed by whole-cell patch clamp, fenofibrate, fenofibric acid, troglitazone, and 15-deoxy-⌬ 12,14 -PGJ 2 reduced the K ATP channel currents, and inhibition continued after washout of these agents. The concentration-response curves of fenofibrate, fenofibric acid, troglitazone, and 15-deoxy-⌬ 12,14

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“…TZDs also prevent progressive ␤-cell dysfunction (17,18). Several mechanisms have been proposed to account for this protective action of TZDs, including a lowering of pancreatic secretory demands (17), a direct positive effect on ␤-cells (19), or the inhibition of the production of pro-inflammatory cytokines (20).…”

mentioning

confidence: 99%

Hypoglycemic Action of Thiazolidinediones/Peroxisome Proliferator–Activated Receptor γ by Inhibition of the c-Jun NH2-Terminal Kinase Pathway

2007

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Type 2 diabetes results from progressive pancreatic ␤-cell dysfunction caused by chronic insulin resistance. Activation of c-Jun NH 2 -terminal kinase (JNK) inhibits insulin signaling in cultured cells and in vivo and thereby promotes insulin resistance. Conversely, the peroxisome proliferator-activated receptor (PPAR) ␥ synthetic ligands thiazolidinediones (TZDs) enhance insulin sensitivity. Here, we show that the TZDs rosiglitazone and troglitazone inhibit tumor necrosis factor-␣-induced JNK activation in 3T3-L1 adipocytes. Our results indicate that PPAR␥ mediates this inhibitory action because 1) it is reproduced by other chemically unrelated PPAR␥ agonist ligands and blocked by PPAR␥ antagonists; 2) it is enhanced by PPAR␥ overexpression; and 3) it is abrogated by PPAR␥ RNA interference. In addition, we show that rosiglitazone inhibits JNK activation and promotes the survival of pancreatic ␤-cells exposed to interleukin-1␤. In vivo, the abnormally elevated JNK activity is inhibited in peripheral tissues by rosiglitazone in two distinct murine models of obesity. Moreover, rosiglitazone fails to enhance insulin-induced glucose uptake in primary adipocytes from ob/ob JNK1 ؊/؊ mice. Accordingly, we demonstrate that the hypoglycemic action of rosiglitazone is abrogated in the diet-induced obese JNK1-deficient mice. In summary, we describe a novel mechanism based on targeting the JNK signaling pathway, which is involved in the hypoglycemic and potentially in the pancreatic ␤-cell protective actions of TZDs/PPAR␥. Diabetes

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Troglitazone can prevent development of type 1 diabetes induced by multiple low-dose streptozotocin in mice

Cited by 24 publications

References 30 publications

Pioglitazone Might Prevent the Progression of Slowly Progressive Type 1 Diabetes

Pioglitazone Might Prevent the Progression of Slowly Progressive Type 1 Diabetes

Fenofibrate, Troglitazone, and 15-Deoxy-Δ^12,14-prostaglandin J₂Close K_ATPChannels and Induce Insulin Secretion

Hypoglycemic Action of Thiazolidinediones/Peroxisome Proliferator–Activated Receptor γ by Inhibition of the c-Jun NH2-Terminal Kinase Pathway

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Troglitazone can prevent development of type 1 diabetes induced by multiple low-dose streptozotocin in mice

Cited by 24 publications

References 30 publications

Pioglitazone Might Prevent the Progression of Slowly Progressive Type 1 Diabetes

Pioglitazone Might Prevent the Progression of Slowly Progressive Type 1 Diabetes

Fenofibrate, Troglitazone, and 15-Deoxy-Δ12,14-prostaglandin J2Close KATPChannels and Induce Insulin Secretion

Hypoglycemic Action of Thiazolidinediones/Peroxisome Proliferator–Activated Receptor γ by Inhibition of the c-Jun NH2-Terminal Kinase Pathway

Contact Info

Product

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Fenofibrate, Troglitazone, and 15-Deoxy-Δ^12,14-prostaglandin J₂Close K_ATPChannels and Induce Insulin Secretion