Probucol preserves pancreatic β-cell function through reduction of oxidative stress in type 2 diabetes

Gorogawa, Shin ichi; Kajimoto, Yoshitaka; Umayahara, Yutaka; Kaneto, Hideaki; Watada, Hirotaka; Kuroda, Akio; Kawamori, Dan; Yasuda, Tetsuyuki; Matsuhisa, Munehide; Yamasaki, Yoshimitsu; Hori, Masatsugu

doi:10.1016/s0168-8227(02)00005-0

Cited by 113 publications

(123 citation statements)

References 30 publications

Supporting

Mentioning

113

Contrasting

Order By: Relevance

“…For these reasons, the levels of these two proteins in the pancreas were quantified using a sandwich ELISA and compared among '/db, db/db, and STR/Ort mice at 5, 10, 15 and 20 weeks of age. The expression level of HSP32 in 15-and 20-week-old db/db mice were higher than that in '/db mice, a result which is consistent with previously reported data (Table 2) (Gorogawa 2002). The expression levels of HSP32 in STR/Ort mice were also significantly higher than in db/m at 5, 15 and 20 weeks of age (Table 2, P B 0.05) and tended to be higher than that of db/m at 10 weeks (Table 1, P 00.069).…”

Section: Resultssupporting

confidence: 93%

“…Although the presence of HSP32 could be detected in the pancreas of STR/ Ort mice, the protein was not detected in '/db mice. Previous studies have reported that the levels of oxidative stress markers HSP32 and HSP47 are elevated in diabetic mouse models (Gorogawa 2002;Ohashi 2004). The expression of HSP32 and HSP47 can also be elevated in response to ROS (Yu and Moriniere 2009).…”

Section: Resultsmentioning

confidence: 95%

“…The type 2 diabetic mouse model db/db was used as a positive control because a higher expression of HSP32 in the pancreas has been observed in these mice (Gorogawa 2002). The mice were reared following uniform standard practices.…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Elevation of pancreatic oxidative stress in STR/Ort mice

Uchida

Naruse

Ogawa

et al. 2011

Journal of Applied Animal Research

View full text Add to dashboard Cite

To gain a better understanding of the causative factors of hyperinsulinaemia, pancreatic oxidative stress in STR/ Ort mice and a type 2 diabetic mouse model (db/db) was evaluated. Expression of oxidative stress marker HSP32 in the pancreas of STR/Ort mice was significantly higher than that in the liver, kidney and spleen. The expression level of HSP32 in STR/Ort was significantly higher than in db/m at 5, 15 and 20 weeks of age (P B 0.05) and tended to be higher than that in db/m (P 0 0.069). The expression level of HSP47 in STR/Ort was also significantly higher than in db/m at 5 and 10 weeks (P B 0.05) and tended to be higher than that of db/m at 15 (P 0 0.086) and 20 weeks (P 0 0.052). Taken together, these results suggest that elevation of oxidative stress in the pancreas during early developmental periods may induce hyperinsulinaemia in STR/Ort mice through impaired insulin metabolism and contribute to the initiation and progression of osteoarthritis.

show abstract

Section: Resultssupporting

confidence: 93%

Section: Resultsmentioning

confidence: 95%

See 1 more Smart Citation

Elevation of pancreatic oxidative stress in STR/Ort mice

Uchida

Naruse

Ogawa

et al. 2011

Journal of Applied Animal Research

View full text Add to dashboard Cite

show abstract

“…Several lines of evidence have implicated oxidative stress in the progression of ␤-cell dysfunction in type 2 diabetes (1)(2)(3)(4)(5)(6)(7)(8). Under diabetic conditions, reactive oxygen species are increased in many tissues and organs through activation of the mitochondrial electron transport chain (9) or acceleration of glycation reactions (1,3) and cause various forms of tissue damage in patients with diabetes (10).…”

mentioning

confidence: 99%

“…Under diabetic conditions, reactive oxygen species are increased in many tissues and organs through activation of the mitochondrial electron transport chain (9) or acceleration of glycation reactions (1,3) and cause various forms of tissue damage in patients with diabetes (10). Extracellular hyperglycemia readily causes intracellular hyperglycemia in ␤-cells, leading to the induction of reactive oxygen species in pancreatic islets of diabetic animals as best represented by the enhanced expression of oxidative stress markers such as 8-hydroxy-2Ј-deoxyguanosine and 4-hydroxy-2,3-nonenal (7,8). In addition, because pancreatic islet cells express a relatively low amount of anti-oxidative enzymes, such as glutathione peroxidase and catalase (11), ␤-cells are likely to be sensitive to oxidative stress.…”

mentioning

confidence: 99%

The Forkhead Transcription Factor Foxo1 Bridges the JNK Pathway and the Transcription Factor PDX-1 through Its Intracellular Translocation

Kawamori

Kaneto

Nakatani

et al. 2006

Journal of Biological Chemistry

Self Cite

238

211

View full text Add to dashboard Cite

It has been shown that oxidative stress and activation of the c-Jun N-terminal kinase (JNK) pathway induce the nucleocytoplasmic translocation of the pancreatic transcription factor PDX-1, which leads to pancreatic ␤-cell dysfunction. In this study, we have shown that the forkhead transcription factor Foxo1/FKHR plays a role as a mediator between the JNK pathway and PDX-1. Under oxidative stress conditions, Foxo1 changed its intracellular localization from the cytoplasm to the nucleus in the pancreatic ␤-cell line HIT-T15. The overexpression of JNK also induced the nuclear localization of Foxo1, but in contrast, suppression of JNK reduced the oxidative stress-induced nuclear localization of Foxo1, suggesting the involvement of the JNK pathway in Foxo1 translocation. In addition, oxidative stress or activation of the JNK pathway decreased the activity of Akt in HIT cells, leading to the decreased phosphorylation of Foxo1 following nuclear localization. Furthermore, adenovirus-mediated Foxo1 overexpression reduced the nuclear expression of PDX-1, whereas repression of Foxo1 by Foxo1-specific small interfering RNA retained the nuclear expression of PDX-1 under oxidative stress conditions. Taken together, Foxo1 is involved in the nucleocytoplasmic translocation of PDX-1 by oxidative stress and the JNK pathway.

show abstract

Current literature in diabetes

2002

Diabetes Metabolism Res

View full text Add to dashboard Cite

In order to keep subscribers up‐to‐date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of diabetes/metabolism. Each bibliography is divided into 17 sections: 1 Books, Reviews & Symposia; 2 General; 3 Genetics; 4 Epidemiology; 5 Immunology; 6 Prediction; 7 Prevention; 8 Intervention: a) General; b) Pharmacology; 9 Pathology: a) General; b) Cardiovascular; c) Neurological; d) Renal; 10 Endocrinology & Metabolism; 11 Nutrition; 12 Animal Studies; 13 Techniques. Within each section, articles are listed in alphabetical order with respect to author (10 Weeks journals ‐ Search completed at 24th July 2002)

show abstract

Probucol preserves pancreatic β-cell function through reduction of oxidative stress in type 2 diabetes

Cited by 113 publications

References 30 publications

Elevation of pancreatic oxidative stress in STR/Ort mice

Elevation of pancreatic oxidative stress in STR/Ort mice

The Forkhead Transcription Factor Foxo1 Bridges the JNK Pathway and the Transcription Factor PDX-1 through Its Intracellular Translocation

Current literature in diabetes

Contact Info

Product

Resources

About