Selenium acts as an insulin-like molecule for the down-regulation of diabetic symptoms via endoplasmic reticulum stress and insulin signalling proteins in diabetes-induced non-obese diabetic mice

Hwang, Dae-Youn; Seo, Sujin; Kim, Yong-Kyu; Kim, Chuel-Kyu; Shim, Sunbo; Jee, Seon-Young; Lee, Suhae; Jang, Mikyong; Kim, Min-Sun; Yim, Suyoun; Lee, Sang Koo; Kang, Byeong‐Cheol; Jang, In-Surk; Cho, Jungsik

doi:10.1007/s12038-007-0072-6

Cited by 49 publications

(29 citation statements)

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“…Selenium has been proved to have a role in prevention of cancer [66], provide optimal endocrine and immune function, and moderate the inflammatory response [35,67]. Selenium had been proven to act as an insulin mimetic by activating key selenoproteins involved in the insulin-signal cascade [68][69][70].…”

Section: Discussionmentioning

confidence: 99%

Effect of experimentally induced diabetes on adult albino ratsʼ ventral prostate gland and role of selenium

El-Haleem

Zidan

2011

The Egyptian Journal of Histology

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IntroductionThe relationship between the occurrence of benign hyperplasia and prostatic cancer with diabetes is a controversial issue. Selenium has been found to alleviate diabetic complications in many organs. Aim of the study To clarify the impact of diabetes on the histological structure of the albino rats' ventral prostate gland and the possible role of selenium supplementation. Materials and methodsThirty adult male albino rats were divided equally into three groups. Group 1 served as control. Group 2 was given a single intraperitoneal injection of 65 mg/kg body weight streptozotocin. Group 3 in which the rats, 1 week after diabetes induction, received 2 mg/kg body weight/day sodium selenite orally. Thirty days after diabetes induction, all rats were weighed, anesthetized, and sacrificed. The ventral prostatic lobes were dissected out, weighed, and processed for light and electron microscope examinations. The area percentage of collagen fibers, epithelial height, and acinar diameter were morphometrically measured. Statistical analysis was carried out using SPSS program. ResultsExamination of the ventral prostate gland of rats from group 2 revealed that the diameter of most acini was highly significantly increased when comparing it with group 1. The epithelial height of their acini was highly significantly decreased when comparing with group 1. Acini were lined by flat-to-low cuboidal cells with few papillary projections. The acinar lining showed focal areas of stratification. Few acini had columnar epithelium. Most cells had irregular-shaped nuclei, a dilated rough endoplasmic reticulum, numerous electron-lucent vacuoles, and few secretory granules. Areas of irregular basement membrane were seen. Thick bundles of collagen fibers and cellular infiltration were seen. Examination of group 3 revealed that it nearly regained its normal architecture. Most acini had many papillary projections and were lined by columnar cells. Acinar cells had euchromatic basal nuclei, rough endoplasmic reticulum, and secretory granules of different sizes and densities, which might seem almost vacuolated with minimum secretory content. The body and prostatic weights were highly significantly lowered in group 2 in comparison with groups 1 and 3. Conclusion Diabetes mellitus had a deleterious effect on the histological structure of the ventral prostate gland, and selenium could ameliorate diabetic effects on the prostate.

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Section: Discussionmentioning

confidence: 99%

Effect of experimentally induced diabetes on adult albino ratsʼ ventral prostate gland and role of selenium

El-Haleem

Zidan

2011

The Egyptian Journal of Histology

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“…Animal model work has also suggested a role for selenium supplementation in reducing some biochemical effects of diabetes. Hwang et al (176) found that selenium supplementation of NOD (nonobese diabetic mice) counteracted ER stress through stimulation of PERKeIF2 and IRE1-JNK pathways and also activating the insulinsignalling pathway. The study also suggested that treatment with selenium may influence aspects of other chronic diseases associated with diabetes, for example, by decreasing the levels of serum markers of liver damage.…”

Section: Diabetesmentioning

confidence: 99%

Selenium in Human Health and Disease

Fairweather‐Tait

Bao

Broadley

et al. 2011

Antioxidants & Redox Signaling

1,070

820

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This review covers current knowledge of selenium in the environment, dietary intakes, metabolism and status, functions in the body, thyroid hormone metabolism, antioxidant defense systems and oxidative metabolism, and the immune system. Selenium toxicity and links between deficiency and Keshan disease and Kashin-Beck disease are described. The relationships between selenium intake/status and various health outcomes, in particular gastrointestinal and prostate cancer, cardiovascular disease, diabetes, and male fertility, are reviewed, and recent developments in genetics of selenoproteins are outlined. The rationale behind current dietary reference intakes of selenium is explained, and examples of differences between countries and/or expert bodies are given. Throughout the review, gaps in knowledge and research requirements are identified. More research is needed to improve our understanding of selenium metabolism and requirements for optimal health. Functions of the majority of the selenoproteins await characterization, the mechanism of absorption has yet to be identified, measures of status need to be developed, and effects of genotype on metabolism require further investigation. The relationships between selenium intake/status and health, or risk of disease, are complex but require elucidation to inform clinical practice, to refine dietary recommendations, and to develop effective public health policies.

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“…In a study using NOD mice, elevated serum enzymes associated with liver damage and apoptosis, as indicated by marked DNA fragmentation were observed and all these changes were decreased with selenium treatment [23]. The BB/WOR diabetic rat is another Type 1 diabetes animal model which has been used extensively to study the effects of hyperglycemia induced injury.…”

Section: Hyperglycemia Induced Changes In Liver In Animal Modelsmentioning

confidence: 99%

Hyperglycemia Induced Changes in Liver: In vivo and In vitro Studies

Dey¹,

Chandrasekaran

2009

CDR

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Diabetes, characterized by chronic hyperglycemia, has reached serious epidemic proportions. It is also not infrequent to find increased incidence of liver injury in diabetics and hyperglycemia plays an important role in promoting liver injury through several mechanisms. The following review identifies the pathways through which hyperglycemia causes changes in liver of various animal models and liver cell culture models, and elucidates the mechanisms and consequences of hyperglycemia induced liver injury in humans. Some of the pathways which are hyperglycemia driven include increased oxidative and nitrosative stress, activation of stress signaling pathways and increased cytokine levels, impairment of protective mechanisms such as the expression of molecular chaperones and proteosome activity, and dysregulation of glucose and lipid metabolism. Thus, hyperglycemia induced changes in the liver's cellular environment in in vitro and in vivo models have been documented extensively in the literature.

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Selenium acts as an insulin-like molecule for the down-regulation of diabetic symptoms via endoplasmic reticulum stress and insulin signalling proteins in diabetes-induced non-obese diabetic mice

Cited by 49 publications

References 50 publications

Effect of experimentally induced diabetes on adult albino ratsʼ ventral prostate gland and role of selenium

Effect of experimentally induced diabetes on adult albino ratsʼ ventral prostate gland and role of selenium

Selenium in Human Health and Disease

Hyperglycemia Induced Changes in Liver: In vivo and In vitro Studies

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