Zinc sulphate induces metallothionein in pancreatic islets of mice and protects against diabetes induced by multiple low doses of streptozotocin

Ohly, Patricia; Dohle, Claudia; Abel, Josef; Seißler, Jochen; Gleichmann, Helga

doi:10.1007/s001250050009

Cited by 111 publications

(93 citation statements)

References 38 publications

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“…Using mZDF rats, angiotensinogen was recently shown to be induced in mesangial cells via ROS/ ERK/JNK pathways (Ohashi et al 2010), and similar mechanisms might be operating in the liver. MT1 is a potent cellular antioxidant that plays important roles in essential trace element homeostasis, metal detoxification and in the protection against various injuries resulting from ROS (Chiaverini & De Ley 2010), including the development of diabetes and its complications (Ohly et al 2000, Cai 2004, Song et al 2005, Ayaz et al 2006, Tang et al 2010. It has also been shown that levels of MT1 are increased in the livers of diabetic rats (Cai et al 2002), which is in agreement with the results obtained in this study.…”

Section: Resultssupporting

confidence: 91%

Sex-dependent hepatic transcripts and metabolites in the development of glucose intolerance and insulin resistance in Zucker diabetic fatty rats

Gustavsson

Soga²,

Wahlström

et al. 2011

Journal of Molecular Endocrinology

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Male Zucker diabetic fatty (mZDF) rats spontaneously develop type 2 diabetes, whereas females only become diabetic when fed a diabetogenic high-fat diet (high-fat-fed female ZDF rat, HF-fZDF). The aim of this study was to investigate if differences in liver functions could provide clues to this sex difference. Non-diabetic obese fZDF rats were compared with either mZDF or HF-fZDF regarding hepatic molecular profiles, to single out those components that might be protective in the females. High-fat feeding in fZDF led to enhanced weight gain, increased blood glucose and insulin levels, reduced insulin sensitivity and a trend towards reduced glucose tolerance, indicative of a prediabetic state. mZDF rats were diabetic, with low levels of insulin, high levels of glucose, reduced insulin sensitivity and impaired glucose tolerance. Transcript profiling and capillary electrophoresis time-of-flight mass spectrometry were used to indentify hepatic transcripts and metabolites that might be related to this. Many diet-induced alterations in transcript and metabolite levels in female rats were towards a 'male-like' phenotype, including reduced lipogenesis, increased fatty acid (FA) oxidation and increased oxidative stress responses. Alterations detected at the level of hepatic metabolites, indicated lower capacity for glutathione (GSH) production in male rats, and higher GSH turnover in females. Taken together, this could be interpreted as if anabolic pathways involving lipogenesis and lipid output might limit the degree of FA oxidation and oxidative stress in female rats. Together with a greater capacity to produce GSH, these hepatic sex differences might contribute to the sex-different development of diabetes in ZDF rats.

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Section: Resultssupporting

confidence: 91%

Sex-dependent hepatic transcripts and metabolites in the development of glucose intolerance and insulin resistance in Zucker diabetic fatty rats

Gustavsson

Soga²,

Wahlström

et al. 2011

Journal of Molecular Endocrinology

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“…dysfunction. The group went on to conclude that these anti-diabetic effects were due to the activation of Zn-induced MT, which provides a defense against OH-groups generated in ~ cell by the inflammatory reactions, most probably due to the MLD-STZ treatment (106).…”

Section: -Zinc and Animal Models Of Type 1 Diabetesmentioning

confidence: 99%

Insulino-mimetic and anti-diabetic effects of zinc

Vardatsikos

Pandey

Srivastava

2013

Journal of Inorganic Biochemistry

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blocked Zn-induced ERKl/2 and PKB phosphorylation, but AG1478, an inhibitor for EGFR was without effect. In CHO cells overexpressing tyrosine kinase deficient IR (CHO-1018), Zn was still able to induce the phosphorylation ERK1/2 and PKB/Akt, whereas insulin-induced ERK1/2 and PKB/Akt phosphorylation was abolished in these cells.Moreover, Zn had no effect on the tyrosine phosphorylation of IR-p-subunit and IRS-l in CHO-IR cells. Furthermore, in IGF-IR knockout cells, both IGF-l and Zn were unable to stimulate the phosphorylation ofERK1/2 and PKB. Taken together, these data suggest that Zn-induced ERK1/2 and PKB/Akt phosphorylation is independent of IR-or EGFR-PTK, but requires IGF-IR-PTK.

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“…STZ is a d-glucopyranose derivative of N-methyl-Nnitrosourea endowed with potent alkylating properties [18] and also acts as a reactive oxygen species-generating agent [19]. While at high doses this agent has diabetogenic potential due to its capacity to selectively promote death of insulin-producing β cells by apoptosis or necrosis, at low doses, STZ generates hydrogen peroxide [20] and induces expression of the glutamic acid decarboxylase autoantigen [21].…”

Section: Introductionmentioning

confidence: 99%

T-cell vaccination leads to suppression of intrapancreatic Th17 cells through Stat3-mediated RORγt inhibition in autoimmune diabetes

et al. 2011

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Zinc sulphate induces metallothionein in pancreatic islets of mice and protects against diabetes induced by multiple low doses of streptozotocin

Cited by 111 publications

References 38 publications

Sex-dependent hepatic transcripts and metabolites in the development of glucose intolerance and insulin resistance in Zucker diabetic fatty rats

Sex-dependent hepatic transcripts and metabolites in the development of glucose intolerance and insulin resistance in Zucker diabetic fatty rats

Insulino-mimetic and anti-diabetic effects of zinc

T-cell vaccination leads to suppression of intrapancreatic Th17 cells through Stat3-mediated RORγt inhibition in autoimmune diabetes

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