Prolactin regulation of the expression of TNF-α, IFN-γ and IL-10 by splenocytes in murine multiple low dose streptozotocin diabetes

Lau, Joey; Börjesson, Andreas; Holstad, Maria; Sandler, Stellan

doi:10.1016/j.imlet.2005.06.006

Cited by 13 publications

(9 citation statements)

References 28 publications

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“…Idd14 covers 36,000,000 bp and 385 genes on chromosome 13, among which six candidates are mapped: prl , CD83, Bmp6, Irf4 , Syk , and cdkal1 . Prolactin PRL enhanced a Th2 response, which may reflect the preventive effect of PRL against development of multiple low-dose STZ diabetes in mice [ 124 , 125 ]. The comparison of mature DCs between patients and controls indicated a difference in CD83 expression.…”

Section: Candidate Genes For Every Known Qtl Of Type 1 Diabetesmentioning

confidence: 99%

Genetic and Molecular Basis of QTL of Diabetes in Mouse: Genes and Polymorphisms

Gao¹,

Jiao²,

Xiong³

et al. 2008

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A systematic study has been conducted of all available reports in PubMed and OMIM (Online Mendelian Inheritance in Man) to examine the genetic and molecular basis of quantitative genetic loci (QTL) of diabetes with the main focus on genes and polymorphisms. The major question is, What can the QTL tell us? Specifically, we want to know whether those genome regions differ from other regions in terms of genes relevant to diabetes. Which genes are within those QTL regions, and, among them, which genes have already been linked to diabetes? whether more polymorphisms have been associated with diabetes in the QTL regions than in the non-QTL regions.Our search revealed a total of 9038 genes from 26 type 1 diabetes QTL, which cover 667,096,006 bp of the mouse genomic sequence. On one hand, a large number of candidate genes are in each of these QTL; on the other hand, we found that some obvious candidate genes of QTL have not yet been investigated. Thus, the comprehensive search of candidate genes for known QTL may provide unexpected benefit for identifying QTL genes for diabetes.

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Section: Candidate Genes For Every Known Qtl Of Type 1 Diabetesmentioning

confidence: 99%

Genetic and Molecular Basis of QTL of Diabetes in Mouse: Genes and Polymorphisms

Gao¹,

Jiao²,

Xiong³

et al. 2008

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“…For normalization of expression data, a 100-bp fragment of 28s (forward: 5Ј TTG AAA ATC CGG GGG AGA G 3Ј, reverse: 5Ј ACA TTG TTC CAA CAT GCC AG 3Ј) was amplified. Primers used to amplify further murine genes were: the rod photoreceptor specific cGMP phosphodiesterase (PDE6b; forward: 5Ј TAC CAC AAC TGG CGC CAC 3Ј, reverse: 5Ј GTA ACC ATG GGC AAG GCC 3Ј, 110-bp fragment); VEGF-A (forward: 5Ј TTA CTG CTG TAC CTC CAC C 3Ј; reverse: 5Ј ACA GGA CGG CTT GAA GAT G 3Ј, 189-bp fragment); tumor necrosis factor (TNF)-␣ (forward: 5Ј GAC CCT CAC ACT CAG ATC ATC TTC 3Ј, reverse: 5Ј CGC TGG CTC AGC CAC TCC 3Ј, 104-bp fragment) 18 ; collagen IV (forward: 5Ј GGT GTC AGC AAT TAG GCA GGT CAA G 3Ј, reverse: 5Ј ACT CCA CGC AGA GCA GAA GCA AGA A 3Ј, 263-bp fragment) 19 ; and laminin ␤1 (forward: 5Ј AGC AGA AAA GGC CCA GGT 3Ј, reverse: 5Ј GGT TTC CTC AGA AGC TGC 3Ј, 118-bp fragment).…”

Section: Determination Of Retinal Hypoxiamentioning

confidence: 99%

Retinopathy Is Reduced during Experimental Diabetes in a Mouse Model of Outer Retinal Degeneration

Gooyer¹,

Stevenson²,

Humphries

et al. 2006

Invest. Ophthalmol. Vis. Sci.

117

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“…For a long time there have been reports of the involvement of immune systems in the pathogenesis of diabetes induced by subdiabetogenic doses of streptozocin (McEvoy et al 1984;Mensah-Brown et al 2001). Also the role of various inflammatory mediators including tumour necrosis factor-a, interferon-g, interleukin-10 (Lau et al 2006), NFkB (Mabley et al 2002) and cyclooxygenase-2 (Tabatabaie et al 2000) have been reported in the diabetogenic effect of low-dose streptozocin in various mouse models. It is noteworthy to mention that most of the antidiabetic hypolipidaemic agents used in this study were reported for their potential antiinflammatory and immunosuppressive (statins) effects in various animal models, and apart from their modulation through their primary mechanisms of action, these drugs could substantially reduce the risk of diabetes by virtue of their anti-inflammatory effect against streptozocin.…”

Section: Discussionmentioning

confidence: 99%

Metabolic effects of various antidiabetic and hypolipidaemic agents on a high-fat diet and multiple low-dose streptozocin (MLDS) mouse model of diabetes

Arulmozhi

Kurian

Bodhankar

et al. 2008

Journal of Pharmacy and Pharmacology

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Insulin resistance and subsequent insulin secretory defect are two main features of type 2 diabetes and associated metabolic disorders. The animal models of type 2 diabetes are very complex and are as heterogeneous as the disease. We have evaluated the effect of various antidiabetic and lipid lowering agents (fenofibrate, rosiglitazone, glimepiride, metformin and simvastatin) on the metabolic abnormalities induced by combining a high-fat diet and multiple low-dose streptozocin (MLDS) in mice. Male Swiss albino mice were orally treated with the above agents and fed with a diet containing high fat for 28 days. On day 15 the animals were injected intraperitoneally with low-dose streptozocin (40 mg kg(-1)), which was administered for five consecutive days. At the end of the 28-day treatment plasma metabolic parameters (glucose, triglyceride and immunoreactive insulin) were estimated. The antidiabetic and hypolipidaemic agents exhibited differential effects on these metabolic parameters. With the exception of fenofibrate all these agents reduced the plasma glucose levels, and the effects of metformin and rosiglitazone on glucose were found to be statistically significant. Although the effect of the test drugs on cholesterol was modest, a significant decrease in triglyceride levels was observed with sub-chronic treatment with these agents. Interestingly, glimepiride mildly elevated the insulin levels while the other antidiabetics and hypolipidaemics reduced the insulin levels, with metformin and rosiglitazone exhibiting statistically significant effects on insulin. To our knowledge this is the first report on the effect of various peroxisome proliferator-activated receptor modulators and newer antidiabetics on the metabolic effects induced by the combined high-fat diet and MLDS model of type 2 diabetes in Swiss albino mice. The results suggested the complexity of the hyperglycaemia, hyperinsulinaemia and hypertriglyceridaemia induced by the high-fat diet and MLDS mouse model, and their correction by various antidiabetics and antihyperlipidaemics may have involved diverse mechanisms.

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Prolactin regulation of the expression of TNF-α, IFN-γ and IL-10 by splenocytes in murine multiple low dose streptozotocin diabetes

Cited by 13 publications

References 28 publications

Genetic and Molecular Basis of QTL of Diabetes in Mouse: Genes and Polymorphisms

Genetic and Molecular Basis of QTL of Diabetes in Mouse: Genes and Polymorphisms

Retinopathy Is Reduced during Experimental Diabetes in a Mouse Model of Outer Retinal Degeneration

Metabolic effects of various antidiabetic and hypolipidaemic agents on a high-fat diet and multiple low-dose streptozocin (MLDS) mouse model of diabetes

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