Please use this identifier to cite or link to this item: http://10.1.7.192:80/jspui/handle/123456789/5230
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dc.contributor.authorPrajapati, Bhumika-
dc.contributor.authorJena, Prasant Kumar-
dc.contributor.authorRajput, Parth-
dc.contributor.authorPurandhar, Kaveri-
dc.contributor.authorSeshadri, Sriram-
dc.date.accessioned2014-12-06T06:54:55Z-
dc.date.available2014-12-06T06:54:55Z-
dc.date.issued2014-
dc.identifier.issn1573-3998-
dc.identifier.urihttp://hdl.handle.net/123456789/5230-
dc.descriptionCurrent Diabetes Reviews, 2014, 10(3), 189-200en_US
dc.description.abstractDiabetes is the most common chronic endocrine disorder having 382 million people in 2013, which will increase to 592 million by 2035 all over the world [1]. Obesity and Type 2 Diabetes (T2D) are often associated with low-grade systematic inflammation, which is regarded as the activation of the immune systems, increased release of the adipocytes derived bioactive metabolites like free fatty acids (FFA), lipids and proinflammatory cytokines and increased gut derived lipopolysaccharide (LPS), leading to the progression of disease [2, 3]. As early as the 1950s, there was little evidence suggesting a correlation or link between inflammation and insulin-resistant states such as obesity, but the mechanism was unknown. In recent times, researchers have found that IL-1􀀂, TNF-􀀁, Interleukin 6 (IL-6) and C-reactive proteins (CRP) are major acute phase responsive proteins, which are the strongest predictors of the development of obesity which further progress to T2D [4].en_US
dc.language.isoenen_US
dc.publisherBentham Science Publishersen_US
dc.subjectAntibioticsen_US
dc.subjectGut microbiotaen_US
dc.subjectInflammationen_US
dc.subjectNLRsen_US
dc.subjectObesityen_US
dc.subjectTLRsen_US
dc.subjectType 2 Diabetesen_US
dc.titleUnderstanding and Modulating the Toll Like Receptors (TLRs) and NOD Like Receptors (NLRs) Cross Talk in Type 2 Diabetesen_US
dc.typeArticleen_US
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