Please use this identifier to cite or link to this item: http://dr.iiserpune.ac.in:8080/xmlui/handle/123456789/3969
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dc.contributor.authorOJHA, AKANKSHAen_US
dc.contributor.authorWATVE, MILINDen_US
dc.date.accessioned2019-09-09T11:36:13Z
dc.date.available2019-09-09T11:36:13Z
dc.date.issued2018-08en_US
dc.identifier.citationEvolution Medicine and Public Health, 2018(1), 186-189.en_US
dc.identifier.issn2050-6201en_US
dc.identifier.urihttp://dr.iiserpune.ac.in:8080/xmlui/handle/123456789/3969
dc.identifier.urihttps://doi.org/10.1093/emph/eoy020en_US
dc.description.abstractLay Summary: Different species of vertebrates have conditions similar to human obesity, insulin resistance and type 2 diabetes. Increasing number of studies are now revealing that the causes and interrelationships between these states are substantially different in different species. Comparative physiology may turn out to be an eye opener for evolutionary theories of diabetes.Obesity induced insulin resistance is believed to be central to type 2 diabetes. Recent work on Mexican cavefish, Astyanax mexicanus, has revealed a hyperglycemic phenotype similar to human type 2 diabetes but here insulin resistance is the cause of obesity rather than an effect. Instead of developing diabetic complications, the hyperglycemic fish lead a healthy and long life. In addition to fish, insulin resistance in hibernating bears, dolphins, horses, bonnet macaques and chimpanzees demonstrate that the relationship between diet, obesity, insulin sensitivity and diabetes is widely different in different species. Evolutionary hypotheses about type 2 diabetes should explain these differences.en_US
dc.language.isoenen_US
dc.publisherOxford University Pressen_US
dc.subjectInsulin resistanceen_US
dc.subjectMexican cavefishen_US
dc.subjecttype 2 diabetesen_US
dc.subjectComparative physiologyen_US
dc.subject2018en_US
dc.titleBlind fish: An eye openeren_US
dc.typeArticleen_US
dc.contributor.departmentDept. of Biologyen_US
dc.identifier.sourcetitleEvolution Medicine and Public Healthen_US
dc.publication.originofpublisherForeignen_US
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