Dysregulated upr and er stress related to a mutation in the sdf2l1 gene are involved in the pathophysiology of diet-induced diabetes in the cohen diabetic rat

HIGHLIGHTS

SUMMARY

This triad, which had been previously implicated in impairing the ability of the pancreas to secrete insulin in other animal models of diabetes, as well as in diabetic humans, did not provide, a sufficiently comprehensive explanation for the full development of the diabetic phenotype in the Cohen susceptible CDs/y strain. Despite the lack of consistent differences in insulin/glucose ratio between CDs/y DD and CDs/y RD during the first 4 weeks of the study, glucose levels in CDs/y DD were already higher than in CDs/y RD or CDr/y . . .

 



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