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题名:Dietary copper supplementation restores beta-cell function of Cohen diabetic rats: a link between mitochondrial function and glucose-stimulated insulin secretion.
作者:WEKSLER-ZANGEN S; JORNS A; TARSI-CHEN L; VERNEA F; AHARON-HANANEL G; SAADA A; LENZEN S; RAZ I;
来源:Am J Physiol Endocrinol Metab. 2013 May;304(10):E1023-34. doi: [ IF= 0.00 ] ]
URL :10.1152/ajpendo.00036.2013
日期:20130606
摘要:beta-Cell mitochondrial dysfunction as well as proinflammatory cytokines have
been suggested to contribute to reduced glucose-stimulated insulin secretion
(GSIS) in type 2 diabetes. We recently demonstrated that Cohen diabetic sensitive
(CDs) rats fed a high-sucrose, low-copper diet (HSD) developed hyperglycemia and
reduced GSIS in association with peri-islet infiltration of fat and interleukin
(IL)-1beta-expressing macrophages, whereas CD resistant (CDr) rats remained
normoglycemic on HSD. We examined: 1) the correlation between copper
concentration in the HSD and progression, prevention, and reversion of
hyperglycemia in CDs rats, 2) the relationship between activity of the
copper-dependent, respiratory-chain enzyme cytochrome c oxidase (COX),
infiltration of fat, IL-1beta-expressing macrophages, and defective GSIS in
hyperglycemic CDs rats. CDs and CDr rats were fed HSD or copper-supplemented HSD
before and during hyperglycemia development. Blood glucose and insulin
concentrations were measured during glucose tolerance tests. Macrophage
infiltration and IL-1beta expression were evaluated in pancreatic sections by
electron-microscopy and immunostaining. COX activity was measured in pancreatic
sections and isolated islets. In CDs rats fed HSD, GSIS and islet COX activity
decreased, while blood glucose and infiltration of fat and IL-1beta-expressing
macrophages increased with time on HSD (P < 0.01 vs. CDr-HSD rats, all
parameters, respectively). CDs rats maintained on copper-supplemented HSD did not
develop hyperglycemia, and in hyperglycemic CDs rats, copper supplementation
restored GSIS and COX activity, reversed hyperglycemia and infiltration of fat
and IL-1beta-expressing macrophages (P < 0.01 vs. hyperglycemic CDs-HSD rats, all
parameters, respectively). We provide novel evidence for a critical role of low
dietary copper in diminished GSIS of susceptible CDs rats involving the combined
consequence of reduced islet COX activity and pancreatic low-grade inflammation.

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