Cocoa-rich diet attenuates beta cell mass loss and function in young Zucker diabetic fatty rats by preventing oxidative stress and beta cell apoptosis
Cocoa-rich diet attenuates beta cell mass loss and function in young Zucker diabetic fatty rats by preventing oxidative stress and beta cell apoptosis
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DOI：
10.1002/mnfr.201400746
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发表时间：
2015-04-01
影响因子：
5.2
通讯作者：
Angeles Martin, Maria
中科院分区：
文献类型：
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作者：
Fernandez-Millan, Elisa;Cordero-Herrera, Isabel;Angeles Martin, Maria
我们最近表明，可可黄烷醇可能通过在体外促进胰腺 β 细胞的存活和功能而具有抗糖尿病潜力。在这项工作中，我们研究了富含可可的饮食是否能够在 2 型糖尿病动物模型中保留 β 细胞质量和功能以及所涉及的机制。我们的研究结果表明，在糖尿病前期状态期间喂食可可可减轻肥胖 Zucker 糖尿病大鼠的高血糖，降低胰岛素抵抗，并增加 β 细胞质量和功能。在分子水平上，富含可可的饮食通过增加 Bcl-xL 水平并降低 Bax 水平和 caspase-3 活性来防止 β 细胞凋亡。可可饮食增强了内源性抗氧化防御的活性，主要是谷胱甘肽过氧化物酶，从而防止了糖尿病前期引起的氧化损伤，并导致细胞凋亡的预防。这些发现提供了第一个体内证据，表明富含可可的饮食可以通过防止氧化应激和β细胞凋亡来延缓功能性β细胞质量的损失并延缓糖尿病的进展。
We have recently shown that cocoa flavanols may have anti-diabetic potential by promoting survival and function of pancreatic beta-cells in vitro. In this work, we investigated if a cocoa-rich diet is able to preserve beta-cell mass and function in an animal model of type 2 diabetes and the mechanisms involved. Our results showed that cocoa feeding during the prediabetic state attenuates hyperglycaemia, reduces insulin resistant, and increases beta cell mass and function in obese Zucker diabetic rats. At the molecular level, cocoa-rich diet prevented beta-cell apoptosis by increasing the levels of Bcl-xL and decreasing Bax levels and caspase-3 activity. Cocoa diet enhanced the activity of endogenous antioxidant defenses, mainly glutathione peroxidase, preventing thus oxidative injury induced by the pre-diabetic condition and leading to apoptosis prevention. These findings provide the first in vivo evidence that a cocoa-rich diet may delay the loss of functional beta-cell mass and delay the progression of diabetes by preventing oxidative stress and beta-cell apoptosis.