डार्क चॉकलेट, एपिकेटेचिन और कोशिकीय ऊर्जा

एपिकेटेचिन से भरपूर डार्क कोको चॉकलेट के टुकड़े, जो कोको से प्राप्त यौगिकों को दर्शाते हैं। Mitozz माइटोकॉन्ड्रियल स्वास्थ्य के प्रति यह दृष्टिकोण, जिसे मणि अग्रवाल, गुइलेर्मो सेबालोस और फ्रांसिस्को विल्लारियल द्वारा विकसित किया गया है।

चॉकलेट को अक्सर उसके स्वाद के लिए पसंद किया जाता है, लेकिन कोको पर किए गए शोध से कुछ और भी गहरी बातें सामने आती हैं। जानिए कैसे एपिकेटेचिन का अध्ययन इस बात के लिए किया गया है कि यह कोशिकाओं द्वारा ऊर्जा उत्पादन और प्रबंधन में कैसे सहायक होता है।

Postprandial Fat Oxidation and Epicatechin

सहकर्मी-समीक्षित अध्ययनों का प्रतिनिधित्व करने वाली पाठ्यपुस्तकों का ढेर (-)-epicatechin और माइटोकॉन्ड्रिया अनुसंधान

This human study assessed short-term metabolic effects of an oral (-)-epicatechin supplement after meals, reporting changes in postprandial fat and carbohydrate handling in normal and overweight participants.

(-)-Epicatechin-induced recovery of mitochondria from simulated diabetes: Potential role of endothelial nitric oxide synthase

(-)-Epicatechin increases indicators associated with mitochondrial biogenesis in endothelial cells and myocardium. We investigated endothelial nitric oxide synthase involvement on (-)-epicatechin-induced increases in indicators associated with mitochondrial biogenesis in human coronary artery endothelial cells cultured in normal-glucose and high-glucose media, as well as to restore indicators of cardiac mitochondria from the effects of simulated diabetes. Here, we demonstrate the role of endothelial nitric oxide synthase on (-)-epicatechin-induced increases in mitochondrial proteins, transcription factors and sirtuin 1 under normal-glucose conditions. In simulated diabetes endothelial nitric oxide synthase function, mitochondrial function–associated and biogenesis-associated indicators were adversely impacted by high glucose, effects that were reverted by (-)-epicatechin. As an animal model of type 2 diabetes, 2-month old C57BL/6 mice were fed a high-fat diet for 16 weeks. Fasting and fed blood glucose levels were increased and NO plasma levels decreased. High-fat-diet-fed mice myocardium revealed endothelial nitric oxide synthase dysfunction, reduced mitochondrial activity and markers of mitochondrial biogenesis. The administration of 1 mg/kg (-)-epicatechin for 15 days by oral gavage shifted these endpoints towards control mice values. Results suggest that endothelial nitric oxide synthase mediates (-)-epicatechin-induced increases of indicators associated with mitochondrial biogenesis in endothelial cells. (-)-Epicatechin also counteracts the negative effects that high glucose or simulated type 2 diabetes has on endothelial nitric oxide synthase function.