AI Article Synopsis

  • Diabetes significantly increases the risk of heart failure, and both green tea extract (GTE) and eicosapentaenoic acid (EPA) may help mitigate these risks.
  • In a study with Wistar rats induced with diabetes, GTE alone showed benefits by reducing inflammation and improving lipid metabolism, while EPA posed a risk by causing rapid death in the animals unless paired with GTE.
  • The combination of EPA and GTE resulted in better coronary reactivity than GTE alone, highlighting the importance of combining antioxidants like GTE with EPA to protect cardiac function and enhance survival in diabetic conditions.

Article Abstract

Diabetes is characterized by a high mortality rate which is often associated with heart failure. Green tea and eicosapentaenoic acid (EPA) are known to lessen some of the harmful impacts of diabetes and to exert cardio-protection. The aim of the study was to determine the effects of EPA, green tea extract (GTE), and a combination of both on the cardiac consequences of diabetes mellitus, induced in Wistar rats by injection of a low dose of streptozotocin (33 mg/kg) combined with a high fat diet. Cardiac mechanical function, coronary reactivity, and parameters of oxidative stress, inflammation, and energy metabolism were evaluated. In the context of diabetes, GTE alone limited several diabetes-related symptoms such as inflammation. It also slightly improved coronary reactivity and considerably enhanced lipid metabolism. EPA alone caused the rapid death of the animals, but this effect was negated by the addition of GTE in the diet. EPA and GTE combined enhanced coronary reactivity considerably more than GTE alone. In a context of significant oxidative stress such as during diabetes mellitus, EPA enrichment constitutes a risk factor for animal survival. It is essential to associate it with the antioxidants contained in GTE in order to decrease mortality rate and preserve cardiac function.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6912216PMC
http://dx.doi.org/10.3390/antiox8110526DOI Listing

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