دانلود رایگان مقاله انگلیسی تغذیه کتوز و میتوهورمونیز: پیامدهای بالقوه برای عملکرد تیروئید و سلامت انسان - هینداوی 2018

عنوان فارسی
تغذیه کتوز و میتوهورمونیز: پیامدهای بالقوه برای عملکرد تیروئید و سلامت انسان
عنوان انگلیسی
Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health
صفحات مقاله فارسی
0
صفحات مقاله انگلیسی
28
سال انتشار
2018
نشریه
هینداوی - Hindawi
فرمت مقاله انگلیسی
PDF
کد محصول
E6211
رشته های مرتبط با این مقاله
پزشکی
گرایش های مرتبط با این مقاله
تغذیه و رژیم درمانی، پزشکی غدد، پزشکی گوش، حلق و بینی
مجله
مجله تغذیه و متابولیسم - Journal of Nutrition and Metabolism
دانشگاه
Department of Human Sciences - College of Education and Human Ecology - The Ohio State University - Columbus - USA
چکیده

Impaired mitochondrial function often results in excessive production of reactive oxygen species (ROS) and is involved in the etiology of many chronic diseases, including cardiovascular disease, diabetes, neurodegenerative disorders, and cancer. Moderate levels of mitochondrial ROS, however, can protect against chronic disease by inducing upregulation of mitochondrial capacity and endogenous antioxidant defense. )is phenomenon, referred to as mitohormesis, is induced through increased reliance on mitochondrial respiration, which can occur through diet or exercise. Nutritional ketosis is a safe and physiological metabolic state induced through a ketogenic diet low in carbohydrate and moderate in protein. Such a diet increases reliance on mitochondrial respiration and may, therefore, induce mitohormesis. Furthermore, the ketone β-hydroxybutyrate (BHB), which is elevated during nutritional ketosis to levels no greater than those resulting from fasting, acts as a signaling molecule in addition to its traditionally known role as an energy substrate. BHB signaling induces adaptations similar to mitohormesis, thereby expanding the potential bene8t of nutritional ketosis beyond carbohydrate restriction. )is review describes the evidence supporting enhancement of mitochondrial function and endogenous antioxidant defense in response to nutritional ketosis, as well as the potential mechanisms leading to these adaptations.

نتیجه گیری

12. Conclusion


Among the chronic and degenerative diseases in which impaired mitochondrial function is a contributing factor, many respond favorably to lifestyle interventions focused on diet and exercise. …e therapeutic potential of nutritional ketosis stands out in this regard. For example, in just the ‰rst 10 weeks of an ongoing clinical trial with hundreds of type 2 diabetics following a ketogenic diet, glycated hemoglobin (HbA1c) decreased to below the diagnostic threshold in more than a third of patients, and prescription medication was reduced or eliminated for more than half of patients [12]. Convincing arguments for a ketogenic diet to be the default treatment for diabetes are a decade old [13] and have continued to gain support since then [14]. Similar arguments are developing for obesity [10, 11], neurodegenerative diseases [19, 20, 27–30], cardiovascular disease [15–17], cancer [18–26], and even aging [31, 32]. Although the mechanisms through which a ketogenic diet may improve these conditions expand beyond mitochondrial function, the great extent to which nutritional ketosis increases reliance on mitochondrial metabolism strongly suggests that mitochondrial adaptation is a central factor.


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