期刊
DIABETES & METABOLIC SYNDROME-CLINICAL RESEARCH & REVIEWS
卷 11, 期 -, 页码 S385-S390出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.dsx.2017.03.022
关键词
Metabolic syndrome; Obesity; Diabetes; Respiratory quotient; Dietary ketosis; Ketogenic diet; Hemoglobin A1c; Insulin; Glucose regulation; BMI
A worsening epidemic of diabetes and its precursor, metabolic syndrome (MetS) is engulfing America. A healthy individual, with proper glucose regulation has an ability to switch between burning fat and carbohydrates. It has been suggested that signaling errors within this homeostatic system, characterized by impaired switching of substrate oxidation from glucose to fat in response to insulin, can contribute to the etiology of metabolic syndrome and occurs before the development of type II diabetes. Glucose regulation with restored insulin sensitivity facilitated through clinically regulated, benign dietary ketosis (BDK), may significantly reduce, regulate and reverse the adverse pathologies common to MetS and obesity. The study assessed if prolonged maintenance of induced and controlled physiological, dietary ketosis, would reverse pathological processes induced by MetS including a reduction in fasting triglycerides, BMI (body mass index) and body fat mass (BFM), weight, a significant decrease and/or normalization of hemoglobin Ale (HgA1c) and an increase in resting metabolic rate (RMR) and blood ketones. A group of 30 adults, previously diagnosed with MetS by their primary care physician, were randomly prescribed to one of three groups: a sustained ketogenic diet with no exercise, standard American diet (SAD) with no exercise or SAD with 3-5 days per week of exercise (30 min.). The results demonstrated that the change over time from week 0 to week 10 was significant (p = 0.001) in the ketogenic group for weight, body fat percentage, BMI, HgA1c and ketones. All variables for the ketogenic group out-performed those of the exercise and non-exercise groups, with five of the seven demonstrating statistical significance. (C) 2017 Diabetes India. Published by Elsevier Ltd. All rights reserved.
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