Glucose And Lipid Homeostasis And Inflammation In Humans Following An Isocaloric Ketogenic Diet
Notes for this study:
||Fasting glucose (mg/dl). Mean + SD. High carb: Week 3: 82 (7). Week 4: 81 (4). Ketogenic diet: Week 3: 81 (7). Week 4: 81 (6). Not statistically significant. Relative postprandial AUC (mg/dL×min). Mean + SD. High carb: ketogenic meal: −102 (595). High carb meal: 685 (687). Ketogenic diet: Ketogenic meal: 713 (1,113). High carb meal 2,004 (1,112). Statistically significant for both.
||Non-randomized controlled trial
|Number of Subjects
In a non-randomized crossover trial, 17 overweight/obese participants were assigned to a ketogenic diet with 5% protein, 5% carbohydrate, and 80% or an isocaloric higher-carbohydrate diet containing 15% protein, 50% carbohydrate, and 35% fat for 4 weeks each, all beginning with the high carbohydrate diet and then switching to the ketogenic diet. Participants were confined to a metabolic ward and all food was provided and consumed under supervision.
Funding issues for this study:
The primary outcomes were anything related to glucose homeostasis. Fasting glucose was normal on average at the beginning of the study, and neither diet caused a change, while the ketogenic diet led to a reduction in insulin and c-peptide. The ketogenic diet led to a statistically significant increase in glucagon, adiponectin, and GIP, a nonsignificant increase in GLP-1, and a statistically significant reduction in FGF21 compared with the high carbohydrate diet. PYY was unchanged, and cortisol was slightly but not significantly elevated after the ketogenic diet. C-reactive protein was significantly higher, and IL-6 was increased initially but went back to baseline after the 4th week. Fasting free fatty acids were significantly elevated by the ketogenic diet.
The researchers also conducted meal tolerance tests characteristic of a typical meal on the ketogenic diet or the higher carbohydrate diet. Results are available above in the values box above.
"Nutrition Science Initiative (NuSI) was the primary funder for this study. NuSI convened the research team, helped formulate the hypotheses, and
provided partial funding. NuSI and its scientific advisors were given the opportunity to comment on the study design and this manuscript, but the investigators retained full
editorial control. This work was also supported, in part, by the Intramural Research Program of the National Institutes of Health (NIH), the National Institute of Diabetes and
Digestive and Kidney Diseases (KDH, MLR), NIH UL1 TR00040 (Columbia Clinical and Translational Science Award, [MR, RL]), and Nutrition Obesity Research Center Grant