The effect of protein source on weight loss, body composition, and substrate oxidation following a 12-week high-protein, ketogenic diet: A randomized trial Rachel Abramczuk Background: Ketogenic diets, diets high in fat and protein and low in carbohydrates, have been shown to be effective for weight loss. Recently, plant-based diets and protein sources have gained in popularity as they are thought to be a healthier alternative to animal-based protein sources. There is limited evidence as to whether protein source impacts ketogenic dietary outcomes.

Objective: The aim of this study is to investigate how plant- and animal-based protein supplementation impact weight loss, body composition, and substrate oxidation following a 12week high-protein, hypocaloric, ketogenic diet in adults with obesity. Methods: Adults with obesity were recruited and randomized (N= 35) to receive a 12-week high-protein ketogenic diet which included plant- or animal-based protein supplements. Body composition was assessed through dual energy x-ray absorptiometry (DEXA) and computed tomography (CT). Substrate oxidation was assessed via indirect calorimetry before and after the intervention.

Results: Both the plant-based and animal-based groups saw significant reductions in overall weight, fat mass, and fat-free mass (p<0.001 for all). The plant-based group saw a significant reduction in carbohydrate oxidation (p=0.037), a trend to suggest an increase in lipid oxidation (p=0.054), and a trend to suggest a decrease in respiratory exchange ratio (p=0.057). There were iii no differences in any body composition variables nor resting energy expenditure following the intervention for either group.

Conclusion: Our results indicate that regardless of protein source, people who followed a 12week high-protein ketogenic diet saw significant loss of weight, fat mass, and fat-free mas. Following a 12-week plant-based high-protein ketogenic diet may lead to a reduction in carbohydrate oxidation and an increase in lipid oxidation, but this may be due to differences in baseline dietary composition and further research is needed to determine the validity of the proposed conclusion.

https://spectrum.library.concordia.ca/id/eprint/994457/1/Abramczuk_MSc_F2024.pdf

https://www.diabetesresearchclinicalpractice.com/article/S0168-8227(24)00808-8/fulltext

Abstract

Aims

This study assessed the five-year effects of a continuous care intervention (CCI) delivered via telemedicine, counseling people with type 2 diabetes (T2D) on a very low carbohydrate diet with nutritional ketosis.

Methods

Participants with T2D were enrolled in a 2-year, open-label, non-randomized study comparing CCI and usual care (UC). After 2 years, 194 of the 262 CCI participants were approached for a three-year extension. Of these, 169 consented, and 122 remained in the study for five years. Primary outcomes were changes in diabetes status assessed using McNemars’ test, including remission and HbA1c < 6.5 % on no glucose lowering medication or only on metformin at 5 years. Changes in body mass, glycemia, and cardiometabolic markers from baseline to 5 years were assessed using linear mixed-effects models.

Results

Twenty percent (n = 24) of the five-year completers achieved remission, with sustained remission observed over three years in 15.8 % (n = 19) and four years in 12.5 % (n = 15). Reversal to HbA1c < 6.5 % without medication or only metformin was seen in 32.5 % (n = 39). Sustained improvements were noted in body mass (−7.6 %), HbA1c (−0.3 %), triglycerides (−18.4 %), HDL-C (+17.4 %), and inflammatory markers, with no significant changes in LDL-C and total cholesterol.

Conclusions

Over five years, the very low carbohydrate intervention showed excellent retention and significant health benefits, including diabetes remission, weight loss, and improved cardiometabolic markers.

Abstract

We and others have previously demonstrated that hypoxia-inducible factor alpha (HIF-1α) stabilization through diet-induced ketosis plays a vital role during brain ischemic injury. We have recently reported that ketosis-stabilized HIF-1α regulates the inflammatory response and contributes to neuroprotection in a rat stroke model. In the current investigation, we examined the downstream mechanism by which the ketogenic (KG) diet protects against brain damage after stroke in mice. Six-seven-week-old male mice were fed the standard diet (SD) or the KG diet to mimic the metabolic state of chronic ketosis. After four weeks, mice were subjected to photothrombotic ischemic stroke. Behavior analysis was recorded at 24 h, 48h, and 72h post-stroke. After 72h, mice were euthanized for infarction, brain edema, hemorrhage, and molecular analysis. Our results showed that the KG diet significantly alleviated infarction, brain edema, and hemorrhage, improved the neurobehavioral outcomes, and attenuated ischemic stroke-induced oxidative/nitrative stress and apoptotic markers at 72h post-stroke. Further, the KG diet upregulated the HIF-1α and interleukin (IL)-10 expression and inhibited thioredoxin-interacting protein (TXNIP), NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation and pro-inflammatory cytokines expression compared to SD-fed mice after stroke. We further showed that the genetic deletion of NLRP3 mediates KG-induced neuroprotection after stroke. Our current study demonstrates that the KG diet exerts neuroprotective effects by inhibiting TXNIP-NLRP3 inflammasome, mainly dependent on heightening the upregulation of IL-10 via HIF-1α stabilization. Thus, the KG diet might be considered a new therapeutic strategy for ischemic patients.

https://www.researchsquare.com/article/rs-4914710/v1