The main objective of this study was to determine whether acute ingestion of a ketone monoester (KME) supplement impacted mixed-meal tolerance test (MMTT) glucose area under the curve (AUC). Nineteen healthy young volunteers (10 males/9 females; age, 24.7 ± 4.9 years; body mass index, 22.7 ± 2.4 kg/m) participated in a double-blind, placebo-controlled crossover study. Following overnight fasting (≥10 h), participants consumed 0.45 mL/kg of a KME supplement or taste-matched placebo followed by an MMTT 15 min later. Blood samples were collected every 15-30 min over 2.5 h. KME supplementation acutely raised β-hydroxybutyrate AUC (590%, < 0.0001, = 2.4) and resulted in decreases in blood glucose AUC (-9.4%, = 0.03, = 0.56) and nonesterified fatty acid (NEFA) AUC (-27.3%, = 0.023, = 0.68) compared with placebo. No differences were found for plasma insulin AUC ( = 0.70) or gastric emptying estimated by co-ingested acetaminophen AUC ( = 0.96) between ketone and placebo. Overall, results indicate that KME supplementation attenuates postprandial glycemic and NEFA responses when taken 15 min prior to a mixed meal in young healthy individuals. Future studies are warranted to investigate whether KME supplementation may benefit individuals with impaired glycemic control. Acute ketone monoester supplementation 15 min prior to a mixed meal decreased postprandial glucose and NEFA levels without significantly impacting postprandial insulin or estimates of gastric emptying. Glucose- and NEFA-lowering effects of ketone monoester supplementation are apparently not mediated by changes in insulin release or gastric emptying.
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http://dx.doi.org/10.1139/apnm-2020-0644 | DOI Listing |
Cardiovasc Res
January 2025
Cardiovascular Research Centre, University of Alberta, Edmonton, Alberta, Canada.
Recent evidence suggests that ketone bodies have therapeutic potential in many cardiovascular diseases including heart failure (HF). Accordingly, this has led to multiple clinical trials that use ketone esters to treat HF patients, which we term ketone therapy. Ketone esters, specifically ketone monoesters, are synthetic compounds which, when consumed, are de-esterified into two β-hydroxybutyrate (βOHB) molecules and increase the circulating βOHB concentration.
View Article and Find Full Text PDFJ Appl Physiol (1985)
January 2025
Physical Activity, Health and Rehabilitation Thematic Research Group, School of Psychology, Sport & Health Sciences, Faculty of Science and Health, University of Portsmouth, Portsmouth, UK.
Type 2 diabetes (T2D) is a metabolic disease associated with cardiovascular dysfunction. The myocardium preferentially uses ketones over free fatty acids as a more energy efficient substrate. The primary aim was to assess the effects of ketone monoester (K) ingestion on cardiac output index ().
View Article and Find Full Text PDFAm J Physiol Cell Physiol
January 2025
School of Health and Exercise Sciences, The University of British Columbia, Okanagan,BC V1V 1V7, Canada.
People with type 2 diabetes (T2D) have a greater risk of developing neurodegenerative diseases, like Alzheimer's disease, in later life. Exogenous ketone supplements containing the ketone body β-hydroxybutyrate (β-OHB) may be a strategy to protect the brain as β-OHB can support cerebral metabolism and promote neuronal plasticity via expression of brain-derived neurotrophic factor (BDNF). Parallel human (ClinicalTrials.
View Article and Find Full Text PDFNutrients
November 2024
Department of Health Behavior, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Cells
October 2024
International Collaboration on Repair Discoveries (ICORD), University of British Columbia, Vancouver, BC V5Z 1M9, Canada.
Spinal cord injury (SCI) pathology and pathophysiology can be attributed to both primary physical injury and secondary injury cascades. Secondary injury cascades involve dysregulated metabolism and energetic deficits directly linked to compromised mitochondrial bioenergetics. Rescuing mitochondrial function and reducing oxidative stress are associated with neuroprotection.
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