Autor: |
Cooper ID; Ageing Biology and Age-Related Diseases, School of Life Sciences, University of Westminster, 115 New Cavendish Street, London W1W 6UW, UK., Kyriakidou Y; Ageing Biology and Age-Related Diseases, School of Life Sciences, University of Westminster, 115 New Cavendish Street, London W1W 6UW, UK., Petagine L; Ageing Biology and Age-Related Diseases, School of Life Sciences, University of Westminster, 115 New Cavendish Street, London W1W 6UW, UK., Edwards K; Cancer Biomarkers and Mechanisms Group, School of Life Sciences, University of Westminster, 115 New Cavendish Street, London W1W 6UW, UK., Soto-Mota A; Metabolic Diseases Research Unit, National Institute of Medical Sciences and Nutrition Salvador Zubiran, Mexico City 14080, Mexico.; School of Medicine, Tecnologico de Monterrey, Mexico City 14380, Mexico., Brookler K; Retired former Research Collaborator, Aerospace Medicine and Vestibular Research Laboratory, Mayo Clinic, Scottsdale, AZ 85259, USA., Elliott BT; Ageing Biology and Age-Related Diseases, School of Life Sciences, University of Westminster, 115 New Cavendish Street, London W1W 6UW, UK. |
Abstrakt: |
Metabolic dysfunctions are among the best documented hallmarks of ageing. Cardiovascular disease, Alzheimer's disease, cancer, type 2 diabetes mellitus, metabolic-dysfunction-associated steatosis liver disease, and fragility fractures are diseases of hyperinsulinaemia that reduce life and healthspan. We studied the effect of suppressing ketosis in 10 lean (BMI 20.5 kg/m 2 ± 1.4), metabolically healthy, pre-menopausal women (age 32.3 ± 8.9 years) maintaining nutritional ketosis (NK) for an average of 3.9 years (± 2.3) who underwent three 21-day phases: nutritional ketosis (NK; P1), suppressed ketosis (SuK; P2), and returned to NK (P3). Ketosis suppression significantly increased insulin, 1.83-fold ( p = 0.0006); glucose, 1.17-fold ( p = 0.0088); homeostasis model assessment for insulin resistance (HOMA-IR), 2.13-fold ( p = 0.0008); leptin, 3.35-fold ( p = 0.0010); total osteocalcin, 1.63-fold ( p = 0.0138); and uncarboxylated osteocalcin, 1.98-fold ( p = 0.0417) and significantly decreased beta-hydroxybutyrate, 13.50-fold ( p = 0.0012) and glucagon-like peptide-1 (GLP-1), 2.40-fold ( p = 0.0209). Sustained NK showed no adverse health effects and may mitigate hyperinsulinemia. All biomarkers returned to basal P1 levels after removing the intervention for SuK, indicating that metabolic flexibility was maintained with long-term euketonaemia. |