Metabolic response to a ketogenic breakfast in the healthy elderly

Freemantle, Erika; Vandal, Milène; Tremblay‐Mercier, Jennifer; Plourde, Mélanie; Poirier, Judes; Cunnane, Stephen C.

doi:10.1007/s12603-009-0026-9

Cited by 44 publications

(71 citation statements)

References 29 publications

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“…The ratio of 13 C: 12 C-CO 2 was used to calculate the b-oxidation of 13 C-DHA recovered in the breath in the form of 13 C-CO 2 . The percentage of dose of 13 C-DHA recovered in the breath as 13 C-CO 2 was calculated as previously described (21) except that basal metabolism was evaluated by using indirect calorimetry (CCM/D; Medgraphics Corp) to measure the volume of CO 2 and O 2 exhaled by participants over 30 min as previously described (22). The cumulative 13 C-DHA b-oxidation was calculated as the AUC of the percentage of dose recovered (PDR) at each time point (GraphPad Prism 5 for Windows software, version 5.03; Graph-Pad).…”

Section: Analytic Methodsmentioning

confidence: 99%

Kinetics of 13C-DHA before and during fish-oil supplementation in healthy older individuals

Plourde¹,

Chouinard‐Watkins²,

Rioux-Perreault³

et al. 2014

The American Journal of Clinical Nutrition

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Section: Analytic Methodsmentioning

confidence: 99%

Kinetics of 13C-DHA before and during fish-oil supplementation in healthy older individuals

Plourde¹,

Chouinard‐Watkins²,

Rioux-Perreault³

et al. 2014

The American Journal of Clinical Nutrition

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“…Breath 13 CO 2 Detection. Fatty acid oxidation was quantified by enrichment of 13 C in breath CO 2 after ingestion of the [U-13 C]linoleic acid using isotope ratio mass spectrometry (Europa 20-20; Sercon Ltd., Crewe, Cheshire, UK) with helium as the carrier gas, as described previously (Freemantle et al, 2009).…”

Section: Methodsmentioning

confidence: 99%

Bezafibrate Mildly Stimulates Ketogenesis and Fatty Acid Metabolism in Hypertriglyceridemic Subjects

Tremblay‐Mercier¹,

Tessier²,

Plourde³

et al. 2010

J Pharmacol Exp Ther

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Our objective was to determine whether bezafibrate, a hypotriglyceridemic drug and peroxisome proliferatoractivated receptor (PPAR)-␣ agonist, is ketogenic and increases fatty acid oxidation in humans. We measured fatty acid metabolism and ketone levels in 13 mildly hypertriglycemic adults (67 Ϯ 11 years old) during 2 metabolic study days lasting 6 h, 1 day before and 1 day after bezafibrate (400 mg of bezafibrate per day for 12 weeks). ␤-Hydroxybutyrate, triglycerides, free fatty acids, fatty acid profiles, insulin, and glucose were measured in plasma, and fatty acid ␤-oxidation was measured in breath after an oral 50-mg dose of the fatty acid tracer [U-13 C]linoleic acid. As expected, 12weeks on bezafibrate decreased plasma triglycerides by 35%. Bezafibrate tended to raise postprandial ␤-hydroxybutyrate, an effect that was significant after normalization to the fasting baseline values (p ϭ 0.03). ␤-Oxidation of [U-13 C]linoleic acid increased by 30% (p ϭ 0.03) after treatment. On the metabolic study day after bezafibrate treatment, postprandial insulin decreased by 26% (p ϭ 0.01), and glucose concentrations were lower 2 to 5 h postprandially. Thus, in hypertriglyceridemic individuals, bezafibrate is mildly ketogenic and significantly changes fatty acid metabolism, effects that may be linked to PPAR␣ stimulation and to moderately improved glucose metabolism.As the population ages, the prevalence of cognitive impairment in the elderly, particularly Alzheimer's disease (AD), is increasing markedly. Glucose is the brain's main energy substrate, providing energy to make ATP to maintain ion gradients, synaptic transmission, protein synthesis (for review, see Hoyer, 1996), and fatty acid turnover in membranes phospholipids (Rapoport et al., 2001). A decline in cerebral glucose metabolism is widely reported in AD (Foster et al., 1984;Blennow et al., 2006;Mosconi et al., 2007). This deterioration in brain fuel supply is progressive, correlates broadly with dementia severity, and may appear during normal aging at which time there can be an approximately 6% reduction in glucose uptake per decade (Petit-Taboué et al., 1998). Reduced brain glucose metabolism can arise before the clinical symptoms of AD (Reiman et al., 2004) and may contribute to neurodegenerative processes leading to AD (Liu 2004(Liu , 2008. As such, an alternative brain fuel to glucose may be therapeutically useful in AD.Physiologically, ketone bodies [or ketones; ␤-hydroxybutyrate (␤-OHB), acetoacetate, and acetone] are the main alternative energy substrate to glucose for brain metabolism and are especially important during periods of glucose deprivation. Ketones can supply up to two thirds of the energy requirement of the brain during starvation (Owen et al., 1967). Mildly increasing ketone synthesis has been proposed as a possible therapeutic approach to correct or bypass brain

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“…Children produce and utilize βOHB more efficiently than adults, a capability crucial in the days immediately after birth when the brain depends on ketone bodies as an energy source, and serum levels can reach 2–3 mM [12]. At the other end of life, the elderly generate ketone bodies after a fast or ketogenic meal to the same extent as younger adults [15, 16]. …”

Section: Metabolism Regulation and Function Of Ketone Bodiesmentioning

confidence: 99%

Ketone bodies as signaling metabolites

Newman

Verdin

2014

Trends in Endocrinology & Metabolism

721

643

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Traditionally, the ketone body β-hydroxybutyrate (βOHB) has been looked upon as a carrier of energy from liver to peripheral tissues during fasting or exercise. However, βOHB also signals via extracellular receptors and acts as an endogenous inhibitor of histone deacetylases (HDACs). These recent findings support a model in which βOHB functions to link the environment, in this case the diet, and gene expression via chromatin modifications. Here, we review the regulation and functions of ketone bodies, the relationship between ketone bodies and calorie restriction, and the implications of HDAC inhibition by the ketone body βOHB in the modulation of metabolism, and diseases of aging.

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Metabolic response to a ketogenic breakfast in the healthy elderly

Abstract: Elderly people in relatively good health have a similar capacity to produce ketones and to oxidize 13C-beta-hydroxybutyrate as middle-aged or young adults, but oxidize 13C-glucose a little more rapidly than healthy middle-aged adults.

Cited by 44 publications

References 29 publications

Kinetics of 13C-DHA before and during fish-oil supplementation in healthy older individuals

Kinetics of 13C-DHA before and during fish-oil supplementation in healthy older individuals

Bezafibrate Mildly Stimulates Ketogenesis and Fatty Acid Metabolism in Hypertriglyceridemic Subjects

Ketone bodies as signaling metabolites

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