ABSTRACT
Background:
Calorie restriction (CR) during daily
nutrition has been shown to
affect the
prognosis of many
chronic diseases such as
metabolic syndrome, diabetes, and
aging. As an alternative
nutrition model, prolonged
intermittent fasting (PF) in
humans is defined by the absence of
food for more than 12 h. In our previous
human studies, CR and PF models were compared and it was concluded that the two models might have differences in
signal transduction mechanisms. We have investigated the effects of these models on
neurons at the molecular level in this study.
Methods:
Neurons (SH-SY5Y) were incubated with normal medium (N), calorie-restricted medium (CR),
fasting medium (PF), and
glucose-free medium (G0) for 16 h. Simultaneously,
ketone (
beta-hydroxybutyrate; bOHB) was added to other experiment flasks containing the same media. Concentrations of
lactate,
lactate dehydrogenase (LDH), bOHB, and
glucose were measured to demonstrate the changes in the
energy metabolism together with the mitochondrial functions of
cells.
Citrate synthase activity and flow cytometric mitochondrial functions were investigated.
Results:
At the end of incubations,
lactate and LDH levels were decreased and mitochondrial activity was increased in all
ketone-added groups (P < .01) regardless of the
glucose concentration in the
environment. In the
fasting model, these differences were more prominent.
Conclusion:
Our results demonstrated that
neurons use
ketones regardless of the amount of
glucose, and bOHB-treated
cells had positive changes in mitochondrial function. We conclude that the presence of bOHB might reverse
neuron damage and that exogenous
ketone treatment may be beneficial in the
treatment of neurological
diseases in the
future.
