Fasting Clinical Trial
Official title:
Evaluation of p21 Induction and Molecular Pathways Related to Short-term Fasting Response
This study will evaluate the effect of short-term fasting (36 hours) in gene expression in blood cells in healthy volunteers.
Fasting is a nutritional intervention consisting on the restriction of nutrient intake during
a relatively long period of time. It elicits a profound metabolic reprogramming aimed at
shifting nutrient supply from external food intake to internal stored nutrients. Periodic
activation of this complex response, termed periodic or intermittent fasting (IF), elicits
numerous protective effects against aging, metabolic alterations, neurological disorders and
cardiovascular health. Short-term fasting is protective in different stress scenarios,
including ischemia reperfusion, bouts of inflammation and chemotherapy-induced toxicity, and
improves the anti-tumor efficacy of chemotherapy. Although the basic physiology of fasting is
well known, the molecular mechanisms underlying its beneficial effects are not yet completely
understood.
In mammals, the response to short-term fasting (from 12 to 48 hours) in terms of nutrient
mobilization through the bloodstream has been extensively studied. Fasting follows sequential
phases, during which nutrients are released from different storing depots. First, glucose is
released from glycogen stores in the liver and muscle. Upon depletion of glycogen, two
fasting mechanisms are activated: fatty acids are exported from the adipose tissue into the
bloodstream in the form of free fatty acids (FFAs), reaching the liver where they are used to
produce ketone bodies, a process termed ketogenesis. Also, gluconeogenesis is activated in
the liver, generating glucose mainly from glycerol (released during lipolysis) and amino
acids, that originate mainly from muscle breakdown. All these physiological responses are
tightly regulated by hormonal and molecular mechanisms.
At the hormonal level, fasting induces a decrease in blood insulin, leptin and ghrelin, and
an increase in glucagon levels, while blood adiponectin remains unchanged. Also, several
signal transduction pathways are affected by fasting. PPARalpha, a nuclear receptor of fatty
acids, becomes activated by the fasting-mediated increase in blood Free fatty Acids (FFAs)
and triggers the expression of many target genes in several tissues, including blood cells.
It has been shown that the Cyclin Dependent Kinase (CDK) inhibitor p21 is highly upregulated
during short-term fasting in many mouse tissues. Moreover, it is known that p21-null mice are
unable to endure normal periods of fasting and that p21 is required for the full activation
of PPARa target genes both in vivo and in isolated hepatocytes.
In the current study, the investigators wanted to study for the first time molecular
mechanisms of fasting that still remained unexplored, specially the expression induction of
p21 and PPARalpha signalling pathway. For this, the investigators analyzed blood samples from
healthy volunteers subjected to 36 hours of fasting, to explore gene expression in Peripheral
Blood Mononuclear Cells (PBMCs).
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