Oliveira HC 2013 Abstract MiP2013

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Oliveira HC, Dorighello GG, Rovani JC, Raposo HF, Paim BA, Vercesi AE (2013) Intermittent fasting improves oxidative stress but not metabolic disturbances and atherosclerosis in hypercholesterolemic mice. Mitochondr Physiol Network 18.08.
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Oliveira HC, Dorighello GG, Rovani JC, Raposo HF, Paim BA, Vercesi AE (2013)

Event: MiPNet18.08_MiP2013

Different regimens of food restriction have been associated with protection against obesity, diabetes and cardiovascular diseases. Food (caloric) restriction can favorably modulate cell and body redox state. In this study, we hypothesized that food restriction could bring benefits for the atherosclerosis-prone hypercholesterolemic LDL receptor–deficient mice.

Two-month-old mice were submitted to an intermittent fasting (IF) regimen (fasting every other day) over a 3-month period that resulted in an overall 20% reduction in food intake. As expected, IF ameliorated two oxidative stress markers, the susceptibility of VLDL to oxidation (increased lag time to oxidation by 25%) and the rate of liver mitochondrial ROS generation (decreased in DCF oxidation by 43%). Unexpectedly, the IF mice had epididymal and carcass fat depots significantly enlarged. Accordingly, plasma levels of leptin were 50% higher in IF mice. In addition, the IF mice presented increased total (37%), VLDL (3-fold) and LDL (50%) cholesterol plasma levels. Glucose homeostasis was also disturbed by IF with elevation of glycemia (40%), insulinemia (50%), glucose intolerance and insulin resistance in IF mice. The systemic inflammatory markers TNF-alpha and C-reactive protein were elevated and spontaneous atherosclerosis development was markedly increased (3-fold).

Although IF caused some benefits on systemic and tissue redox state, this type of food restriction induced obesity and diabetes and worsened atherosclerosis in these LDL receptor–deficient mice. Thus, IF is not beneficial in the context of genetic hypercholesterolemia.

Keywords: Atherosclerosis

O2k-Network Lab: BR Campinas Vercesi AE


Labels: MiParea: Exercise physiology;nutrition;life style, mt-Medicine  Pathology: Cardiovascular, Diabetes, Obesity  Stress:Oxidative stress;RONS  Organism: Mouse  Tissue;cell: Liver  Preparation: Intact organism, Homogenate, Isolated mitochondria 

Regulation: Redox state  Coupling state: ROUTINE  Pathway:


MiP2013 

Affiliations and author contributions

1 - Dept Structural and Functional Biology, State University of Campinas, Brazil

2 - Dept Clinical Pathology, State University of Campinas, Brazil.

Email: ho98@unicamp.br

Supported by Fapesp, CNPq and Capes Brazilian Research Agencies.