Intermittent Fasting - another mechanism

There are quite a few of us now that have an interest in Intermittent Fasting (IF). I have just seen this abstract which looks at another mechanism associated with IF. This mechanism could add to the fat-burning effect of fasting.

You may have heard of l-carnitine - it has been sold as a supplement allegedly to increase fat burning and prevent fatigue. The description below is from Wikipedia:

Carnitine, also known as L-carnitine or levocarnitine, is a quaternary ammonium compound biosynthesized from the amino acids lysine and methionine.[1] It helps in the consumption and disposal of fat in the body because it is responsible for the transport of fatty acids from the cytosol into the mitochondria. It is often sold as a nutritional supplement.

One of the supplement advertisements explains:

L-carnitine transfers long-chain fatty acids, such as triglycerides into mitochondria (a cell's energy powerhouse), where they may be oxidized to produce energy. L-carnitine is a very popular supplement that promotes growth and development. It is also used for fat-burning, increasing energy, and improving resistance to muscle fatigue. L-carnitine has also been shown to help build muscle. is also great in dieting, as it reduces feelings of hunger and weakness.

OK, that is the context.

Now there is this study, Fasting and Caloric Restriction Increases mRNA Concentrations of Novel Organic Cation Transporter-2 and Carnitine Concentrations in Rat Tissues.

The study shows that fasting and caloric restriction lead to an upregulation of OCTN2 in several tissues, probably mediated by activation of PPAR. Increased tissue carnitine concentrations in fasted and calorie-restricted rats might be at least in part due to increased uptake of carnitine by OCTN2.


The study identifies a particular mechanism but the key issue is that fasting and calorie restriction (CR) lead to increased carnitine concentrations.


So that which athletes and bodybuilders seek to achieve via supplementation is possible - at least in rats - via fasting or calorie restriction...



Background: Recently, we have shown that activation of peroxisome proliferator-activated receptor (PPAR)- by clofibrate leads to an upregulation of novel organic cation transporter (OCTN)-2, a carnitine transporter, and in turn increases the carnitine concentration in the liver of rats. In this study, we tested the hypothesis that fasting and caloric restriction, conditions under which PPAR activation also occurs, cause similar effects. Methods: Three groups of rats received the diet either ad libitum (control rats) or 10.5 g diet/day (70% of energy requirement for maintenance, E70 rats) or 6 g diet/day (40% of energy requirement for maintenance, E40 rats) for 10 days. A 4th group received the diet ad libitum for 9 days and was then fasted for 24 h (fasted rats). Results: Fasted and calorie-restricted rats had increased mRNA concentrations of acyl-CoA oxidase and carnitine palmitoyltransferase-1 in the liver, heart and kidneys compared to control rats (p < 0.05), indicative of activation of PPAR in these tissues. E70 rats had increased OCTN2 mRNA concentrations in liver (2.6-fold) and kidneys (1.5-fold) and increased total carnitine concentrations in these tissues compared to control rats. E40 rats had increased OCTN2 mRNA concentrations in the liver (3.3-fold), skeletal muscle (2.2-fold), heart (2.3-fold) and kidneys (3.5-fold) and increased total carnitine concentrations in these four tissues compared to control rats. Fasted rats had increased OCTN2 mRNA concentrations in the liver (4.0-fold), heart (2.1-fold) and kidneys (2.0-fold) and increased total carnitine concentrations in these three tissues (p < 0.05). Conclusion: The study shows that fasting and caloric restriction lead to an upregulation of OCTN2 in several tissues, probably mediated by activation of PPAR. Increased tissue carnitine concentrations in fasted and calorie-restricted rats might be at least in part due to increased uptake of carnitine by OCTN2.