The Carnitine-Hypoglycemia Story: The role of Carnitine in Fatty Acid Oxidation and Why It Does Not Work In Hypoglycaemics

by Bryan Walsh

Carnitine is a nitrogen-containing non-protein compound that can be synthesized by the body. Carnitine is thought to help transport long chain fatty acids across the inner mitochondrial membrane to be used as a source for ATP synthesis (beta oxidation).

Conventional nutritional wisdom suggests that because our body can make carnitine, we should easily have enough. But this assumes we have the necessary ingredients. To make carnitine, we need the amino acids lysine and methionine, as well as vitamin C, vitamin B6, iron, and oxygen. Many people lack one or more of these raw materials.

[Nature's Sunshine Mega-Chel contains most of the required nutrients for your body to make carnitine (minus the oxygyen, that you will have to suck in yourself).  Mega Chel contains 58mg of l-methionine, 2,220% of RDA of vitamin C, 2,500% of RDA of vitamin B6, and 3.2mg of iron.]

Carnitine can also be consumed in our diet, with the highest amounts occurring in red meat and pork. Some diets may be deficient.

Hypoglycemia

When our blood sugar starts to drop between meals, two processes should kick in to help maintain normal levels – glycogenolysis and gluconeogenesis. The pancreatic hormone glucagon is thought to stimulate these processes.
But glucagon doesn’t seem to work correctly in hypoglycemics. What could be going on?
First, a quick review of the pathways:

1. When glucose starts to drop, insulin will often drop and glucagon will often increase.
2. This situation (low insulin, high glucagon) can stimulate lipolysis, or the liberation of fatty acids from adipocytes (fat cells).
3. These fatty acids can make their way to the liver to be used for energy (ATP) synthesis.
4. Fatty acids must enter into the mitochondria of cells, where they will be broken down into acetyl coenzyme A (acetyl-CoA), and used to produce ATP in the citric acid cycle.
5. During low energy states, (e.g. low glucose), high levels of acetyl-CoA up-regulates the enzyme pyruvate into oxaloacetate, which can then be converted into phosphoenoylpyruvate (PEP) and used in hepatic gluconeogenesis. Conversely, low levels of acetyl-CoA down-regulates pyruvate carboxylase and thus gluconeogenesis will suffer.

So why, during low energy states, can acetyl CoA levels drop within the mitochondria?

Enter carnitine

During periods of low glucose, carnitine helps break down fatty acids into acetyl-CoA in the mitochondria and shuttles long chain fatty acids across the inner mitochondrial membrane.
Without carnitine, these changes  won’t occur and acetyl-CoA levels may drop. Thus low carnitine can lead to low levels of acetyl-CoA and effectively inhibit new glucose production.
(As a side note, glycogen phosphorylase, the enzyme necessary for converting stored glycogen into glucose, also requires vitamin B6, and thus may also play an unacknowledged role in hypoglycemia.)
Carnitine deficiency is relatively common during and after pregnancy, and in vegetarians.

Source: http://www.precisionnutrition.com/doctor-detective-hypoglycemia