Magnesium is a cofactor for many enzymes involved in glucose metabolism

It is well-established that magnesium is a cofactor for many enzymes involved in glucose metabolism. For this reason, in the event that someone experiences a magnesium deficiency, his/her enzymes necessary for glucose metabolism may remain underactive.  The underactivity of glucose-metabolizing enzymes could lead to elevated blood glucose levels (hyperglycemia), as a byproduct of magnesium deficiency.

Research shows that increasing magnesium concentrations is capable of improving homeostatic glucose and insulin levels.  This is likely due to the fact that when magnesium intake increases (either through diet or supplementation), enzymes metabolize glucose more efficiently and less insulin secretion is necessary to shuttle glucose out of the bloodstream.  If your blood glucose levels spike unpredictably to high levels, it’s possible that a lack of magnesium in your diet could be a partial cause.

In fact, a study by Lal, Vasudev, Kela, and Jain (2003) discovered a greater occurrence of hypomagnesemia among persons with Type 2 diabetes than non-diabetic patients, indicative of the fact that chronically low magnesium may induce glucose abnormalities.  In the event that glucose abnormalities (e.g. hyperglycemia) result from an underlying magnesium deficiency, supplementation with magnesium could decrease severity or hyperglycemia via augmentation of enzymatic glucose metabolism, islet Beta-cell response, and reversal of insulin resistance.  Moreover, a vicious circle may occur in which hyperglycemia (resulting from low magnesium) exacerbates magnesium depletion (through frequent urination or insulin resistance), and the depletion of magnesium promotes increased likelihood of future hyperglycemia.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/2253826
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/8091358
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/12693452

Full article about Magnesium Deficiency Symptoms, Causes, & Treatments read at http://mentalhealthdaily.com/

Magnesium rich foods

by Cedars-Sinai Medical Center >> CP0403MagnesiumRichFoods.pdf

Citicoline increases glucose metabolism

Citicoline increases glucose metabolism in the brain and cerebral blood flow. [1]

Cocaine dependence is associated with depleted dopamine levels in the central nervous system. In cocaine-dependent individuals citicoline increases brain dopamine levels and reduces cravings.[2]

In the general population citicoline increases brain responses to food stimuli, specifically in the amygdala, insula, and lateral orbitofrontal cortex, which correlate with decreased appetite.[3]

Natural synthesis

The brain prefers to use choline to synthesize acetylcholine. This limits the amount of choline available to synthesize phosphatidylcholine. When the availability of choline is low or the need for acetylcholine increases, phospholipids containing choline can be catabolized from neuronal membranes. These phospholipids include sphingomyelin and phosphatidylcholine. [4]

Food sources of Choline

  • Shrimp
  • Eggs
  • Scallops
  • Chicken
  • Turkey
  • Tuna
  • Cod
  • Salmon
  • Beef
  • Collard Greens

Links for food sources of choline:

Chemical formula

Citicoline


Citicholine


References

  1. Watanabe S, Kono S, Nakashima Y, Mitsunobu K, Otsuki S (1975). “Effects of various cerebral metabolic activators on glucose metabolism of brain”. Folia Psychiatrica et Neurologica Japonica. 29 (1): 67–76.
  2. Renshaw PF, Daniels S, Lundahl LH, Rogers V, Lukas SE (Feb 1999). “Short-term treatment with citicoline (CDP-choline) attenuates some measures of craving in cocaine-dependent subjects: a preliminary report”. Psychopharmacology. 142 (2): 132–8.
  3. Killgore WD, Ross AJ, Kamiya T, Kawada Y, Renshaw PF, Yurgelun-Todd DA (Jan 2010). “Citicoline affects appetite and cortico-limbic responses to images of high-calorie foods”. The International Journal of Eating Disorders. 43 (1): 6–13.
  4. Adibhatla RM, Hatcher JF, Dempsey RJ (Jan 2002). “Citicoline: neuroprotective mechanisms in cerebral ischemia”. Journal of Neurochemistry. 80 (1): 12–23.