Acetyl L-Carnitine and Diabetes

Longer Life for Diabetics

Acetyl L-carnitine is involved in the transport of certain fatty acids into cells. As a result of the process of oxidation, energy is released by the cell mitochondria. Diabetics stand to gain benefits from acetyl L-carnitine supplementation.

Most chronic diseases of aging reflect loss of mitochondrial function and numbers, limiting the energy available to cells as we age. Poorly-functioning mitochondria also impose huge oxidant stress on their parent cells, further accelerating aging and shortening life.

Acetyl L-carnitine, a natural molecule with several related forms, provides mitochondria with both the energy they need and the antioxidant protection that they must have to retain their youthful function.

This is important because diabetics are at especially high risk for cardiovascular complications and early death. A part of this is that diabetics are more deficient in acetyl L-carnitine than others of the same age groups.^{4, 5}

Since acetyl L-carnitine helps the mitochondria utilize energy, it can play a critical role in reducing the occurrence and impact of diabesity.⁶ Recent studies show that in addition to helping the mitochondria burn fat as energy, acetyl-l-carnitine is also vital for removing waste products from mitochondria.⁷ This is important because we now recognize that the buildup of mitochondrial waste products is one of the most important contributors to insulin resistance, which further promotes high blood sugar and obesity.⁸

Acetyl L-carnitine supplements extend life by increasing energy to tissues throughout the body. It has proven effective in reducing fatigue, enhancing cardiovascular function, improving body composition and promoting weight loss, lowering blood sugar levels, and delaying or reversing brain degeneration.

Help for Heart Conditions

Acetyl L-carnitine has a protective effect on heart muscles and function, thus diabetics may benefit from this supplement, as diabetes increases the risk of developing heart conditions. In clinical research, acetyl L-carnitine has been found to enhance the efficacy of conventional drugs in improving glucose and lipid levels in diabetics.

Diabetics suffer from both ischemic (low blood flow) and non-ischemic heart muscle dysfunction. These can be reduced by long-term acetyl L-carnitine supplements. Animal studies show that whether you’re a diabetic or not, oral supplementation with acetyl-l-carnitine helps your heart muscle pump harder and more efficiently.⁹ Even more impressive, acetyl L-carnitine’s mitochondria-friendly actions help reduce body fat mass, which in turn improves insulin sensitivity and may help control blood sugar levels.¹⁰

(Another study published in the April 2010 issue of “Nutrition and Metabolism” assessed the benefits of acetyl L-carnitine for various health conditions. In relation to diabetes, researchers concluded that there is increased evidence that supplementing with acetyl L-carnitine helps improve cardiovascular conditions.)

Diabesity

As obesity rates skyrocket, more and more Americans are developing type II diabetes as a result, this is now being called “diabesity.” We’ve seen how acetyl L-carnitine improves the usage of fat as a source of energy, lowers cholesterol and triglyceride levels and may reduce the risk of health problems in diabetics who have impaired fat metabolism.

Obesity and aging contribute to low carnitine levels, which compromises mitochondrial performance and increases insulin resistance, promoting further obesity and acetyl L-carnitine reduction.¹¹ Restoring carnitine levels to their youthful values is an effective way to break this deadly cycle.

Supplemented patients used their fat for energy, burning it 22% faster than control patients, without any increase in muscle protein breakdown.¹⁴ Another study demonstrated a loss of total fat mass of 4 pounds, with a gain in lean muscle mass of 8.4 pounds.¹⁵

Animal studies confirm and extend these findings, showing that acetyl L-carnitine decreases body weight gain, food intake, and fat composition, while improving insulin resistance. All of which convinces us that acetyl L-carnitine needs to be part of our Dia-Mazing supplement.

Nerve Pain

Diabetic polyneuropathy (DPN) is the most common late complication of diabetes and is commonly associated with neuropathic pain.¹¹ DPN shows a dynamic history of early reversible metabolic abnormalities.  These become progressively replaced by less reversible structural lesions and functional deficits.⁸

Data has shown significant improvements in sural nerve fiber numbers and regenerating nerve fiber clusters. Vibration perception improved in both studies. Pain, as the most bothersome symptom, showed significant improvement taking 1,000 mg ALC.¹²

These studies demonstrate that ALC treatment is effective in alleviating symptoms, particularly pain, and improves nerve fiber regeneration and vibration perception in patients with established diabetic neuropathy.

We use the acetyl L-carnitine form because it is more active in moving fat molecules across the mitochondrial membrane.  It readily crosses into the brain from the bloodstream, and its extra acetyl molecule provides additional energy directly to brain cells.¹³

References

1. Mingorance C, Gonzalez del Pozo M, Dolores Herrera M, Alvarez de Sotomayor M. Oral supplementation of propionyl-l-carnitine reduces body weight and hyperinsulinaemia in obese Zucker rats. Br J Nutr. 2009 Oct;102(8):1145-53.

2. Noland RC, Koves TR, Seiler SE, et al. Carnitine insufficiency caused by aging and overnutrition compromises mitochondrial performance and metabolic control. J Biol Chem. 2009 Aug 21;284(34):22840-52.

3. Terman A, Kurz T, Navratil M, Arriaga EA, Brunk UT. Mitochondrial turnover and aging of long-lived postmitotic cells: the mitochondrial-lysosomal axis theory of aging. Antioxid Redox Signal. 2010 Apr;12(4):503-35.

4. Scarpini E, Doneda P, Pizzul S, Chiodi P, Ramacci MT, Baron P, Conti G, Sacilotto G, Arduini A, Scarlato G: L-carnitine and acetyl-L-carnitine in human nerves from normal and diabetic subjects. J Peripher Nerv Syst 1:157–163, 1996.

5. Ido Y, McHowat J, Chang KC, Arrigoni-Martelli E, Orfalian Z, Kilo C, Corr PB, Williamson JR: Neural dysfunction and metabolic imbalances in diabetic rats: prevention by acetyl-L-carnitine. Diabetes 43:1469–1477, 1994.

6. Sugimoto K, Murakawa Y, Sima AAF: Diabetic neuropathy: a continuing enigma. Diabetes Metab Res Rev 16: 408–433, 2000.

7. Sima AAF: New insights into the metabolic and molecular basis for diabetic neuropathy. Cell Mol Life Sci 60:2445–2464, 2003.

8. Dyck PJ, Thomas PK: Diabetic polyneuropathy. In Diabetic Neuropathy. Philadelphia, W.B. Saunders, 1999, p. 239–406.

9. Mingorance C, Duluc L, Chalopin M, et al. Propionyl-L-carnitine corrects metabolic and cardiovascular alterations in diet-induced obese mice and improves liver respiratory chain activity. PLoS One. 2012;7(3):e34268.

10. Mingorance C, Rodriguez-Rodriguez R, Justo ML, Herrera MD, de Sotomayor MA. Pharmacological effects and clinical applications of propionyl-L-carnitine. Nutr Rev. 2011 May;69(5):279-90.

11. Sima AAF: New insights into the metabolic and molecular basis for diabetic neuropathy. Cell Mol Life Sci 60:2445–2464, 2003.

12. Anders A.F. Sima, MD, PHD1, Menotti Calvani, MD2, Munish Mehra, PHD3, Antonino Amato, Acetyl-l-Carnitine Improves Pain, Nerve Regeneration, and Vibratory Perception in Patients With Chronic Diabetic Neuropathy. Diabetes Care 2005 Jan; 28(1): 89-94.

13. Scafidi S, Fiskum G, Lindauer SL, et al. Metabolism of acetyl-L-carnitine for energy and neurotransmitter synthesis in the immature rat brain. J Neurochem. 2010 Aug;114(3):820-31.

14. Wutzke KD, Lorenz H. The effect of l-carnitine on fat oxidation, protein turnover, and body composition in slightly overweight subjects. Metabolism. 2004 Aug;53(8):1002-6.

15. Malaguarnera M, Cammalleri L, Gargante MP, Vacante M, Colonna V, Motta M. L-Carnitine treatment reduces severity of physical and mental fatigue and increases cognitive functions in centenarians: a randomized and controlled clinical trial. Am J Clin Nutr. 2007 Dec;86(6):1738-44.