AMPK Activation

// Corey Schuler, RN, MS, CNS, DC


AMPK (5' adenosine monophosphate-activated protein kinase) is activated during exercise prompting glucose uptake into cells, making exercise an important factor for regulating glucose metabolism within normal limits.

Mitochondria diagram

What is AMPK?

AMPK is an insulin independent mechanism.1 Insulin is the hormone that helps regulate blood glucose levels. When serum glucose levels are normally elevated due to dietary intake or ho-meostatic need, insulin is released from the beta cells of the pancreas to facilitate the uptake of glucose into cells for energy. During exercise, AMPK is activated which increases a series of enzymes, including GSK-3b (glycogen synthase kinase 3b), CRTC2 (CRE-binding protein [CREB]-regulated transcription coactivator 2) and FOXO1 (forkhead box O1) that play a role in glucose metabolism.2,3 According to DeFronzo and Tripathy, skeletal muscle is responsible for around 80% of insulin-stimulated glucose uptake.4 Exercise, like insulin, increases the glucose transport in skeletal muscle, resulting in glucose clearance from the blood through GLUT4 transporters in skeletal muscle.

How does AMPK work?

MAMPK is an enzyme that acts as an energy sensor when the ATP/ADP (adenosine triphosphate/ adenosine diphosphate) ratio changes. ATP is needed to produce energy via mitochondria, so when ATP supplies run low, AMPK is activated. AMPK is expressed primarily in the liver, skeletal muscle and the brain, all involved in energy intake and consumption.5 The ATP/ADP shift can occur for many reasons, including normally low serum glucose concentrations, changes in blood flow, oxygen, hormones, and, of course, exercise.6 Once activated, the energy consuming pathways are turned off and the energy producing pathways are turned on in order to restore energy balance.5 By turning on the energy producing pathways, glycogen storage is normally limited and appropriate changes in glucose uptake and insulin sensitivity are observed.7

1Hilder TL, Baer LA, Fuller PM, et al. Insulin-independent pathways mediating glucose uptake in hindlimb-suspended skeletal muscle. Journ App Phys. 2005; 99(6):2181-8.

2Zhang BB, Zhou G, Li C. AMPK: an emerging drug target for diabetes and the metabolic syndrome. Cell Metab. 2009; 9(5): 407–16.

3O’Neill, HM. AMPK and Exercise: Glucose Uptake and Insulin Sensitivity. Diabetes Metab J. 2013 Feb; 37(1): 1-21.

4DeFronzo RA, Tripathy D. Skeletal muscle insulin resistance is the primary defect in type 2 diabetes. Diabetes Care. 2009;32(Suppl 2):S157–S163

5Carling D, Mayer FV, Sanders MJ, Gamblin SJ. AMP-activated protein kinase: nature’s energy sensor. Nat Chem Biol. 201;7(8):512–8.

6Hardie DG. AMP-activated protein kinase: an energy sensor that regulates all aspects of cell function. Genes Dev. 2011;25(18):1895–908.

7Jensen J, Rustad PI, Kolnes AJ, et al. The role of skeletal muscle glycogen breakdown for regulation of insulin sensitivity by exercise. Front Physiol. 2011; 2: 112.


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