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AMPK and Exercise: Glucose Uptake and Insulin Sensitivity
Hayley M. O'Neill
Diabetes Metab J. 2013;37(1):1-21.   Published online February 15, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.1.1
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AbstractAbstract PDFPubReader   

AMPK is an evolutionary conserved sensor of cellular energy status that is activated during exercise. Pharmacological activation of AMPK promotes glucose uptake, fatty acid oxidation, mitochondrial biogenesis, and insulin sensitivity; processes that are reduced in obesity and contribute to the development of insulin resistance. AMPK deficient mouse models have been used to provide direct genetic evidence either supporting or refuting a role for AMPK in regulating these processes. Exercise promotes glucose uptake by an insulin dependent mechanism involving AMPK. Exercise is important for improving insulin sensitivity; however, it is not known if AMPK is required for these improvements. Understanding how these metabolic processes are regulated is important for the development of new strategies that target obesity-induced insulin resistance. This review will discuss the involvement of AMPK in regulating skeletal muscle metabolism (glucose uptake, glycogen synthesis, and insulin sensitivity).

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Original Articles
The Role of Akt-1/PKBalpha on Insulin Action in 3T3-L1 Adipocyte.
Jung Min Lee, Hyun Shik Son, Hyuk Sang Kwon, Seung Ki Kwack, Seung Hyun Ko, Sang Ah Chang, Kun Ho Yoon, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang, Prem Sharma
Korean Diabetes J. 2002;26(4):274-285.   Published online August 1, 2002
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BACKGROUND
S: Akt/PKB as a serine/threonine kinase is stimulated by insulin and other growth factors. And insulin stimulates glucose uptake by promoting the translocation of glucose transporter 4 (GLUT4) to the cell membrane. But, it is not clear that Akt/PKB, a downstream target of PI 3-kinase, is involved in glucose uptake pathway. In this study, we investigated the role of Akt/PKB, especially Akt-1, on insulin action in 3T3-L1 adipocyte. METHODS: We made recombinant Ad5.Akt-1 vector by the insertion of Akt-1 gene to adenoviral vector. And then, we overexpressed Akt-1 proteins(wild type and kinase inactive type) in 3T3-L1 adipocytes by using a adenoviral transfection method. We observed the changes of glucose uptake, glycogen synthesis, activities of mitogen-activated protein kinase (MAPK, also called extracellular signal-regulated kinase), p70 ribosomal s6 protein kinase (p70s6k), and glycogen synthase kinase 3 (GSK3) according to Akt-1 activity and insulin treatment. RESULTS: First, overexpression of Akt-1 did not affect to glucose uptake, whether insulin stimulates or not. Second, overexpression of Akt-1 did not affect the phosphorylation of p44/42-MAPK, either. Third, the glycogen synthesis was increased by overexpression of Akt-1. CONCLUSION: Akt-1 activation is necessary for glycogen synthesis, but is not essential for glucose transport in 3T3-L1 adipocytes.
The Effect of Elevated Plasma Free Fatty Acids on Non-Insulin-Mediated Glucose Uptake and Insulin Resistance.
Yong Ki Min, Jong Ho Ahn, Jae Joon Koh, Hong Kyu Lee, Hun Ki Min
Korean Diabetes J. 1998;22(1):47-55.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
In vivo glucose uptake occurs via two mechanisms, namely insulin-mediated glucose uptake(IMGU) and non-insulin-mediated glucose up-take(NIMGU). NIMGU accaunts for about 70~85% of postabsorptive glucose uptake. Despite many studies, it is still controversial how an increase in lipolysis affects glucose metabolism in man. More specifically, the effect of free fatty acid(FFA) on NIMGU has not been exanuned. METHOD: Two-step(euglycemia- hyperglycemia) glucose clamp techique with [3-H]-glucose infusion was performed in 6 normal men. Each man was studied twice, with(test experiement) and without (control experiment) the administration of lipid and heparin at an interval of at least 4 weeks in random order. The subjects received an insulin infusion at 1.1 pmol/kg. min in conjuction with the infusion of somatostatin(step 1, 153 nmol/h; step 2, 458 nmol/h). Result: Plasma glucose levels during step 1 were 5.4+0.1 mmol/L(control experiment), 5.4+0.1 mmol/ L(test experiment), and were raised to 14.7+0.2 mmol/L, 14.6+0.1 mmol/L, respectively, during step 2. Plasma insulin levels during step 1 were 56+4 pmol/L(control experiment), 52+4 pmol/L(test experiment), and were 65+3 pmol/L, 62+4 pmol/L, respectively, during step 2. In control experiment, plasma FFA levels were 0.24+0.02 mmol/L during step 1 and 0.11+0.01 mmol/L during step 2. In test experiment, plasma FFA levels increased significantly to 1.08+0.06 mmol/L during step 1 and 1.01 +0.04 mmol/L during step 2, respectively(p<0.01). Glucose infusion rate(GIR) to increase glucose concentrations to the desired levels were 7.7+0.8 pnol/ kg,min during step 1 and 29.7+3.7 pmol/kg.min during step 2 in control experiment. In test experiment, GIR decreawd significantly to 3.8+0.9 pmol/ kg.min during step 1 and 20.7+1.2 pmol/kg.min during step 2, respectively(p<0.05). There was no significant difference between NIMGU, estimated by the difference between glucose disapperance rate of step 1 and step 2 of lipid infusion test experiment and that of control experiment. CONCLUSION: These results showed that artificial elevation of plasma FFA levels led to a state of insulin resistance, however, the change of FFA level did not influence NIMGU in man.

Diabetes Metab J : Diabetes & Metabolism Journal
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