scholarly journals Endogenous Ligand for GPR120, Docosahexaenoic Acid, Exerts Benign Metabolic Effects on the Skeletal Muscles via AMP-activated Protein Kinase Pathway

2015 ◽  
Vol 290 (33) ◽  
pp. 20438-20447 ◽  
Author(s):  
Nami Kim ◽  
Jung Ok Lee ◽  
Hye Jeong Lee ◽  
Hyung Ip Kim ◽  
Joong Kwan Kim ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Docosahexaenoic Acid ◽  
Skeletal Muscles ◽  
Metabolic Effects ◽  
Endogenous Ligand ◽  
Amp Activated Protein Kinase ◽  
Kinase Pathway

scholarly journals Regulation of glycogen synthesis by the laforin–malin complex is modulated by the AMP-activated protein kinase pathway

2007 ◽  
Vol 17 (5) ◽  
pp. 667-678 ◽  
Author(s):  
Maria Carmen Solaz-Fuster ◽  
José Vicente Gimeno-Alcañiz ◽  
Susana Ros ◽  
Maria Elena Fernandez-Sanchez ◽  
Belen Garcia-Fojeda ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Glycogen Synthesis ◽  
Amp Activated Protein Kinase ◽  
Kinase Pathway

scholarly journals Docosahexaenoic acid regulates 5′ AMP‐activated protein kinase in adipocytes

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Chao-Wei Huang ◽  
Yu Jen Chen ◽  
Yuan-Yu Lin ◽  
Harry John Mersmann ◽  
Shih-Torng Ding
Keyword(s):  
Protein Kinase ◽  
Docosahexaenoic Acid ◽  
Amp Activated Protein Kinase

scholarly journals mTOR Inhibitor Therapy and Metabolic Consequences: Where Do We Stand?

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Aleksandra Kezic ◽  
Ljiljana Popovic ◽  
Katarina Lalic
Keyword(s):  
Protein Kinase ◽  
Glucose Metabolism ◽  
Calorie Restriction ◽  
Mtor Inhibitor ◽  
Hepatic Glucose Production ◽  
Mtor Inhibitors ◽  
Glucose Production ◽  
Metabolic Effects ◽  
Solid Organ ◽  
Amp Activated Protein Kinase

mTOR (mechanistic target of rapamycin) protein kinase acts as a central integrator of nutrient signaling pathways. Besides the immunosuppressive role after solid organ transplantations or in the treatment of some cancers, another promising role of mTOR inhibitor as an antiaging therapeutic has emerged in the recent years. Acute or intermittent rapamycin treatment has some resemblance to calorie restriction in metabolic effects such as an increased insulin sensitivity. However, the chronic inhibition of mTOR by macrolide rapamycin or other rapalogs has been associated with glucose intolerance and insulin resistance and may even provoke type II diabetes. These metabolic adverse effects limit the use of mTOR inhibitors. Metformin is a widely used drug for the treatment of type 2 diabetes which activates AMP-activated protein kinase (AMPK), acting as calorie restriction mimetic. In addition to the glucose-lowering effect resulting from the decreased hepatic glucose production and increased glucose utilization, metformin induces fatty acid oxidations. Here, we review the recent advances in our understanding of the metabolic consequences regarding glucose metabolism induced by mTOR inhibitors and compare them to the metabolic profile provoked by metformin use. We further suggest metformin use concurrent with rapalogs in order to pharmacologically address the impaired glucose metabolism and prevent the development of new-onset diabetes mellitus after solid organ transplantations induced by the chronic rapalog treatment.

Polyphenols targeting diabetes via the AMP-activated protein kinase pathway; future approach to drug discovery

2019 ◽  
Vol 56 (7) ◽  
pp. 472-492 ◽  
Author(s):  
Saeideh Momtaz ◽  
Armin Salek-Maghsoudi ◽  
Amir Hossein Abdolghaffari ◽  
Eghbal Jasemi ◽  
Shamsali Rezazadeh ◽  
...  
Keyword(s):  
Drug Discovery ◽  
Protein Kinase ◽  
Amp Activated Protein Kinase ◽  
Kinase Pathway

scholarly journals Sex Differences in the Metabolic Effects of Testosterone in Sheep

Endocrinology ◽  
2012 ◽  
Vol 153 (1) ◽  
pp. 123-131 ◽  
Author(s):  
Scott D. Clarke ◽  
Iain J. Clarke ◽  
Alexandra Rao ◽  
Michael A. Cowley ◽  
Belinda A. Henry
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Uncoupling Protein ◽  
Specific Effect ◽  
Metabolic Effects ◽  
Mrna Levels ◽  
Nonesterified Fatty Acids ◽  
Glucose Levels ◽  
Amp Activated Protein Kinase ◽  
The Brain

Adiposity is regulated in a sexually divergent manner. This is partly due to sex steroids, but the differential effects of androgens in males and females are unclear. We investigated effects of testosterone on energy balance in castrated male (n = 6) and female sheep (n = 4), which received 3 × 200 mg testosterone implants for 2 wk or blank implants (controls). Temperature probes were implanted into retroperitoneal fat and skeletal muscle. Blood samples were taken to measure metabolites and insulin. In males, muscle and fat biopsies were collected to measure uncoupling protein (UCP) mRNA and phosphorylation of AMP-activated protein kinase and Akt. Testosterone did not change food intake in either sex. Temperature in muscle was higher in males than females, and testosterone reduced heat production in males only. In fat, however, temperature was higher in the castrate males compared with females, and there was no effect of testosterone treatment in either sex. Preprandial glucose levels were lower, but nonesterified fatty acids were higher in females compared with males, irrespective of testosterone. In males, the onset of feeding increased UCP1 and UCP3 mRNA levels in skeletal muscle, without an effect of testosterone. During feeding, testosterone reduced glucose levels in males only but did not alter the phosphorylation of AMP-activated protein kinase or Akt in muscle. Thus, testosterone maintains lower muscle and fat temperatures in males but not females. The mechanism underlying this sex-specific effect of testosterone is unknown but may be due to sexual differentiation of the brain centers controlling energy expenditure.

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