scholarly journals AMP-Activated Protein Kinase (AMPK) and Energy-Sensing in the Brain

2012 ◽  
Vol 21 (2) ◽  
pp. 52-60 ◽  
Author(s):  
Santosh Ramamurthy ◽  
Gabriele Ronnett
Keyword(s):  
Protein Kinase ◽  
Energy Sensing ◽  
Amp Activated Protein Kinase ◽  
The Brain

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.

scholarly journals Phosphorylation of ULK1 (hATG1) by AMP-Activated Protein Kinase Connects Energy Sensing to Mitophagy

Science ◽  
2010 ◽  
Vol 331 (6016) ◽  
pp. 456-461 ◽  
Author(s):  
D. F. Egan ◽  
D. B. Shackelford ◽  
M. M. Mihaylova ◽  
S. Gelino ◽  
R. A. Kohnz ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Energy Sensing ◽  
Amp Activated Protein Kinase

AMP-activated protein kinase in the brain

2008 ◽  
Vol 32 (S4) ◽  
pp. S42-S48 ◽  
Author(s):  
G V Ronnett ◽  
S Aja
Keyword(s):  
Protein Kinase ◽  
Amp Activated Protein Kinase ◽  
The Brain

scholarly journals Effects of AMP-Activated Protein Kinase in Cerebral Ischemia

2009 ◽  
Vol 30 (3) ◽  
pp. 480-492 ◽  
Author(s):  
Jun Li ◽  
Louise D McCullough
Keyword(s):  
Protein Kinase ◽  
In Vivo Studies ◽  
Ampk Activation ◽  
Vigorous Exercise ◽  
Nitric Oxide Signaling ◽  
Reductase Inhibitors ◽  
Amp Activated Protein Kinase ◽  
The Brain

AMP-activated protein kinase (AMPK) is a serine threonine kinase that is highly conserved through evolution. AMPK is found in most mammalian tissues including the brain. As a key metabolic and stress sensor/effector, AMPK is activated under conditions of nutrient deprivation, vigorous exercise, or heat shock. However, it is becoming increasingly recognized that changes in AMPK activation not only signal unmet metabolic needs, but also are involved in sensing and responding to ‘cell stress’, including ischemia. The downstream effect of AMPK activation is dependent on many factors, including the severity of the stressor as well as the tissue examined. This review discusses recent in vitro and in vivo studies performed in the brain/neuronal cells and vasculature that have contributed to our understanding of AMPK in stroke. Recent data on the potential role of AMPK in angiogenesis and neurogenesis and the interaction of AMPK with 3-hydroxy-3-methy-glutaryl-CoA reductase inhibitors (statins) agents are highlighted. The interaction between AMPK and nitric oxide signaling is also discussed.

scholarly journals Neuronal AMPK coordinates mitochondrial energy sensing and hypoxia resistance

2020 ◽  
Author(s):  
Brandon J. Berry ◽  
Aksana Baldzizhar ◽  
Andrew P. Wojtovich
Keyword(s):  
Protein Kinase ◽  
Mitochondrial Function ◽  
Stress Resistance ◽  
Atp Synthesis ◽  
Protonmotive Force ◽  
Electrochemical Gradient ◽  
Energy Sensing ◽  
Amp Activated Protein Kinase ◽  
Spatiotemporal Control

ABSTRACTOrganisms adapt to their environment through coordinated changes in mitochondrial function and metabolism. The mitochondrial protonmotive force (PMF) is an electrochemical gradient that powers ATP synthesis and adjusts metabolism to energetic demands via cellular signaling. It is unknown how or where transient PMF changes are sensed and signaled due to lack of precise spatiotemporal control in vivo. We addressed this by expressing a light-activated proton pump in mitochondria to spatiotemporally “turn off” mitochondrial function through PMF dissipation in tissues with light. We applied our construct – mitochondria-OFF (mtOFF) – to understand how metabolic status impacts hypoxia resistance, a response that relies on mitochondrial function. mtOFF activation induced starvation-like behavior mediated by AMP-activated protein kinase (AMPK). We found prophylactic mtOFF activation increased survival following hypoxia, and that protection relied on neuronal AMPK. Our study links spatiotemporal control of mitochondrial PMF to cellular metabolic changes that mediate behavior and stress resistance.

scholarly journals LKB1 Is Physiologically Required for Sleep from Drosophila to the Mouse

2021 ◽  
Author(s):  
Ziyi Liu ◽  
Lifen Jiang ◽  
Chaoyi Li ◽  
Chengang Li ◽  
Jingqun Yang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Physiological Role ◽  
Adenosine Monophosphate ◽  
Nrem Sleep ◽  
Eeg Analysis ◽  
Loss Of Function ◽  
Sleep Regulation ◽  
Amp Activated Protein Kinase ◽  
The Brain ◽  
Mediated Reduction

LKB1 is known as a master kinase for 14 kinases related to the adenosine monophosphate (AMP)-activated protein kinase (AMPK). Two of them (SIK3 and AMPKa;) have previously been implicated in sleep regulation. We generated loss-of-function (LOF) mutants for Lkb1 in both Drosophila and mice. Sleep was reduced in Lkb1-mutant flies and in flies with neuronal deletion of Lkb1. Sleep was reduced in mice after virally mediated reduction of Lkb1 in the brain. Electroencephalography (EEG) analysis showed that non-rapid eye movement (NREM) sleep and sleep need were both reduced in Lkb1-mutant mice. These results indicate that LKB1 plays a physiological role in sleep regulation conserved from flies to mice.

scholarly journals StimulatingS-adenosyl-l-methionine synthesis extends lifespan via activation of AMPK

2016 ◽  
Vol 113 (42) ◽  
pp. 11913-11918 ◽  
Author(s):  
Takafumi Ogawa ◽  
Ryohei Tsubakiyama ◽  
Muneyoshi Kanai ◽  
Tetsuya Koyama ◽  
Tsutomu Fujii ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Protein Kinase ◽  
Cell Survival ◽  
Metabolic Effects ◽  
Model Organisms ◽  
Lifespan Extension ◽  
Beneficial Effects ◽  
Energy Sensing ◽  
Amp Activated Protein Kinase ◽  
Methionine Synthesis

Dietary restriction (DR), such as calorie restriction (CR) or methionine (Met) restriction, extends the lifespan of diverse model organisms. Although studies have identified several metabolites that contribute to the beneficial effects of DR, the molecular mechanism underlying the key metabolites responsible for DR regimens is not fully understood. Here we show that stimulatingS-adenosyl-l-methionine (AdoMet) synthesis extended the lifespan of the budding yeastSaccharomyces cerevisiae. The AdoMet synthesis-mediated beneficial metabolic effects, which resulted from consuming both Met and ATP, mimicked CR. Indeed, stimulating AdoMet synthesis activated the universal energy-sensing regulator Snf1, which is theS. cerevisiaeortholog of AMP-activated protein kinase (AMPK), resulting in lifespan extension. Furthermore, our findings revealed thatS-adenosyl-l-homocysteine contributed to longevity with a higher accumulation of AdoMet only under the severe CR (0.05% glucose) conditions. Thus, our data uncovered molecular links between Met metabolites and lifespan, suggesting a unique function of AdoMet as a reservoir of Met and ATP for cell survival.

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