Institution
Fraternal Order of Eagles
Education•Grove City, Ohio, United States•
About: Fraternal Order of Eagles is a education organization based out in Grove City, Ohio, United States. It is known for research contribution in the topics: Skeletal muscle & Insulin. The organization has 178 authors who have published 199 publications receiving 4134 citations. The organization is also known as: F.O.E. & Aeries Lodge.
Topics: Skeletal muscle, Insulin, Insulin resistance, Adipose tissue, Autophagy
Papers
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TL;DR: Reduced BBB GLUT1 expression worsens Alzheimer's disease cerebrovascular degeneration, neuropathology and cognitive function, suggesting thatGLUT1 may represent a therapeutic target for Alzheimer's Disease vasculo-neuronal dysfunction and degeneration.
Abstract: The glucose transporter GLUT1 at the blood-brain barrier (BBB) mediates glucose transport into the brain. Alzheimer's disease is characterized by early reductions in glucose transport associated with diminished GLUT1 expression at the BBB. Whether GLUT1 reduction influences disease pathogenesis remains, however, elusive. Here we show that GLUT1 deficiency in mice overexpressing amyloid β-peptide (Aβ) precursor protein leads to early cerebral microvascular degeneration, blood flow reductions and dysregulation and BBB breakdown, and to accelerated amyloid β-peptide (Aβ) pathology, reduced Aβ clearance, diminished neuronal activity, behavioral deficits, and progressive neuronal loss and neurodegeneration that develop after initial cerebrovascular degenerative changes. We also show that GLUT1 deficiency in endothelium, but not in astrocytes, initiates the vascular phenotype as shown by BBB breakdown. Thus, reduced BBB GLUT1 expression worsens Alzheimer's disease cerebrovascular degeneration, neuropathology and cognitive function, suggesting that GLUT1 may represent a therapeutic target for Alzheimer's disease vasculo-neuronal dysfunction and degeneration.
447 citations
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TL;DR: It is shown that acute treadmill running in mice causes mitochondrial oxidative stress at 3–12 h and mitophagy at 6’h post-exercise in skeletal muscle and that Ulk1 activation is dependent on Ampk, and that exercise-induced metabolic adaptation requiresUlk1.
Abstract: Mitochondrial health is critical for skeletal muscle function and is improved by exercise training through both mitochondrial biogenesis and removal of damaged/dysfunctional mitochondria via mitophagy. The mechanisms underlying exercise-induced mitophagy have not been fully elucidated. Here, we show that acute treadmill running in mice causes mitochondrial oxidative stress at 3–12 h and mitophagy at 6 h post-exercise in skeletal muscle. These changes were monitored using a novel fluorescent reporter gene, pMitoTimer, that allows assessment of mitochondrial oxidative stress and mitophagy in vivo, and were preceded by increased phosphorylation of AMP activated protein kinase (Ampk) at tyrosine 172 and of unc-51 like autophagy activating kinase 1 (Ulk1) at serine 555. Using mice expressing dominant negative and constitutively active Ampk in skeletal muscle, we demonstrate that Ulk1 activation is dependent on Ampk. Furthermore, exercise-induced metabolic adaptation requires Ulk1. These findings provide direct evidence of exercise-induced mitophagy and demonstrate the importance of Ampk-Ulk1 signaling in skeletal muscle.
297 citations
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TL;DR: The molecular mechanisms underpinning resistance to leptin and ghrelin are discussed and how they can be exploited as targets for pharmacological management of obesity are discussed.
Abstract: Obesity, a major risk factor for the development of diabetes mellitus, cardiovascular diseases and certain types of cancer, arises from a chronic positive energy balance that is often due to unlimited access to food and an increasingly sedentary lifestyle on the background of a genetic and epigenetic vulnerability. Our understanding of the humoral and neuronal systems that mediate the control of energy homeostasis has improved dramatically in the past few decades. However, our ability to develop effective strategies to slow the current epidemic of obesity has been hampered, largely owing to the limited knowledge of the mechanisms underlying resistance to the action of metabolic hormones such as leptin and ghrelin. The development of resistance to leptin and ghrelin, hormones that are crucial for the neuroendocrine control of energy homeostasis, is a hallmark of obesity. Intensive research over the past several years has yielded tremendous progress in our understanding of the cellular pathways that disrupt the action of leptin and ghrelin. In this Review, we discuss the molecular mechanisms underpinning resistance to leptin and ghrelin and how they can be exploited as targets for pharmacological management of obesity.
277 citations
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TL;DR: Intravascular infusion is the most popular route for therapeutic multipotent mesenchymal stromal/stem cell (MSC) delivery in hundreds of clinical trials and suitable strategies for assessing and controlling hemocompatibility and optimized cell delivery are crucial for the development of safer and more effective MSC therapies.
260 citations
Authors
Showing all 181 results
Name | H-index | Papers | Citations |
---|---|---|---|
John F. Engelhardt | 88 | 340 | 26574 |
E. Dale Abel | 82 | 264 | 24402 |
Curt D. Sigmund | 74 | 318 | 16689 |
Wei Bao | 59 | 306 | 15466 |
Eric B. Taylor | 58 | 206 | 13760 |
Kamal Rahmouni | 55 | 177 | 12209 |
Kaikobad Irani | 51 | 115 | 12083 |
Mark A. Yorek | 49 | 174 | 15502 |
Christopher M. Adams | 47 | 126 | 12123 |
Long-Sheng Song | 47 | 123 | 10879 |
Sue C. Bodine | 39 | 103 | 12105 |
Kimberly K. Leslie | 39 | 181 | 4821 |
Aloysius J. Klingelhutz | 38 | 96 | 7104 |
Brandon S.J. Davies | 37 | 57 | 3335 |
Brian T. O’Neill | 37 | 157 | 5132 |