scholarly journals The Potential Role of Glucose Transport Changes in Hot Flash Physiology: A Hypothesis

2008 ◽  
Vol 10 (3) ◽  
pp. 241-247 ◽  
Author(s):  
Sharon L. Dormire
Keyword(s):  
Potential Role ◽  
Glucose Transporter ◽  
Hot Flashes ◽  
Menopausal Woman ◽  
Hot Flash ◽  
Research Directions ◽  
Glucose Transporter 1 ◽  
Brain Glucose ◽  
New Research

Purpose: The purpose of this article is to detail a novel hypothesis regarding the role of changes in brain glucose delivery in menopausal hot flashes. Organizing Framework: The impaired glucose delivery hypothesis of menopausal hot flashes is presented as a potential model of hot flash physiology. As foundational to the hypothesis, brain glucose physiology, specifically neurobarrier coupling, is presented in detail. With brain activation, glucose needs immediate increase; additional glucose is supplied through increased production of glucose transporter 1 (GLUT1) at the blood—brain barrier (BBB) and through vasodilation. Estrogen is important to this system in stimulating production of GLUT1. As estrogen declines at menopause, upregulation of GLUT1 is less efficient. As a consequence, neurobarrier coupling overcompensates with an excess neurovascular response, or a hot flash. Research supporting this hypothesis is briefly reviewed and new questions raised are reviewed. Conclusions: The impaired glucose hypothesis of menopausal hot flashes proposes an inadequate neurobarrier response to neurometabolic stimulation as estrogen declines, resulting in additional neurometabolic stimulation with consequent neurovascular stimulation. In this model, the menopausal woman has diminished ability to respond to fluctuations in blood glucose over the course of the day, which results in hot flashes as a counter-regulatory response. This perspective accounts for observed physiological changes that have not been previously detailed. New research directions are identified.

MATERIAL HANDLING MACHINES AND SYSTEMS – UMI-TWINN PROJECT CONTRIBUTION

2019 ◽  
Vol 12 (1) ◽  
pp. 7-20
Author(s):  
Péter Telek ◽  
Béla Illés ◽  
Christian Landschützer ◽  
Fabian Schenk ◽  
Flavien Massi
Keyword(s):  
Material Handling ◽  
Digital Data ◽  
Flow Process ◽  
Research Directions ◽  
Scientific Excellence ◽  
Research Activities ◽  
New Research ◽  
Eu Project ◽  
The University

Nowadays, the Industry 4.0 concept affects every area of the industrial, economic, social and personal sectors. The most significant changings are the automation and the digitalization. This is also true for the material handling processes, where the handling systems use more and more automated machines; planning, operation and optimization of different logistic processes are based on many digital data collected from the material flow process. However, new methods and devices require new solutions which define new research directions. In this paper we describe the state of the art of the material handling researches and draw the role of the UMi-TWINN partner institutes in these fields. As a result of this H2020 EU project, scientific excellence of the University of Miskolc can be increased and new research activities will be started.

Abstract 112: A Pathological Role of Endothelial p53 in the Regulation of Endothelial Function and Glucose Metabolism

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Masataka YOKOYAMA ◽  
Yoshio KOBAYASHI ◽  
Tohru MINAMINO
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cell ◽  
Glucose Metabolism ◽  
Endothelial Function ◽  
Mitochondrial Biogenesis ◽  
Glucose Transporter ◽  
Diabetic Patients ◽  
Glucose Transporter 1 ◽  
P53 Activation

Cellular senescence is a state of irreversible growth arrest induced by various stresses such as oncogenic stimuli. This response is controlled by negative regulators of the cell cycle like the p53 tumor suppressor protein. Accumulating evidence has suggested a role of p53 activation in various age-associated conditions including atherosclerosis, heart failure and diabetes. Here we show that endothelial p53 activation plays a pathological role in the regulation of endothelial function and glucose metabolism under diabetic conditions. Endothelial expression of p53 was markedly up-regulated in a streptozotocin-induced diabetes model. Endothelial function such as acetylcholine-dependent vasodilatation was markedly impaired in this model. Although hyperglycemia was not altered, impairment of endothelial function was significantly improved in mice with endothelial cell-specific p53 deficiency. In same way, p53 was markedly activated in ischemic vessels, and endothelial p53 deficiency enhanced ischemia-induced angiogenesis. Mechanistically, endothelial p53 up-regulated the expression of PTEN that negatively regulated the Akt-eNOS pathway, and therefore disruption of p53 improved endothelial dysfunction. We also found that endothelial p53 was markedly activated, and the Akt-eNOS pathway was attenuated in a diet-induced obesity model. Disruption of endothelial p53 activation improved dietary inactivation of eNOS that up-regulated the expression of PGC-1α in skeletal muscle, thereby increasing mitochondrial biogenesis and oxygen consumption. Inhibition of endothelial p53 also improved dietary impairment of glucose transport into skeletal muscle by up-regulating endothelial expression of glucose transporter 1. Consequently, mice with endothelial cell-specific p53 deficiency fed a high-calorie diet showed improvement of insulin sensitivity and less fat accumulation compared with control littermates. These results indicate that endothelial p53 negatively regulates endothelium-dependent vasodilatation, ischemia-induced angiogenesis, and mitochondrial biogenesis by inhibiting the Akt-eNOS pathway and suggest that inhibition of endothelial p53 could be a novel therapeutic target in diabetic patients.

Topography of brain glucose hypometabolism and epileptic network in glucose transporter 1 deficiency

2015 ◽  
Vol 110 ◽  
pp. 206-215 ◽  
Author(s):  
Cigdem Inan Akman ◽  
Frank Provenzano ◽  
Dong Wang ◽  
Kristin Engelstad ◽  
Veronica Hinton ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Glucose Transporter 1 ◽  
Brain Glucose ◽  
Glucose Hypometabolism

Analyzing the response to epidemics: concept of evidence-based Haddon matrix

2017 ◽  
Vol 7 (3) ◽  
pp. 266-283 ◽  
Author(s):  
Azrah Anparasan ◽  
Miguel Lejeune
Keyword(s):  
Physical Environment ◽  
Evidence Based ◽  
Research Directions ◽  
Content Type ◽  
Humanitarian Organizations ◽  
The Matrix ◽  
New Research ◽  
Future Work ◽  
Haddon Matrix

Purpose The purpose of this paper is to propose a novel evidence-based Haddon matrix that identifies intervention options for organizations and governments responding to an epidemic in a developing economy. Design/methodology/approach A literature review of articles published within a year of the cholera outbreak in Haiti. Two separate types of literature sources are used – academic and non-academic – to apprehend the value and role of interventions implemented and/or identified. Findings The Haddon matrix helps break down the challenges involved in the containment of an epidemic into smaller, manageable components. This research shows that the matrix enables visualization of past evidence, help dissect various informational sources, and increase collaboration across humanitarian organizations. It will also serve as a building block for academics to identify new research directions to respond to epidemic outbreaks. Research limitations/implications The analysis focuses on the cholera epidemic in Haiti. Future work will be directed to generalize the identified recommendations and insights to a broader context. Originality/value This paper presents an evidence-based Haddon matrix that infers recommendations and insights based on past evidence for each phase (pre-event, response, and post-event) and factor (agent, host, physical environment, and socio-cultural environment) of an epidemic and for various stakeholders (humanitarian organizations, governments, and academics). The matrix provides a structured framework to identify interventions and best practices to address challenges during an epidemic outbreak.

scholarly journals Up-regulation of key glycolysis proteins in cancer development

2018 ◽  
Vol 13 (1) ◽  
pp. 569-581
Author(s):  
Nicole Nowak ◽  
Anna Kulma ◽  
Jan Gutowicz
Keyword(s):  
Cancer Cells ◽  
Glucose Transporter ◽  
Lactate Production ◽  
Cancer Development ◽  
Glucose Transporter 1 ◽  
Expression Of Genes ◽  
Glycolysis Pathway ◽  
Cancer Cell Survival ◽  
Glycolytic Rate

AbstractIn rapid proliferating cancer cells, there is a need for fast ATP and lactate production, therefore cancer cells turn off oxidative phosphorylation and turn on the so called "Warburg effect". This regulating the expression of genes involved in glycolysis. According to many studies, glucose transporter 1, which supplies glucose to the cell, is the most abundantly expressed transporter in cancer cells. Hexokinase 2, is one of four hexokinase isoenzymes, is also another highly expressed enzyme in cancer cells and it functions to enhance the glycolytic rate. The up-regulation of these two proteins has been established as an important factor in promoting development and metastasis in many types of cancer. Furthermore, other enzymes involved in glycolysis pathway such as phosphoglucose isomerase and glyceraldehyde 3-phosphate dehydrogenase, exhibit additional functions in promoting tumor growth in a non-glycolytic way. This review demonstrates the pivotal role of GLUT1, HK2, PGI and GAPDH in cancer development. In particular, we look at how the multifunctional proteins, PGI and GAPDH, affect cancer cell survival. We also present various clinical cancer cases in terms of the overexpression of selected proteins, which may be considered as a therapeutic target.

The role of molecular analysis of SLC2A1 in the diagnostic workup of glucose transporter 1 deficiency syndrome

2020 ◽  
Vol 416 ◽  
pp. 117041
Author(s):  
Satoru Takahashi ◽  
Ryosuke Tanaka ◽  
Ryo Takeguchi ◽  
Mami Kuroda ◽  
Yuichi Akaba ◽  
...  
Keyword(s):  
Molecular Analysis ◽  
Glucose Transporter ◽  
Deficiency Syndrome ◽  
Diagnostic Workup ◽  
Glucose Transporter 1
Sign in / Sign up

Export Citation Format

Share Document