Proline: Metabolic Sensing and Parametabolic Regulation

2014 ◽  
pp. 320-343 ◽  
Keyword(s):  
Metabolic Sensing

scholarly journals Nutrient and Metabolic Sensing in T Cell Responses

2017 ◽  
Vol 8 ◽  
Author(s):  
Jun Wei ◽  
Jana Raynor ◽  
Thanh-Long M. Nguyen ◽  
Hongbo Chi
Keyword(s):  
T Cell ◽  
T Cell Responses ◽  
Cell Responses ◽  
Metabolic Sensing

scholarly journals Electro-Metabolic Sensing Through Capillary ATP-Sensitive K+ Channels and Adenosine to Control Cerebral Blood Flow

2021 ◽  
Author(s):  
Maria Sancho ◽  
Nicholas R. Klug ◽  
Amreen Mughal ◽  
Thomas J. Heppner ◽  
David Hill-Eubanks ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Function ◽  
Brain Activity ◽  
List Type ◽  
Capillary Endothelial Cells ◽  
Metabolic Sensing ◽  
Cellular Components

SUMMARYThe dense network of capillaries composed of capillary endothelial cells (cECs) and pericytes lies in close proximity to all neurons, ideally positioning it to sense neuro/glial-derived compounds that regulate regional and global cerebral perfusion. The membrane potential (VM) of vascular cells serves as the essential output in this scenario, linking brain activity to vascular function. The ATP-sensitive K+ channel (KATP) is a key regulator of vascular VM in other beds, but whether brain capillaries possess functional KATP channels remains unknown. Here, we demonstrate that brain capillary ECs and pericytes express KATP channels that robustly control VM. We further show that the endogenous mediator adenosine acts through A2A receptors and the Gs/cAMP/PKA pathway to activate capillary KATP channels. Moreover, KATP channel stimulation in vivo causes vasodilation and increases cerebral blood flow (CBF). These findings establish the presence of KATP channels in cECs and pericytes and suggest their significant influence on CBF.HIGHLIGHTSCapillary network cellular components—endothelial cells and pericytes—possess functional KATP channels.Activation of KATP channels causes profound hyperpolarization of capillary cell membranes.Capillary KATP channels are activated by exogenous adenosine via A2A receptors and cAMP-dependent protein kinase.KATP channel activation by adenosine or synthetic openers increases cerebral blood flow.

Metabolic sensing and regulation by the hypothalamus

2008 ◽  
Vol 294 (5) ◽  
pp. E809-E809 ◽  
Author(s):  
Martin G. Myers
Keyword(s):  
Metabolic Sensing

scholarly journals Metabolic‐sensing of the skeletal muscle clock coordinates fuel oxidation

2020 ◽  
Vol 34 (5) ◽  
pp. 6613-6627 ◽  
Author(s):  
Hongshan Yin ◽  
Weini Li ◽  
Somik Chatterjee ◽  
Xuekai Xiong ◽  
Pradip Saha ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fuel Oxidation ◽  
Metabolic Sensing

scholarly journals Metabolic Sensing and the Brain: Who, What, Where, and How?

Endocrinology ◽  
2011 ◽  
Vol 152 (7) ◽  
pp. 2552-2557 ◽  
Author(s):  
Barry E. Levin ◽  
Christophe Magnan ◽  
Ambrose Dunn-Meynell ◽  
Christelle Le Foll
Keyword(s):  
Energy Homeostasis ◽  
Distributed Network ◽  
Metabolic Substrates ◽  
Hepatic Portal Vein ◽  
Metabolic Sensing ◽  
Hepatic Portal ◽  
And Function ◽  
The Brain ◽  
Local Brain ◽  
Brain Barriers

Unique subpopulations of specialized metabolic sensing neurons reside in a distributed network throughout the brain and respond to alterations in ambient levels of various metabolic substrates by altering their activity. Variations in local brain substrate levels reflect their transport across the blood- and cerebrospinal-brain barriers as well as local production by astrocytes. There are a number of mechanisms by which such metabolic sensing neurons alter their activity in response to changes in substrate levels, but it is clear that these neurons cannot be considered in isolation. They are heavily dependent on astrocyte and probably tanycyte metabolism and function but also respond to hormones (e.g. leptin and insulin) and cytokines that cross the blood-brain barrier from the periphery as well as hard-wired neural inputs from metabolic sensors in peripheral sites such as the hepatic portal vein, gastrointestinal tract, and carotid body. Thus, these specialized neurons are capable of monitoring and integrating multiple signals from the periphery as a means of regulating peripheral energy homeostasis.

Energy and metabolic sensing G protein–coupled receptors during lactation-induced changes in energy balance

2014 ◽  
Vol 48 ◽  
pp. 33-41 ◽  
Author(s):  
P. Friedrichs ◽  
B. Saremi ◽  
S. Winand ◽  
J. Rehage ◽  
S. Dänicke ◽  
...  
Keyword(s):  
Energy Balance ◽  
G Protein ◽  
G Protein Coupled Receptors ◽  
Metabolic Sensing ◽  
Induced Changes ◽  
G Protein Coupled

scholarly journals Progenitor-intrinsic Metabolic Sensing Promotes Hematopoietic Homeostasis

2021 ◽  
Author(s):  
Hannah A Pizzato ◽  
Yahui Wang ◽  
Michael Wolfgang ◽  
Brian Finck ◽  
Gary J Patti ◽  
...  
Keyword(s):  
Myeloid Cells ◽  
Cell Loss ◽  
Acid Oxidation ◽  
Hematopoietic Progenitors ◽  
Metabolic Switch ◽  
Genetic Ablation ◽  
Mitochondrial Pyruvate Carrier ◽  
Stem And Progenitor Cells ◽  
Metabolic Sensing ◽  
Extrinsic Feedback

Hematopoietic homeostasis is maintained by stem and progenitor cells in part by extrinsic feedback cues triggered by mature cell loss. We demonstrate a different mechanism by which hematopoietic progenitors intrinsically anticipate and prevent the loss of mature progeny through metabolic switches. We examined hematopoiesis in mice conditionally deficient in long-chain fatty acid oxidation (carnitine palmitoyltransferase 2, Cpt2), glutaminolysis (glutaminase, Gls), or mitochondrial pyruvate import (mitochondrial pyruvate carrier 2, Mpc2). While genetic ablation of Cpt2 or Gls minimally impacted most blood lineages, deletion of Mpc2 led to a sharp decline in mature myeloid cells. However, MPC2-deficient myeloid cells rapidly recovered due to a transient increase in myeloid progenitor proliferation. Competitive bone marrow chimera and stable isotope tracing experiments demonstrated that this proliferative burst was intrinsic to MPC2-deficient progenitors and accompanied by a metabolic switch to glutaminolysis. Thus, hematopoietic progenitors intrinsically adjust to metabolic perturbations independently of feedback from downstream mature cells to maintain homeostasis.

scholarly journals NQO1 binds and supports SIRT1 function

2017 ◽  
Author(s):  
Peter Tsvetkov ◽  
Julia Adler ◽  
Yaarit Adamovich ◽  
Gad Asher ◽  
Nina Reuven ◽  
...  
Keyword(s):  
Target Genes ◽  
Protective Role ◽  
Class Iii ◽  
Mitochondrial Stress ◽  
Protein Levels ◽  
Related Enzyme ◽  
Metabolic Sensing ◽  
Regulatory Loop ◽  
Nadh Oxidoreductase

AbstractSilent information regulator 2-related enzyme 1 (SIRT1) is an NAD+-dependent class III deacetylase and a key component of the cellular metabolic sensing pathway. The requirement of NAD+ for SIRT1 activity led us to assume that NQO1, an NADH oxidoreductase producing NAD+, regulates SIRT1 activity. We show here that SIRT1 is capable of increasing NQO1 (NAD(P)H Dehydrogenase Quinone 1) transcription and protein levels. NQO1 physically interacts with SIRT1 but not with an enzymatically dead SIRT1 H363Y mutant. The interaction of NQO1 with SIRT1 is markedly increased under mitochondrial inhibition. Interestingly, under this condition the nuclear pool of NQO1 is elevated. Depletion of NQO1 compromises the role of SIRT1 in inducing transcription of several target genes and eliminates the protective role of SIRT1 following mitochondrial inhibition. Our results suggest that SIRT1 and NQO1 form a regulatory loop where SIRT1 regulates NQO1 expression and NQO1 binds and mediates the protective role of SIRT1 during mitochondrial stress. The interplay between an NADH oxidoreductase enzyme and an NAD+ dependent deacetylase may act as a rheostat in sensing mitochondrial stress.

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