Perspectives on Leptin�s Role as a Metabolic Signal for the Onset of Puberty

1999 ◽  
pp. 87-105 ◽  
Author(s):  
C.C. Cheung ◽  
D.K. Clifton ◽  
R.A. Steiner
Keyword(s):  
Metabolic Signal

scholarly journals Subfornical organ neurons integrate cardiovascular and metabolic signals

2017 ◽  
Vol 312 (2) ◽  
pp. R253-R262 ◽  
Author(s):  
Nicole M. Cancelliere ◽  
Alastair V. Ferguson
Keyword(s):  
Patch Clamp ◽  
Subfornical Organ ◽  
Ang Ii ◽  
Metabolic Homeostasis ◽  
Circumventricular Organ ◽  
Autonomic Functions ◽  
Bath Application ◽  
Metabolic Signal ◽  
Metabolic Hormone

The subfornical organ (SFO) is a critical circumventricular organ involved in the control of cardiovascular and metabolic homeostasis. Despite the plethora of circulating signals continuously sensed by the SFO, studies investigating how these signals are integrated are lacking. In this study, we use patch-clamp techniques to investigate how the traditionally classified “cardiovascular” hormone ANG II, “metabolic” hormone CCK and “metabolic” signal glucose interact and are integrated in the SFO. Sequential bath application of CCK (10 nM) and ANG (10 nM) onto dissociated SFO neurons revealed that 63% of responsive SFO neurons depolarized to both CCK and ANG; 25% depolarized to ANG only; and 12% hyperpolarized to CCK only. We next investigated the effects of glucose by incubating and recording neurons in either hypoglycemic, normoglycemic, or hyperglycemic conditions and comparing the proportions of responses to ANG ( n = 55) or CCK ( n = 83) application in each condition. A hyperglycemic environment was associated with a larger proportion of depolarizing responses to ANG ( χ2, P < 0.05), and a smaller proportion of depolarizing responses along with a larger proportion of hyperpolarizing responses to CCK ( χ2, P < 0.01). Our data demonstrate that SFO neurons excited by CCK are also excited by ANG and that glucose environment affects the responsiveness of neurons to both of these hormones, highlighting the ability of SFO neurons to integrate multiple metabolic and cardiovascular signals. These findings have important implications for this structure’s role in the control of various autonomic functions during hyperglycemia.

scholarly journals Understanding the role of gut microbiome–host metabolic signal disruption in health and disease

2011 ◽  
Vol 19 (7) ◽  
pp. 349-359 ◽  
Author(s):  
Elaine Holmes ◽  
Jia V. Li ◽  
Thanos Athanasiou ◽  
Hutan Ashrafian ◽  
Jeremy K. Nicholson
Keyword(s):  
Gut Microbiome ◽  
Health And Disease ◽  
Metabolic Signal

scholarly journals AMPK: A Critical Metabolic Signal

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Laurie J. Goodyear ◽  
Ho‐Jin Koh ◽  
Nobuharu Fujii ◽  
Taro Toyoda ◽  
Carol A. Witczak ◽  
...  
Keyword(s):  
Metabolic Signal

Fructose 2,6-bisphosphate is essential for glucose-regulated gene transcription of glucose-6-phosphatase and other ChREBP target genes in hepatocytes

2012 ◽  
Vol 443 (1) ◽  
pp. 111-123 ◽  
Author(s):  
Catherine Arden ◽  
Susan J. Tudhope ◽  
John L. Petrie ◽  
Ziad H. Al-Oanzi ◽  
Kirsty S. Cullen ◽  
...  
Keyword(s):  
Essential Role ◽  
Target Genes ◽  
Covalent Modification ◽  
Bifunctional Enzyme ◽  
Selective Depletion ◽  
Genes Encoding ◽  
Element Binding Protein ◽  
Metabolic Signal ◽  
Allosteric Mechanisms ◽  
Active Variant

Glucose metabolism in the liver activates the transcription of various genes encoding enzymes of glycolysis and lipogenesis and also G6pc (glucose-6-phosphatase). Allosteric mechanisms involving glucose 6-phosphate or xylulose 5-phosphate and covalent modification of ChREBP (carbohydrate-response element-binding protein) have been implicated in this mechanism. However, evidence supporting an essential role for a specific metabolite or pathway in hepatocytes remains equivocal. By using diverse substrates and inhibitors and a kinase-deficient bisphosphatase-active variant of the bifunctional enzyme PFK2/FBP2 (6-phosphofructo-2-kinase–fructose-2,6-bisphosphatase), we demonstrate an essential role for fructose 2,6-bisphosphate in the induction of G6pc and other ChREBP target genes by glucose. Selective depletion of fructose 2,6-bisphosphate inhibits glucose-induced recruitment of ChREBP to the G6pc promoter and also induction of G6pc by xylitol and gluconeogenic precursors. The requirement for fructose 2,6-bisphosphate for ChREBP recruitment to the promoter does not exclude the involvement of additional metabolites acting either co-ordinately or at downstream sites. Glucose raises fructose 2,6-bisphosphate levels in hepatocytes by reversing the phosphorylation of PFK2/FBP2 at Ser32, but also independently of Ser32 dephosphorylation. This supports a role for the bifunctional enzyme as the phosphometabolite sensor and for its product, fructose 2,6-bisphosphate, as the metabolic signal for substrate-regulated ChREBP-mediated expression of G6pc and other ChREBP target genes.

Brain glucose-sensing mechanisms: ubiquitous silencing by aglycemia vs. hypothalamic neuroendocrine responses

2001 ◽  
Vol 281 (4) ◽  
pp. E649-E654 ◽  
Author(s):  
Charles V. Mobbs ◽  
Lee-Ming Kow ◽  
Xue-Jun Yang
Keyword(s):  
Glucose Concentration ◽  
Glucose Sensing ◽  
Hypothalamic Neurons ◽  
Brain Glucose ◽  
Malonyl Coa ◽  
Extracellular Glucose Concentration ◽  
Extracellular Glucose ◽  
Neuroendocrine Responses ◽  
Metabolic Signal

Interest in brain glucose-sensing mechanisms is motivated by two distinct neuronal responses to changes in glucose concentrations. One mechanism is global and ubiquitous in response to profound hypoglycemia, whereas the other mechanism is largely confined to specific hypothalamic neurons that respond to changes in glucose concentrations in the physiological range. Although both mechanisms use intracellular metabolism as an indicator of extracellular glucose concentration, the two mechanisms differ in key respects. Global hyperpolarization (inhibition) in response to 0 mM glucose can be reversed by pyruvate, implying that the reduction in ATP levels acting through ATP-dependent potassium (K-ATP) channels is the key metabolic signal for the global silencing in response to 0 mM glucose. In contrast, neuroendocrine hypothalamic responses in glucoresponsive and glucose-sensitive neurons (either excitation or inhibition, respectively) to physiological changes in glucose concentration appear to depend on glucokinase; neuroendocrine responses also depend on K-ATP channels, although the role of ATP itself is less clear. Lactate can substitute for glucose to produce these neuroendocrine effects, but pyruvate cannot, implying that NADH (possibly leading to anaplerotic production of malonyl-CoA) is a key metabolic signal for effects of glucose on glucoresponsive and glucose-sensitive hypothalamic neurons.

scholarly journals Nitric oxide as a developmental and metabolic signal in filamentous fungi

2020 ◽  
Vol 113 (5) ◽  
pp. 872-882 ◽  
Author(s):  
Yanxia Zhao ◽  
Jieyin Lim ◽  
Jianyang Xu ◽  
Jae‐Hyuk Yu ◽  
Weifa Zheng
Keyword(s):  
Nitric Oxide ◽  
Filamentous Fungi ◽  
Metabolic Signal

scholarly journals Lipoexpediency: de novo lipogenesis as a metabolic signal transmitter

2011 ◽  
Vol 22 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Irfan J. Lodhi ◽  
Xiaochao Wei ◽  
Clay F. Semenkovich
Keyword(s):  
De Novo ◽  
De Novo Lipogenesis ◽  
Metabolic Signal

Variation in hydrogen stable isotopes in cellulose and n-alkanes: phylogenetic signal and related traits

2020 ◽  
Author(s):  
Jochem Baan ◽  
Meisha Holloway-Phillips ◽  
Ansgar Kahmen
Keyword(s):  
Organic Compounds ◽  
Plant Traits ◽  
Phylogenetic Signal ◽  
Isotope Analysis ◽  
Botanical Garden ◽  
Leaf Water ◽  
Physiological Traits ◽  
Large Set ◽  
Metabolic Signal ◽  
Species Specific

&lt;p&gt;Hydrogen (H) stable isotope analysis of specific plant organic compounds has become of interest as a tool for ecological, environmental and palaeoclimatological studies. Aside from the influence of leaf water evaporative enrichment on the &amp;#948;&lt;sup&gt;2&lt;/sup&gt;H composition of organic compounds, hydrogen isotope fractionation occurs during carbon metabolism in the plant (&amp;#949;&lt;sub&gt;bio&lt;/sub&gt;). To get a better understanding of the metabolic signal recorded in &amp;#949;&lt;sub&gt;bio&lt;/sub&gt;, we explored the variation of &amp;#948;&lt;sup&gt;2&lt;/sup&gt;H in cellulose and n-alkanes, and its relationship with phylogeny and other plant traits. Leaf material of a large set of species in the eudicot clade was collected in the botanical garden at the University of Basel, cellulose and n-alkanes were extracted, &amp;#948;&lt;sup&gt;2&lt;/sup&gt;H in both compounds and &amp;#948;&lt;sup&gt;18&lt;/sup&gt;O in cellulose were analysed. It was found that modelled leaf water differences only explain part of the observed variation of &amp;#948;&lt;sup&gt;2&lt;/sup&gt;H in organic compounds. &amp;#948;&lt;sup&gt;2&lt;/sup&gt;H appears to be related to phylogeny and a wider assessment of trait data is currently being undertaken to test for signal associations with physiological traits. This study helps address at which taxonomic level the variation of &amp;#948;&lt;sup&gt;2&lt;/sup&gt;H is found; illuminate plant physiological traits that can be responsible for shaping species specific &amp;#948;&lt;sup&gt;2&lt;/sup&gt;H values in organic compounds; as well as, provide novel insights into the &amp;#948;&lt;sup&gt;2&lt;/sup&gt;H covariation between cellulose and n-alkanes.&lt;/p&gt;

The NADH oxidizing system of the plasma membrane and metabolic signal control

PROTOPLASMA ◽  
1995 ◽  
Vol 184 (1-4) ◽  
pp. 158-162 ◽  
Author(s):  
H. L�w ◽  
F. L. Crane
Keyword(s):  
Plasma Membrane ◽  
Signal Control ◽  
Metabolic Signal
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