Relevant bibliographies by topics / Energy and glucose homeostasis

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Energy and glucose homeostasis'

Author: Grafiati
Published: 28 September 2024

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Journal articles on the topic "Energy and glucose homeostasis"

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Lam, Carol K. L., Madhu Chari, and Tony K. T. Lam. "CNS Regulation of Glucose Homeostasis." Physiology 24, no. 3 (June 2009): 159–70. http://dx.doi.org/10.1152/physiol.00003.2009.

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The past decade has hosted a remarkable surge in research dedicated to the central control of homeostatic mechanisms. Evidence indicates that the brain, in particular the hypothalamus, directly senses hormones and nutrients to initiate behavioral and metabolic responses to control energy and nutrient homeostasis. Diabetes is chiefly characterized by hyperglycemia due to impaired glucose homeostatic regulation, and a primary therapeutic goal is to lower plasma glucose levels. As such, in this review, we highlight the role of the hypothalamus in the regulation of glucose homeostasis in particular and discuss the cellular and molecular mechanisms by which this neural pathway is orchestrated.
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Pattaranit, Ratchada, and Hugo Antonius van den Berg. "Mathematical models of energy homeostasis." Journal of The Royal Society Interface 5, no. 27 (July 8, 2008): 1119–35. http://dx.doi.org/10.1098/rsif.2008.0216.

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Diabetes and obesity present a mounting global challenge. Clinicians are increasingly turning to mechanism-based mathematical models for a quantitative definition of physiological defects such as insulin resistance, glucose intolerance and elevated obesity set points, and for predictions of the likely outcomes of therapeutic interventions. However, a very large range of such models is available, making a judicious choice difficult. To better inform this choice, here we present the most important models published to date in a uniform format, discussing similarities and differences in terms of the decisions faced by modellers. We review models for glucostasis, based on the glucose–insulin feedback control loop, and consider extensions to long-term energy balance, dislipidaemia and obesity.
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Marty, Nell, Michel Dallaporta, and Bernard Thorens. "Brain Glucose Sensing, Counterregulation, and Energy Homeostasis." Physiology 22, no. 4 (August 2007): 241–51. http://dx.doi.org/10.1152/physiol.00010.2007.

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Neuronal circuits in the central nervous system play a critical role in orchestrating the control of glucose and energy homeostasis. Glucose, beside being a nutrient, is also a signal detected by several glucose-sensing units that are located at different anatomical sites and converge to the hypothalamus to cooperate with leptin and insulin in controlling the melanocortin pathway.
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López-Gambero, A. J., F. Martínez, K. Salazar, M. Cifuentes, and F. Nualart. "Brain Glucose-Sensing Mechanism and Energy Homeostasis." Molecular Neurobiology 56, no. 2 (May 24, 2018): 769–96. http://dx.doi.org/10.1007/s12035-018-1099-4.

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Soty, Maud, Amandine Gautier-Stein, Fabienne Rajas, and Gilles Mithieux. "Gut-Brain Glucose Signaling in Energy Homeostasis." Cell Metabolism 25, no. 6 (June 2017): 1231–42. http://dx.doi.org/10.1016/j.cmet.2017.04.032.

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Wang, Yan, Markey C. McNutt, Serena Banfi, Michael G. Levin, William L. Holland, Viktoria Gusarova, Jesper Gromada, Jonathan C. Cohen, and Helen H. Hobbs. "Hepatic ANGPTL3 regulates adipose tissue energy homeostasis." Proceedings of the National Academy of Sciences 112, no. 37 (August 24, 2015): 11630–35. http://dx.doi.org/10.1073/pnas.1515374112.

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Angiopoietin-like protein 3 (ANGPTL3) is a circulating inhibitor of lipoprotein and endothelial lipase whose physiological function has remained obscure. Here we show that ANGPTL3 plays a major role in promoting uptake of circulating very low density lipoprotein-triglycerides (VLDL-TGs) into white adipose tissue (WAT) rather than oxidative tissues (skeletal muscle, heart brown adipose tissue) in the fed state. This conclusion emerged from studies of Angptl3−/− mice. Whereas feeding increased VLDL-TG uptake into WAT eightfold in wild-type mice, no increase occurred in fed Angptl3−/− animals. Despite the reduction in delivery to and retention of TG in WAT, fat mass was largely preserved by a compensatory increase in de novo lipogenesis in Angptl3−/− mice. Glucose uptake into WAT was increased 10-fold in KO mice, and tracer studies revealed increased conversion of glucose to fatty acids in WAT but not liver. It is likely that the increased uptake of glucose into WAT explains the increased insulin sensitivity associated with inactivation of ANGPTL3. The beneficial effects of ANGPTL3 deficiency on both glucose and lipoprotein metabolism make it an attractive therapeutic target.
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Seo, J., E. S. Fortuno, J. M. Suh, D. Stenesen, W. Tang, E. J. Parks, C. M. Adams, T. Townes, and J. M. Graff. "Atf4 Regulates Obesity, Glucose Homeostasis, and Energy Expenditure." Diabetes 58, no. 11 (August 18, 2009): 2565–73. http://dx.doi.org/10.2337/db09-0335.

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Giridharan, NV. "Glucose & energy homeostasis: Lessons from animal studies." Indian Journal of Medical Research 148, no. 5 (2018): 659. http://dx.doi.org/10.4103/ijmr.ijmr_1737_18.

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Pepino, Marta Y., and Christina Bourne. "Non-nutritive sweeteners, energy balance, and glucose homeostasis." Current Opinion in Clinical Nutrition and Metabolic Care 14, no. 4 (July 2011): 391–95. http://dx.doi.org/10.1097/mco.0b013e3283468e7e.

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van Praag, H., M. Fleshner, M. W. Schwartz, and M. P. Mattson. "Exercise, Energy Intake, Glucose Homeostasis, and the Brain." Journal of Neuroscience 34, no. 46 (November 12, 2014): 15139–49. http://dx.doi.org/10.1523/jneurosci.2814-14.2014.

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Dissertations / Theses on the topic "Energy and glucose homeostasis"

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Forsyth, Robert J. "The contribution of astrocyte glycogen to brain energy homeostasis." Thesis, University of Newcastle Upon Tyne, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361387.

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Burke, Luke Kennedy. "Neurocircuitry underlying serotonin's effects on energy and glucose homeostasis." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708592.

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Matthäus, Dörte. "The role of CADM1 in energy and glucose homeostasis." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2014. http://dx.doi.org/10.18452/16905.

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Mehr als 300 Millionen Menschen sind weltweit von Diabetes betroffen, die Mehrheit davon leidet an Typ-2-Diabetes. Typ-2-Diabetes ist durch eine Insulinresistenz charakterisiert, welche meistens durch Übergewicht und Adipositas verursacht wird. Diese Insulinresistenz kann zunächst durch eine erhöhte pankreatische Insulinsekretion kompensiert werden, jedoch können langfristig die pankreatischen beta-Zellen den erhöhten Insulinbedarf nicht mehr decken. Dies verursacht einen starken Anstieg der Blutglucosespiegel und stellt den Beginn der Typ-2-Diabetes Erkrankung dar. Neben genetischen Veränderungen sind Umweltfaktoren, wie erhöhte Nahrungsaufnahme und reduzierte Bewegung, wichtige Faktoren in der Pathogenese des Typ-2-Diabetes. Frühere Forschungsergebnisse zeigten eine wichtige Rolle von microRNA 375 (miR-375) im Wachstum und in der Funktion der Insulin produzierenden beta-Zellen. Die Genexpression von miR-375 ist in diabetischen Nagetieren und Menschen verändert, was auf eine wichtige Rolle dieser microRNA in der Pathogenese des Typ-2-Diabetes hindeutet. Gene, die durch miR-375 reguliert werden, wurden in den pankreatischen beta-Zellen beschrieben, jedoch ist der Mechanismus wie miR-375 das Wachstum und die Funktion der pankreatischen beta-Zellen beeinflusst noch nicht im Detail verstanden. Das Cell Adhesion Molecule 1 (CADM1) ist ein bekanntes Zielgen der miR-375 und vor allem im Gehirn als Regulator von Anzahl und Funktion der Synapsen bekannt. Da es außerdem in den pankreatischen beta Zellen exprimiert ist, könnte es auch dort an der Regulation von beta-Zellwachstum und –funktion beteiligt sein und die Glucose- und Energiehomöostase verändern. Ziel dieser Arbeit war es, in vollständig oder konditionell Cadm1-defizienten Mäusen den Einfluss von CADM1 in pankreatischen beta-Zellen und neuronalem Gewebe an der Regulation von Glucose- und Energiehomöostase zu untersuchen.
More than 300 million people world-wide are affected by diabetes, the majority suffering from type 2 diabetes. Type 2 diabetes is characterized by insulin resistance, usually caused by obesity and overweight. Enhanced pancreatic insulin secretion largely compensates insulin resistance for years. A failure of pancreatic beta-cells to meet increased insulin demands drastically increases blood glucose levels and marks the onset of type 2 diabetes. Besides environmental influences, mainly elevated food intake and reduced physical activity, also genetic mutations are important factors in the pathophysiology of type 2 diabetes. Recent literature highlights the role of microRNA 375 (miR-375) in the growth and function of pancreatic insulin-producing beta-cells. MiR-375 gene expression is regulated in diabetic humans and rodents, suggesting that this microRNA is involved in the pathogenesis of type 2 diabetes. Genes regulated by miR-375 have been described in pancreatic beta-cells. Nevertheless, the exact mechanisms how miR-375 regulates beta-cell growth and insulin secretion have not been understood. Cell adhesion molecule 1 (CADM1) is a known target of miR-375 and has mainly been described as regulator of synapse number and synaptic function in the brain. CADM1 is also expressed in pancreatic beta-cells and might regulate beta-cell growth and function and might be involved in the control of glucose and energy homeostasis. The aim of this work was to investigate whether CADM1 in pancreatic beta-cells or neuronal tissue contributes to the regulation of energy and glucose homeostasis by using total and conditional Cadm1 deficient mice. Total Cadm1 deficient (Cadm1KO) mice showed increased sensitivity to glucose and insulin as well as enhanced glucose-stimulated insulin secretion compared to littermate control mice. Elevated glucose-stimulated insulin secretion after Cadm1 depletion could be confirmed in an in vitro beta-cell model.
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Wang, Xun. "IRF3 is a Critical Regulator of Adipose Glucose and Energy Homeostasis." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10537.

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Obesity is associated with a state of chronic inflammation, which is believed to contribute to insulin resistance. We previously identified interferon regulatory factor 3 (IRF3) as an anti-adipogenic transcription factor with high expression in adipocytes. Because IRF3 is known to drive expression of pro-inflammatory genes in immune cells, we hypothesized that it may also promote inflammation and insulin resistance in adipocytes. Consistent with our expectations, we found that the expression of inflammatory genes in adipocytes was induced by IRF3 overexpression, while knockdown of IRF3 had the opposite effect. Despite this effect on local adipocyte gene expression, we found that \(Irf3^{-/-}\) mice did not show evidence of altered systemic inflammation. Nonetheless, \(Irf3^{-/-}\) mice did display altered metabolism relative to their wild type (WT) littermates. For example, high fat diet (HFD) fed \(Irf3^{-/-}\) mice exhibited increased lean mass and decreased fat mass compared to WT, accompanied by increased food intake and energy expenditure. Further investigation showed that the white adipose tissue (WAT) of \(Irf3^{-/-}\) mice had increased expression of brown adipocyte selective genes compared to WT, and the inguinal WAT of the \(Irf3^{-/-}\) mouse contain multilocular adipocytes that resemble brown adipocytes. These data suggest that IRF3 affects energy homeostasis by regulating the development of brown adipocyte-like cells in WAT. Additionally, \(Irf3^{-/-}\) mice are significantly more insulin sensitive and glucose tolerant compared to WT when kept on HFD. Consistent with in vivo observations, IRF3 knockdown in 3T3-L1 adipocytes resulted in enhanced insulin-stimulated glucose uptake and lipogenesis, while overexpression of constitutively active IRF3 had the opposite effect. Several IRF3 target genes in adipocytes were identified using transcriptional profiling. Interestingly, the expression level of Slc2a4 (encoding the Glut4 protein) was inversely correlated with that of IRF3 in both WAT and cultured adipocytes. Analysis of the Slc2a4 proximal promoter identified a putative IRF3 binding site upstream of the transcription start site, and luciferase assay in 3T3-L1 adipocytes showed that IRF3 negatively regulates Slc2a4 expression via this site. Taken together, these data indicate that IRF3 plays a role in whole body glucose homeostasis by repressing thermogenic gene expression as well as the expression of adipose Glut4.
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Hall, Jessica Ann. "Thyroid Hormone and Insulin Metabolic Actions on Energy and Glucose Homeostasis." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11663.

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Faced with an environment of constantly changing nutrient availability, mammals have adapted complex homeostatic mechanisms to maintain energy balance. Deviations from this balance are largely corrected through a concerted, multi-organ effort that integrates hormonal signals with transcriptional regulatory networks. When these relationships are altered, as with over-nutrition and insulin resistance, metabolic disease ensues. Here, I present data concerning two distinct transcriptional pathways--one for thyroid hormone (TH) and one for insulin--that confer hormone responsiveness on metabolic gene programs that preserve energy homeostasis.
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Rahman, S. A. "Investigating the role of gut hormones in energy and glucose homeostasis." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1417078/.

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Obesity is associated with type-2 diabetes mellitus. Gut hormones are peptides secreted in response to nutrient intake that act to regulate food intake, energy and glucose homeostasis. Thus, alterations in gut hormone abundance and/or signalling can contribute to the development of the obese and T2DM phenotype. The incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic hormone augment glucose-mediated insulin secretion. Peptide YY is released from the gut post-prandially and acts primarily as a satiety signal. Recently studies have highlighted a role for PYY in regulating glucose homeostasis, which to date remains partially understood. Dipeptidyl peptidase-4 is involved in the biological inactivation of the incretins hence; DPP-4 inhibition is used to treat T2DM. DPP-4 also regulates PYY. Thus, DPP-4 inhibition may potentially impact on pancreatic PYY function and signalling and may alter the effects of the PYY system on glucose homeostasis. In addition, gut peptides have been identified as possible contributors to cases of hyperinsulinaemic-hypoglycaemia resulting from bariatric surgery. Therefore, this thesis aimed to (1) determine the contribution of pancreatic PYY deletion to the intra-islet PYY system; glucose homeostasis and body weight phenotype and (2) establish the impact of hyperinsulinism on DPP-4 and its gut hormone substrates. To address the first point, pancreatic-specific Pyy null mice were phenotyped for changes in the pancreatic endocrine system, followed by body weight and glucose metabolism, in vivo. Further investigations measuring gut hormone mRNA suggested the intra-islet system was contributing to the observed reduction in weight gain and hyperinsulinaemia. Finally, patients with congenital forms of HI were evaluated for PYY, the incretins and DPP-4. This study highlighted a role for DPP-4, PYY and GIP in mediating HI. In conclusion, this thesis demonstrates a role for gut hormones in energy and glucose homeostasis. Further work is required to understand the interaction of gut peptides on islet function.
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Stump, Madeliene. "The role of brain PPAR[gamma] in regulation of energy balance and glucose homeostasis." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/6000.

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The Peroxisome Proliferator-Activated Receptor gamma (PPARγ), a master regulator of adipogenesis, has been shown to influence energy balance through its actions in the brain rather than in the adipose tissue alone. Deletion of PPARγ in mouse brain results in resistance to weight gain in response to high fat diet. Activation of PPARγ leads to change in the firing pattern of melanocortin system neurons (POMC and AgRP), which are critical for energy homeostasis. To determine the effects of modulation of brain PPARγ on food intake and energy expenditure we generated a novel transgenic mouse model in which a dominant-negative (DN) mutant form of PPARγ (P467L) or a wild type (WT) form that is conditionally expressed in either the entire central nervous system (CNS) or specifically in POMC or AgRP neurons. Interference with brain PPARγ results in impaired insulin and glucose regulation. This in turn has significant implications in altering the growth rate and metabolic homeostasis. In light of the well-established role of PPARγ in regulating insulin sensitivity, this is the first report implicating brain PPARγ in controlling peripheral insulin levels. Overexpression of the WT PPARγ in the CNS leads to failure to thrive and early death due to microcephaly and severe distortion of brain architecture with notable agenesis of the corpus callosum. Our results show that the levels of PPARγ in the brain are tightly regulated and perturbations leading to “too much” or “too little” functional PPARγ result in major shifts in structural organization of the brain or metabolic balance. The herein presented data show that chronic interference with the function of neuronal PPARγ affects energy balance only under certain dietary conditions and through specific neuronal populations. We show that POMC, but not AgRP neurons, are particularly sensitive to modulation of PPARγ activity. These observations give support to the notion that cellular adaptations in POMC neurons, driven by PPARγ, represent critical components in the regulation of metabolic homeostasis.
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Aatsinki, S. M. (Sanna-Mari). "Regulation of hepatic glucose homeostasis and Cytochrome P450 enzymes by energy-sensing coactivator PGC-1α." Doctoral thesis, Oulun yliopisto, 2015. http://urn.fi/urn:isbn:9789526208053.

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Abstract Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is a master regulator of energy metabolism and mitochondrial biology in high-energy cell types and tissues. The regulation of PGC-1α is versatile, and both transcriptional and post-transcriptional mechanisms play major roles. External stimuli affect PGC-1α-regulation which in turn adapts cellular signals to meet them. For example, conditions like fasting and diabetes mellitus (DM) are known to activate PGC-1α expression in the liver, resulting in enhanced de novo glucose production, gluconeogenesis. In the present study, the mechanisms of hepatic PGC-1α regulation and PGC-1α-regulated functions were elucidated. We found that PGC-1α was induced by oral type 2 diabetes therapeutic metformin, via AMPK and SIRT1, regulating the mitochondrial gene response, against previous assumptions. Simultaneously, gluconeogenesis was repressed by other means. Furthermore, PGC-1α upregulated the anti-inflammatory interleukin 1 receptor antagonist (IL1Rn). PGC-1α also diminished interleukin 1β-mediated inflammatory response in hepatocytes. Novel, xenobiotic and endobiotic metabolizing Cytochrome P450 enzymes regulated by PGC-1α were also identified in this thesis. CYP2A5 was induced by PGC-1α through hepatocyte nuclear factor 4α (HNF-4α) coactivation. Also, vitamin D metabolizing CYP2R1 and CYP24A1 were identified as novel genes regulated by PGC-1α, suggesting a role for PGC-1α in the regulation of active vitamin D levels. The findings presented in this thesis provide insight into the pathology of glucose perturbations such as type 2 diabetes, and stimulate discovery of therapeutic agents to treat this disease. Furthermore, the findings suggest that vitamin D metabolism and energy metabolism are tightly linked, with PGC-1α emerging as a novel mediator
Tiivistelmä Peroksisomiproliferaattori-aktivoituvan reseptori γ:n koaktivaattori 1α (PGC-1α) on merkittävä glukoosiaineenvaihdunnan ja mitokondrioiden toiminnan säätelijä korkeaenergisissä soluissa ja kudoksissa. PGC-1α:a säädellään monin tavoin: sekä transkriptionaalisella säätelyllä että transkription jälkeisellä muokkauksella on merkittävä rooli. Monet ulkoiset tekijät säätelevät PGC-1α:n aktiivisuutta, joka puolestaan säätelee solunsisäisiä signaalireittejä vastaamaan tähän signaaliin. Esimerkiksi paasto ja diabetes mellitus (DM) ovat fysiologisia tiloja, jotka lisäävät voimakkaasti PGC-1α:n ilmentymistä maksassa, jolloin glukoosin uudistuotanto eli glukoneogeneesi kiihtyy. Tässä väitöskirjassa tutkittiin PGC-1α:n säätelyä sekä PGC-1α -säädeltyjä signaalireittejä maksassa. Osoitimme, että tyypin 2 diabeteslääke metformiini indusoi PGC-1α:n ilmentymistä maksassa, vastoin aikaisempia käsityksiä. PGC-1α indusoitui AMPK:n ja SIRT1:n välityksellä, säädelleen edelleen mitokondriaalisten geenien aktiivisuutta. Samalla glukoneogeneesi kuitenkin repressoitui muilla mekanismeilla. Lisäksi osoitimme, että PGC-1α indusoi tulehdusreaktiota vaimentavaa interleukiini 1 reseptorin antagonistia (IL1Rn). PGC-1α esti interleukiini 1β:n aiheuttamaa tulehdusvastetta hepatosyyteissä. Lisäksi väitöskirjassa tunnistettiin uusia, PGC-1α -säädeltyjä lääkeaineita ja elimistön sisäisiä yhdisteitä metaboloivia sytokromi P450 -entsyymejä (CYP). Hiiren CYP2A5:n ilmentymisen osoitettiin olevan PGC-1α- ja HNF4α-välitteistä. Lisäksi osoitettiin, että D-vitamiinia metaboloivat CYP2R1 ja CYP24A1 ovat uusia PGC-1α -säädeltyjä geenejä. Tämä löydös viittaa siihen, että PGC-1α:lla on rooli aktiivisen D-vitamiinin säätelyssä. Tämän väitöskirjan löydökset lisäävät tietoa glukoosiaineenvaihdunnan häiriöiden kuten tyypin 2 diabeteksen molekulaarisista mekanismeista, joita voidaan hyödyntää mahdollisten uusien lääkeaineiden kehittämisessä. Lisäksi väitöskirjassa osoitettiin, että D-vitamiinimetabolia on kytköksissä energia-aineenvaihduntaan ja että PGC-1α:lla on tässä rooli, jota ei aiemmin ole tunnettu
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Eftychidis, Vasileios. "Elucidating the principal role of cholecystokinin neurons of the ventromedial hypothalamic nucleus in energy homeostasis." Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:906a0aa6-847a-43b8-a527-458252aca825.

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The central nervous system (CNS) has a crucial role in the maintenance of energy homeostasis by orchestrating a plethora of signals from peripheral organs about the state of energy stores and the current energy intake needed to match energy expenditure. These signals converge into the hypothalamic regions and its complex local circuitry. CNS-derived cholecystokinin (CCK) is acting at central level to modulate energy balance by regulating the neuronal activity of hypothalamic neuronal populations that regulate food intake, energy storage and consumption. Moreover, our recent published work identifies CCK neurons as key integrators of the neuroendocrine negative feedback of glucocorticoids to the PVN. Glucose sensing neurons of the Ventromedial Hypothalamus (VMH) are integrating energy signals and are essential for mounting a counter-regulatory response and glucose homeostasis. VMH is also important in energy expenditure by regulating body weight and thermogenesis. CCK neurons are present in high density in the VMH.The source of endogenous CCK that acts on distinct neuronal components has not been elucidated. The research so far does not address the purpose of CCK neurons in the hypothalamus and their potential role in the network dynamics regarding energy homeostasis. In this study, we untangle the role of CCK neurons in the VMH nucleus by employing stereotactic intracranial delivery of adeno-associated viruses that result in cell-type specific chemogenetic inhibition or ablation of these neurons. Acute silencing of their neurotransmission with the cre-dependent AAV expression of the chemogenetic tool of Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) increases their daily food intake due to increased meal numbers and eating frequency without meal size or meal duration being affected. CCK ablation by a newly generated double-recombinase-mediated Diphtheria Toxin Receptor (DTR) mouse line or AAV-DTA-mediated ablation resulted in hyperphagia, obesity and hyperglycaemia. We conclude that CCKVMH neurons are implicated in the regulation of food intake, body weight and glucose homeostasis in the adult brain.
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Birkenfeld, Andreas L. [Verfasser]. "The role of natriuretic peptides in the regulation of energy metabolism, lipid- and glucose homeostasis / Andreas L. Birkenfeld." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1035182424/34.

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Books on the topic "Energy and glucose homeostasis"

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Mladen, Vranic, Efendić Suad, and Hollenberg Charles H. 1930-, eds. Fuel homeostasis and the nervous system. New York: Plenum Press, 1991.

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institutet, Karolinska, ed. Food deprivation and glucose homeostasis in hemorrhagic stress. Stockholm: [s.n.], 1987.

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1950-, Pagliassotti Michael J., Davis Stephen N. 1955-, and Cherrington Alan 1946-, eds. The role of the liver in maintaining glucose homeostasis. Austin: Landes, 1994.

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Polakof, Sergio. Brain glucosensing: Physiological implications. Hauppauge, N.Y: Nova Science Publishers, 2010.

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Sarabia, Vivian E. Calcium homeostasis and regulation of glucose uptake in human skeletal muscle cells in culture. Ottawa: National Library of Canada, 1990.

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Hodakoski, Cindy Marie. P-REX2 PH Domain Inhibition of PTEN Regulates Transformation, Insulin Signaling, and Glucose Homeostasis. [New York, N.Y.?]: [publisher not identified], 2012.

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Miller, Janette Brand. The new glucose revolution pocket guide to sugar & energy. New York: Marlowe, 2004.

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Gema, Frühbeck, and Nutrition Society (Great Britain), eds. Peptides in energy balance and obesity. Wallingford, Oxfordshire: CABI Pub. in association with the Nutrition Society, 2009.

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Muromt͡sev, V. A. Medit͡sina v XXI veke: Ot drevneĭshikh tradit͡siĭ do vysokikh tekhnologiĭ. Sankt-Peterburg: Izd-vo "Intan", 1998.

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Pool, Ontario Assessment Instrument, ed. Energy and the living cell: Draft. Toronto: Minister of Education, Ontario, 1989.

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Book chapters on the topic "Energy and glucose homeostasis"

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Kirchner, Henriette, Matthias Tschöp, and Jenny Tong. "GOAT and the Regulation of Energy and Glucose Homeostasis." In Ghrelin in Health and Disease, 131–47. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-903-7_7.

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Kamstra, Kaj, and Alexander Tups. "Neuroendocrine Interactions in the Control of Glucose- and Energy Homeostasis." In Physiological Consequences of Brain Insulin Action, 63–78. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003079927-5.

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Mounien, Lourdes, and Bernard Thorens. "Central Glucose Sensing and Control of Food Intake and Energy Homeostasis." In Metabolic Syndrome, 29–51. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470910016.ch2.

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Guillaume, Maeva, Alexandra Montagner, Coralie Fontaine, Françoise Lenfant, Jean-François Arnal, and Pierre Gourdy. "Nuclear and Membrane Actions of Estrogen Receptor Alpha: Contribution to the Regulation of Energy and Glucose Homeostasis." In Sex and Gender Factors Affecting Metabolic Homeostasis, Diabetes and Obesity, 401–26. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-70178-3_19.

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Alsahli, Mazen, and John E. Gerich. "Normal Glucose Homeostasis." In Principles of Diabetes Mellitus, 1–20. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20797-1_2-1.

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Alsahli, Mazen, Muhammad Z. Shrayyef, and John E. Gerich. "Normal Glucose Homeostasis." In Principles of Diabetes Mellitus, 1–20. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-20797-1_2-2.

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Gerich, John E., Steven D. Wittlin, and Christian Meyer. "Normal Glucose Homeostasis." In Principles of Diabetes Mellitus, 39–56. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4757-6260-0_2.

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Alsahli, Mazen, Muhammad Z. Shrayyef, and John E. Gerich. "Normal Glucose Homeostasis." In Principles of Diabetes Mellitus, 23–42. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-18741-9_2.

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Shrayyef, Muhammad Z., and John E. Gerich. "Normal Glucose Homeostasis." In Principles of Diabetes Mellitus, 19–35. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-09841-8_2.

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Ferrannini, Ele, and Marta Seghieri. "Overview of Glucose Homeostasis." In Endocrinology, 1–22. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-45015-5_1.

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Conference papers on the topic "Energy and glucose homeostasis"

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Ahmed, Sumaya, and Nasser Rizk. "The Expression of Bile Acid Receptor TGR5 in Adipose Tissue in Diet-Induced Obese Mice." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0212.

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Bile acids are significant physiological factors for digestion, solubilization, absorption, toxic metabolites and xenobiotics. In addition, bile acids are responsible of signal transduction as well as metabolic regulation that activate several receptors such as farnesoid X receptor (FXR) and the membrane G-protein receptor 5 (TGR5). Activation of TGR5 by bile acids is associated with prevention of obesity as well as ameliorating the resistance to insulin via increasing energy expenditure. The objective of this research is to investigate TGR5 gene expression level in different fat depots including visceral or epididymal adipose tissue (eWAT), brown adipose tissue and inguinal adipose tissue (iWAT) and to study the response of TGR5 gene expression to the antiobesity treatment (SFN). Three groups of male CD1 mice were used in this study; lean group fed with SCD, DIO mice on HFD and DIO obese mice treated with anti-obesity treatment. Body weight (BW) and phenotype data were evaluated by weekly including blood samples for analysis of glucose, insulin, leptin, triglycerides (TG). Total RNA was extracted from different fat depots and RT-PCR profiler array technology was used to in order to assess the mRNA expression of TGR5 and leptin. There was significant downregulation of TGR5 gene expression level in obese (DIO) mice and remarkable upregulation of TGR5 gene expression after successful weight loss in DIO mice treated with SFN in time dependent manner at 1 weeks and 4 weeks of ip applications. In conclusion, obesity is associated with decrease in expression of TGR5 in different fat depots and treatment with anti-obesity drug (Sulforaphane) causes stepwise upregulation of TGR5 gene expression in epididymal white adipose tissue parallel stepwise decrease in body weight. Increase of expression of TGR5 in DIO mice in eWAT is accompanied by improvement in glucose homeostasis and insulin action.
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Belmon, Anchana P., and Jeraldin Auxillia. "An Unprecedented PSO-PID Optimized Glucose Homeostasis." In 2020 International Conference on Smart Technologies in Computing, Electrical and Electronics (ICSTCEE). IEEE, 2020. http://dx.doi.org/10.1109/icstcee49637.2020.9277306.

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Kim, Jaeyeon, Gerald M. Saidel, John P. Kirwan, and Marco E. Cabrera. "Computational Model of Glucose Homeostasis During Exercise." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.260736.

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Kim, Jaeyeon, Gerald M. Saidel, John P. Kirwan, and Marco E. Cabrera. "Computational Model of Glucose Homeostasis During Exercise." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4397397.

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Panwar, Madhuri, Amit Acharyya, and Rishad A. Shafik. "Non-invasive Blood Glucose Estimation Methodology Using Predictive Glucose Homeostasis Models." In 2018 8th International Symposium on Embedded Computing and System Design (ISED). IEEE, 2018. http://dx.doi.org/10.1109/ised.2018.8703991.

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Singh, Neeraj Kumar, and Hao Wang. "Virtual Environment Model of Glucose Homeostasis for Diabetes Patients." In 2019 IEEE International Conference on Industrial Cyber Physical Systems (ICPS). IEEE, 2019. http://dx.doi.org/10.1109/icphys.2019.8780383.

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Villa E, Yisel C., and Julian M. Garcia G. "Modeling of the Human Pancreas Function in Glucose Homeostasis." In 2018 Argentine Conference on Automatic Control (AADECA). IEEE, 2018. http://dx.doi.org/10.23919/aadeca.2018.8577449.

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Shrestha, Man Mohan, Chun-Yan Lim, and Weiping Han. "Actin Cytoskeletal Remodeling in the Regulation of Glucose Homeostasis." In International Conference on Photonics and Imaging in Biology and Medicine. Washington, D.C.: OSA, 2017. http://dx.doi.org/10.1364/pibm.2017.t1b.2.

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Nevis, Ruiz M., Colorado G. Vivian, and Lema-Perez Laura. "A Coupled Model of Glucose Homeostasis From a Fieldbus View." In 2019 IEEE 4th Colombian Conference on Automatic Control (CCAC). IEEE, 2019. http://dx.doi.org/10.1109/ccac.2019.8920895.

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Berggren, Per-Olof. "The islet of Langerhans is a master regulator of glucose homeostasis." In 2010 IEEE Photonics Society Winter Topicals Meeting Series (WTM 2010). IEEE, 2010. http://dx.doi.org/10.1109/photwtm.2010.5421943.

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Reports on the topic "Energy and glucose homeostasis"

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Puigserver, Pere. Maintenance of Glucose Homeostasis through Acetylation of the Metabolic Transcriptional Coactivator PGC-1alpha. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ada467976.

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Puigserver, Pere. Maintenance of Glucose Homeostasis Through Acetylation of the Metabolic Transcriptional Coactivator PGC1-alpha. Fort Belvoir, VA: Defense Technical Information Center, February 2011. http://dx.doi.org/10.21236/ada551301.

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Sosa Munguía, Paulina del Carmen, Verónica Ajelet Vargaz Guadarrama, Marcial Sánchez Tecuatl, Mario Garcia Carrasco, Francesco Moccia, and Roberto Berra-Romani. Diabetes mellitus alters intracellular calcium homeostasis in vascular endothelial cells: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0104.

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Review question / Objective: What are the effects of diabetes mellitus on the calcium homeostasis in vascular endothelial cells? -To describe the effects of diabetes on the mechanisms that regulate intracellular calcium; -To describe other molecules/mechanisms that alters intracellular Ca2+ homeostasis. Condition being studied: Diabetes mellitus is a pathology with a high incidence in the population, characterized by an increase in blood glucose. People with diabetes are 2-4 times more likely to suffer from a cardiovascular complication, such as total or partial loss of sight, myocardial infarction, kidney failure, among others. Cardiovascular complications have been reported to derive from dysfunction of endothelial cells, which have important functions in blood vessels. In order to understand the etiology of this poor function of endothelial cells, it is necessary to study the molecular mechanisms involved in these functions, to identify the effects of diabetes and thus, develop new research that will mitigate the effects of this pathology.
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frydman, judith. Mechanism and function of the chaperonin from Methanococcus maripaludis: implications for archaeal protein homeostasis and energy production. Office of Scientific and Technical Information (OSTI), March 2018. http://dx.doi.org/10.2172/1429063.

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Chen, Jiankun, Yingming Gu, Lihong Yin, Minyi He, Na Liu, Yue Lu, Changcai Xie, Jiqiang Li, and Yu Chen. Network meta-analysis of curative efficacy of different acupuncture methods on obesity combined with insulin resistance. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0075.

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Review question / Objective: Population：Patients diagnosed as obesity with insulin resistance. Obesity reference: Consensus of experts on the Prevention and treatment of adult obesity in China in 2011 and Consensus of Chinese experts on medical nutrition therapy for overweight/obesity in 2016 were developed by the Obesity Group of Chinese Society of Endocrinology(CSE); BMI≥28. IR reference: According to the Expert opinions on insulin resistance evaluation published by Chinese Diabetes Society, HOMA-IR≥2.68 is regarded as the standard for the diagnosis of IR. Regardless of age, gender and course of disease. Patients diagnosed as obesity with insulin resistance. Intervention：Any kind of acupuncture, moxibustion, acupuncture+moxibustion, warm acupuncture, electropuncture, auricular point, acupoint application and acupoint catgut embedding. Comparison：Other acupuncture treatments, Drug therapy or blank control. Outcome：Primary outcomes: ①Fasting blood-glucose (FBG); ②Fasting serum insulin (FINS); ③Homeostasis model assessment-IR (HOMA-IR); ④Body Mass Index (BMI). Secondary outcomes: ①Waistline; ②Waist-hip ratio;③Triglyceride (TG); ④Total cholesterol (TC); ⑤High-density lipoprotein (HDL); ⑥Low-density lipoprotein (LDL). Study: Randomized controlled trials (RCTs) of different acupuncture methods in the treatment on obesity with insulin resistance, blind method and language are not limited. Randomized controlled trials (RCTs).
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Corscadden, Louise, and Anjali Singh. Metabolism And Measurable Metabolic Parameters. ConductScience, December 2022. http://dx.doi.org/10.55157/me20221213.

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Metabolism is the sum of chemical reactions involved in sustaining the life of organisms.[1] It constantly provides your body with the energy to perform essential functions. The process is categorized into two groups:[2] Catabolism: It’s the process of breaking down molecules to obtain energy. For example, converting glucose to pyruvate by cellular respiration. Anabolism: It’s the process of synthesis of compounds required to run the metabolic process of the organisms. For example, carbohydrates, proteins, lipids, and nucleic acids.[2] Metabolism is affected by a range of factors, such as age, sex, muscle mass, body size, and physical activity affect metabolism or BMR (the basal metabolic rate). By definition, BMR is the minimum amount of calories your body requires to function at rest.[2] Now, you have a rough idea about the concept. But, you might wonder why you need to study it. What and how metabolic parameters are measured to determine the metabolism of the organism? Find the answer to all these questions in this article.
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Cahaner, Avigdor, Sacit F. Bilgili, Orna Halevy, Roger J. Lien, and Kellye S. Joiner. effects of enhanced hypertrophy, reduced oxygen supply and heat load on breast meat yield and quality in broilers. United States Department of Agriculture, November 2014. http://dx.doi.org/10.32747/2014.7699855.bard.

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Original objectivesThe objectives of this project were to evaluate the growth performance, meat yield and quality attributes of broiler strains widely differing in their genetic potential under normal temperature vs. warm temperature (short and long-term) conditions. Strain differences in breast muscle accretion rate, metabolic responses under heat load and, gross and histopathological changes in breast muscle under thermal load was also to be characterized. BackgroundTremendous genetic progress has been made in broiler chicken growth rate and meat yield since the 1950s. Higher growth rate is driven by higher rates of feed intake and metabolism, resulting in elevated internal heat production. Hot rearing conditions negatively affect broiler growth by hindering dissipation of heat and may lead to a lethal elevation in body temperature. To avoid heat-induced mortality, broilers reduce feed intake, leading to depressed growth rate, lower weight gain, reduce breast meat yield and quality. Thus, the genetic potential of contemporary commercial broilers (CCB) is not fully expressed under hot conditions. Major conclusions, solutions, and achievementsResearch conducted in Israel focused on three broiler strains – CCB, Featherless, Feathered sibs (i.e., sharing similar genetic background). Complimentary research trials conducted at Auburn utilized CCB (Cobb 500, Cobb 700, Ross 308, Ross 708), contrasting their performance to slow growing strains. Warm rearing conditions consistently reduced feed intake, growth rate, feed efficiency, body weight uniformity and breast muscle yield, especially pronounced with CCB and magnified with age. Breast meat quality was also negatively affected, as measured by higher drip loss and paler meat color. Exposure to continuous or short-term heat stress induced respiratory alkalosis. Breast muscle histomorphometrics confirmed enhanced myofiber hypertrophy in CCB. Featherless broilers exhibited a significant increase in blood-vessel density under warm conditions. Rapid growth and muscle accretion rate was correlated to various myopathies (white striping, woody and necrotic) as well as to increases in plasma creatinekinase levels. Whether the trigger(s) of muscle damage is loss of cellular membrane integrity due to oxidative damage or tissue lactate accumulation, or to loss of inter-compartmental cation homeostasis is yet to be determined. Based on genome-wide single-nucleotide polymorphism array genotyping, identification of the gene with the recessive mutation Scaleless (sc) facilitated the development a dCAPS assay to discriminate between sc carrier (sc/+) and non-carrier (+/+) individuals. ImplicationsThis project confirmed that featherless broiler strains grow efficiently with high yield and quality of breast meat, even under warm rearing conditions that significantly depress the overall performance of CCB. Therefore, broiler meat production in hot regions and climates can be substantially improved by introducing the featherless gene into contemporary commercial broiler stocks. This approach has become more feasible with the development of dCAPS assay. A novel modification of the PCR protocol (using whole blood samples instead of extracted DNA) may contribute to the efficient development of commercial featherless broiler strains. Such strains will allow expansion of the broiler meat production in developing countries in warm climates, where energy intensive environmental control of rearing facilities are not economical and easily achievable.
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Gothilf, Yoav, Roger Cone, Berta Levavi-Sivan, and Sheenan Harpaz. Genetic manipulations of MC4R for increased growth and feed efficiency in fish. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7600043.bard.

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The hypothalamic melanocortin system plays a central role in the regulation of food consumption and energy homeostasis in mammals. Accordingly, our working hypothesis in this project was that genetic editing of the mc4r gene, encoding Melanocortin Receptor 4 (MC4R), will enhance food consumption, feed efficiency and growth in fish. To test this hypothesis and to assess the utility of mc4r editing for the enhancement of feed efficiency and growth in fish, the following objectives were set: Test the effect of the mc4r-null allele on feeding behavior, growth, metabolism and survival in zebrafish. Generate mc4r-null alleles in tilapia and examine the consequences for growth and survival, feed efficiency and body composition. Generate and examine the effect of naturally-occurring mc4r alleles found in swordfish on feeding behavior, growth and survival in zebrafish. Define the MC4R-mediated and MC4R-independent effects of AgRP by crossing mc4r- null strains with fish lacking AgRP neurons or the agrpgene. Our results in zebrafish did not support our hypothesis. While knockout of the agrpgene or genetic ablation of hypothalamic AgRP neurons led to reduced food intake in zebrafish larvae, knockout (KO) of the mc4r gene not only did not increase the rate of food intake but even reduced it. Since Melanocortin Receptor 3 (MC3R) has also been proposed to be involved in hypothalamic control of food intake, we also tested the effectofmc3r gene KO. Again, contrary to our hypothesis, the rate of food intake decreased. The next step was to generate a double mutant lucking both functional MC3R and MC4R. Again, the double KO exhibited reduced food intake. Thus, the only manipulation within the melanocortin system that affected food intake in consistent with the expected role of the system was seen in zebrafish larvae upon agrpKO. Interestingly, despite the apparent reduced food intake in the larval stage, these fish grow to be of the same size as wildtype fish at the adult stage. Altogether, it seems that there is a compensatory mechanism that overrides the effect of genetic manipulations of the melanocortin system in zebrafish. Under Aim 3, we introduced the Xna1, XnB1l, and XnB2A mutations from the Xiphophorus MC4R alleles into the zebrafish MC4R gene. We hypothesized that these MC4R mutations would act as dominant negative alleles to increase growth by suppressing endogenous MC4R activity. When we examined the activity of the three mutant alleles, we were unable to document any inhibition of a co-transfected wild type MC4R allele, hence we did not introduce these alleles into zebrafish. Since teleost fish possess two agrpgenes we also tested the effect of KO of the agrp2 gene and ablation of the AgRP2 cells. We found that the AgRP2 system does not affect food consumption but may rather be involved in modulating the stress response. To try to apply genetic editing in farmed fish species we turned to tilapia. Injection of exogenous AgRP in adult tilapia induced significant changes in the expression of pituitary hormones. Genetic editing in tilapia is far more complicated than in zebrafish. Nevertheless, we managed to generate one mutant fish carrying a mutation in mc4r. That individual died before reaching sexual maturity. Thus, our attempt to generate an mc4r-mutant tilapia line was almost successful and indicate out non-obvious capability to generate mutant tilapia.
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Boisclair, Yves R., and Arieh Gertler. Development and Use of Leptin Receptor Antagonists to Increase Appetite and Adaptive Metabolism in Ruminants. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697120.bard.

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Objectives The original project had 2 major objectives: (1) To determine the effects of centrally administered leptin antagonist on appetite and adaptive metabolism in the sheep; (2) To develop and prepare second-generation leptin antagonists combining high binding affinity and prolonged in vivo half-life. Background Periods of suboptimal nutrition or exaggerated metabolic activity demands lead to a state of chronic energy insufficiency. Ruminants remain productive for a surprisingly long period of time under these circumstances by evoking adaptations sparing available energy and nutrients. The mechanism driving these adaptations in ruminant remains unknown, but could involve a reduction in plasma leptin, a hormone acting predominantly in the brain. In laboratory animals, reduced leptin signaling promotes survival during nutritional insufficiency by triggering energy sparing adaptations such as reduced thyroid hormone production and insulin resistance. Our overall hypothesis is that similar adaptations are triggered by reduced leptin signaling in the brain of ruminants. Testing of this hypothesis in ruminants has not been possible due to inability to block the actions of endogenous leptin and access to ruminant models where leptin antagonistic therapy is feasible and effective. Major achievements and conclusions The Israeli team had previously mutated 3 residues in ovine leptin, with no effect on receptor binding. This mutant was renamed ovine leptin antagonist (OLA) because it cannot activate signaling and therefore antagonizes the ability of wild type leptin to activate its receptor. To transform OLA into an effective in vivo antagonist, the Israeli made 2 important technical advances. First, it incorporated an additional mutation into OLA, increasing its binding affinity and thus transforming it into a super ovine leptin antagonist (SOLA). Second, the Israeli team developed a method whereby polyethylene glycol is covalently attached to SOLA (PEG-SOLA) with the goal of extending its half-life in vivo. The US team used OLA and PEG-SOLA in 2 separate animal models. First, OLA was chronically administered directly into the brain of mature sheep via a cannula implanted into the 3rdcerebroventricule. Unexpectedly, OLA had no effect of voluntary feed intake or various indicators of peripheral insulin action but reduced the plasma concentration of thyroid hormones. Second, the US team tested the effect of peripheral PEG-SOLA administration in an energy sensitive, rapidly growing lamb model. PEG-SOLA was administered for 14 consecutive days after birth or for 5 consecutive days before sacrifice on day 40 of life. Plasma PEG-SOLA had a half-life of over 16 h and circulated in 225- to 288-fold excess over endogenous leptin. PEG-SOLA administration reduced plasma thyroid hormones and resulted in a higher fat content in the carcass at slaughter, but had no effects on feed intake, body weight, plasma glucose or insulin. These results show that the team succeeded in developing a leptin antagonist with a long in vivo half-life. Moreover, in vivo results show that reduced leptin signaling promotes energy sparing in ruminants by repressing thyroid hormone production. Scientific and agricultural implications The physiological role of leptin in ruminants has been difficult to resolve because peripheral administration of wild type leptin causes little effects. Our work with leptin antagonists show for the first time in ruminants that reduced leptin signaling induces energy sparing mechanisms involving thyroid hormone production with little effect on peripheral insulin action. Additional work is needed to develop even more potent leptin antagonists, to establish optimal administration protocols and to narrow down phases of the ruminant life cycle when their use will improve productivity.
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Granot, David, Scott Holaday, and Randy D. Allen. Enhancing Cotton Fiber Elongation and Cellulose Synthesis by Manipulating Fructokinase Activity. United States Department of Agriculture, 2008. http://dx.doi.org/10.32747/2008.7613878.bard.

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a. Objectives (a) Identification and characterization of the cotton fiber FRKs; (b) Generating transgenic cotton plants overproducing either substrate inhibited tomato FRK or tomato FRK without substrate inhibition; (c) Generating transgenic cotton plants with RNAi suppression of fiber expressed FRKs; (d) Generating Arabidopsis plants that over express FRK1, FRK2, or both genes, as additional means to assess the contribution of FRK to cellulose synthesis and biomass production. b. Background to the topic: Cellulose synthesis and fiber elongation are dependent on sugar metabolism. Previous results suggested that FRKs (fructokinase enzymes that specifically phosphorylate fructose) are major players in sugar metabolism and cellulose synthesis. We therefore hypothesized that increasing fructose phosphorylation may enhance fiber elongation and cellulose synthesis in cotton plants. Accordinlgy, the objectives of this research were: c. Major conclusions and achievements: Two cotton FRKs expressed in fibers, GhFRK2 and GhFRK3, were cloned and characterized. We found that GhFRK2 enzyme is located in the cytosol and GhFRK3 is located within plastids. Both enzymes enable growth on fructose (but not on glucose) of hexose kinase deficient yeast strain, confirming the fructokinase activity of the cloned genes. RNAi constructs with each gene were prepared and sent to the US collaborator to generate cotton plants with RNAi suppression of these genes. To examine the effect of FRKs using Arabidopsis plants we generated transgenic plants expressing either LeFRK1 or LeFRK2 at high level. No visible phenotype has been observed. Yet, plants expressing both genes simultaneously are being created and will be tested. To test our hypothesis that increasing fructose phosphorylation may enhance fiber cellulose synthesis, we generated twenty independent transgenic cotton plant lines overexpressing Lycopersicon (Le) FRK1. Transgene expression was high in leaves and moderate in developing fiber, but enhanced FRK activity in fibers was inconsistent between experiments. Some lines exhibited a 9-11% enhancement of fiber length or strength, but only one line tested had consistent improvement in fiber strength that correlated with elevated FRK activity in the fibers. However, in one experiment, seed cotton mass was improved in all transgenic lines and correlated with enhanced FRK activity in fibers. When greenhouse plants were subjected to severe drought during flowering and boll development, no genotypic differences in fiber quality were noted. Seed cotton mass was improved for two transgenic lines but did not correlate with fiber FRK activity. We conclude that LeFRK1 over-expression in fibers has only a small effect on fiber quality, and any positive effects depend on optimum conditions. The improvement in productivity for greenhouse plants may have been due to better structural development of the water-conducting tissue (xylem) of the stem, since stem diameters were larger for some lines and the activity of FRK in the outer xylem greater than observed for wild-type plants. We are testing this idea and developing other transgenic cotton plants to understand the roles of FRK in fiber and xylem development. We see the potential to develop a cotton plant with improved stem strength and productivity under drought for windy, semi-arid regions where cotton is grown. d. Implications, scientific and agricultural: FRKs are probably bottle neck enzymes for biomass and wood synthesis and their increased expression has the potential to enhance wood and biomass production, not only in cotton plants but also in other feed and energy renewable plants.
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