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  • 1
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    Furan fatty acid as an anti-inflammatory component from the green-lipped mussel Perna canaliculus [Pharmacology] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-10-19
    Description: A lipid extract of Perna canaliculus (New Zealand green-lipped mussel) has reportedly displayed anti-inflammatory effects in animal models and in human controlled studies. However, the anti-inflammatory lipid components have not been investigated in detail due to the instability of the lipid extract, which has made the identification of the distinct active components a formidable task. Considering the instability of the active component, we carefully fractionated a lipid extract of Perna canaliculus (Lyprinol) and detected furan fatty acids (F-acids). These naturally but rarely detected fatty acids show potent radical-scavenging ability and are essential constituents of plants and algae. Based on these data, it has been proposed that F-acids could be potential antioxidants, which may contribute to the protective properties of fish and fish oil diets against chronic inflammatory diseases. However, to date, in vivo data to support the hypothesis have not been obtained, presumably due to the limited availability of F-acids. To confirm the in vivo anti-inflammatory effect of F-acids in comparison with that of eicosapentaenoic acid (EPA), we developed a semisynthetic preparation and examined its anti-inflammatory activity in a rat model of adjuvant-induced arthritis. Indeed, the F-acid ethyl ester exhibited more potent anti-inflammatory activity than that of the EPA ethyl ester. We report on the in vivo activity of F-acids, confirming that the lipid extract of the green-lipped mussel includes an unstable fatty acid that is more effective than EPA.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    Determination of the stress in rock unaffected by boreholes or drifts, from measured strains or deformations (1968)
    In:  Int. J. Rock. Mech. Min. Sci., Hannover, Conseil de l'Europe, vol. 5, no. 10, pp. 337-353, pp. 5100101, (ISSN 0343-5164)
    Details
    Publication Date: 1968
    Keywords: Stress ; Elasticity ; Stress measurements ; Crustal deformation (cf. Earthquake precursor: deformation or strain) ; Rock mechanics
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    BIBLIOGRAPHY SEISMOLOGY
  • 3
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    Caps2-dex mouse shows autistic-like behaviors [Neuroscience] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-12-19
    Description: Ca2+-dependent activator protein for secretion 2 (CAPS2 or CADPS2) potently promotes the release of brain-derived neurotrophic factor (BDNF). A rare splicing form of CAPS2 with deletion of exon3 (dex3) was identified to be overrepresented in some patients with autism. Here, we generated Caps2-dex3 mice and verified a severe impairment in...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Conformational changes of the phenyl and naphthyl isocyanate-DNA adducts during DNA replication and by minor groove binding molecules (2013)
    Oxford University Press
    Details
    Publication Date: 2013-10-08
    Description: DNA lesions produced by aromatic isocyanates have an extra bulky group on the nucleotide bases, with the capability of forming stacking interaction within a DNA helix. In this work, we investigated the conformation of the 2'-deoxyadenosine and 2'-deoxycytidine derivatives tethering a phenyl or naphthyl group, introduced in a DNA duplex. The chemical modification experiments using KMnO 4 and 1-cyclohexyl-3 -(2-morpholinoethyl) carbodiimide metho- p -toluenesulfonate have shown that the 2'-deoxycytidine lesions form the base pair with guanine while the 2'-deoxyadenosine lesions have less ability of forming the base pair with thymine in solution. Nevertheless, the kinetic analysis shows that these DNA lesions are compatible with DNA ligase and DNA polymerase reactions, as much as natural DNA bases. We suggest that the adduct lesions have a capability of adopting dual conformations, depending on the difference in their interaction energies between stacking of the attached aromatic group and base pairing through hydrogen bonds. It is also presented that the attached aromatic groups change their orientation by interacting with the minor groove binding netropsin, distamycin and synthetic polyamide. The nucleotide derivatives would be useful for enhancing the phenotypic diversity of DNA molecules and for exploring new non-natural nucleotides.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 5
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    The cells and peripheral representation of sodium taste in mice (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-01-29
    Description: Salt taste in mammals can trigger two divergent behavioural responses. In general, concentrated saline solutions elicit robust behavioural aversion, whereas low concentrations of NaCl are typically attractive, particularly after sodium depletion. Notably, the attractive salt pathway is selectively responsive to sodium and inhibited by amiloride, whereas the aversive one functions as a non-selective detector for a wide range of salts. Because amiloride is a potent inhibitor of the epithelial sodium channel (ENaC), ENaC has been proposed to function as a component of the salt-taste-receptor system. Previously, we showed that four of the five basic taste qualities-sweet, sour, bitter and umami-are mediated by separate taste-receptor cells (TRCs) each tuned to a single taste modality, and wired to elicit stereotypical behavioural responses. Here we show that sodium sensing is also mediated by a dedicated population of TRCs. These taste cells express the epithelial sodium channel ENaC, and mediate behavioural attraction to NaCl. We genetically engineered mice lacking ENaCalpha in TRCs, and produced animals exhibiting a complete loss of salt attraction and sodium taste responses. Together, these studies substantiate independent cellular substrates for all five basic taste qualities, and validate the essential role of ENaC for sodium taste in mice.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849629/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849629/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandrashekar, Jayaram -- Kuhn, Christina -- Oka, Yuki -- Yarmolinsky, David A -- Hummler, Edith -- Ryba, Nicholas J P -- Zuker, Charles S -- R01 DC003160/DC/NIDCD NIH HHS/ -- R01 DC003160-05/DC/NIDCD NIH HHS/ -- Z01 DE000561-13/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Mar 11;464(7286):297-301. doi: 10.1038/nature08783. Epub 2010 Jan 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Neurobiology, University of California at San Diego, La Jolla, California 92093-0649, USA〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20107438" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior/physiology ; Epithelial Sodium Channels/genetics/metabolism ; Mice ; Mice, Transgenic ; Sodium/*physiology ; Taste/*genetics ; Taste Buds/cytology/metabolism/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    Thirst driving and suppressing signals encoded by distinct neural populations in the brain (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-01-28
    Description: Thirst is the basic instinct to drink water. Previously, it was shown that neurons in several circumventricular organs of the hypothalamus are activated by thirst-inducing conditions. Here we identify two distinct, genetically separable neural populations in the subfornical organ that trigger or suppress thirst. We show that optogenetic activation of subfornical organ excitatory neurons, marked by the expression of the transcription factor ETV-1, evokes intense drinking behaviour, and does so even in fully water-satiated animals. The light-induced response is highly specific for water, immediate and strictly locked to the laser stimulus. In contrast, activation of a second population of subfornical organ neurons, marked by expression of the vesicular GABA transporter VGAT, drastically suppresses drinking, even in water-craving thirsty animals. These results reveal an innate brain circuit that can turn an animal's water-drinking behaviour on and off, and probably functions as a centre for thirst control in the mammalian brain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4401619/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4401619/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oka, Yuki -- Ye, Mingyu -- Zuker, Charles S -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Apr 16;520(7547):349-52. doi: 10.1038/nature14108. Epub 2015 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Biochemistry and Molecular Biophysics, Columbia College of Physicians and Surgeons, Howard Hughes Medical Institute, Columbia University, New York, New York 10032, USA [2] Department of Neuroscience, Columbia College of Physicians and Surgeons, Howard Hughes Medical Institute, Columbia University, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25624099" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; DNA-Binding Proteins/metabolism ; Dehydration/physiopathology ; Drinking ; Drinking Behavior/*physiology ; Drinking Water ; Lasers ; Mice ; Optogenetics ; Satiety Response ; Subfornical Organ/*cytology/*physiology ; Thirst/*physiology ; Transcription Factors/metabolism ; Vesicular Inhibitory Amino Acid Transport Proteins/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
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    Regulation of pancreatic beta cell mass by neuronal signals from the liver (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-22
    Description: Metabolic regulation in mammals requires communication between multiple organs and tissues. The rise in the incidence of obesity and associated metabolic disorders, including type 2 diabetes, has renewed interest in interorgan communication. We used mouse models to explore the mechanism whereby obesity enhances pancreatic beta cell mass, pathophysiological compensation for insulin resistance. We found that hepatic activation of extracellular regulated kinase (ERK) signaling induced pancreatic beta cell proliferation through a neuronal-mediated relay of metabolic signals. This metabolic relay from the liver to the pancreas is involved in obesity-induced islet expansion. In mouse models of insulin-deficient diabetes, liver-selective activation of ERK signaling increased beta cell mass and normalized serum glucose levels. Thus, interorgan metabolic relay systems may serve as valuable targets in regenerative treatments for diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Imai, Junta -- Katagiri, Hideki -- Yamada, Tetsuya -- Ishigaki, Yasushi -- Suzuki, Toshinobu -- Kudo, Hirohito -- Uno, Kenji -- Hasegawa, Yutaka -- Gao, Junhong -- Kaneko, Keizo -- Ishihara, Hisamitsu -- Niijima, Akira -- Nakazato, Masamitsu -- Asano, Tomoichiro -- Minokoshi, Yasuhiko -- Oka, Yoshitomo -- New York, N.Y. -- Science. 2008 Nov 21;322(5905):1250-4. doi: 10.1126/science.1163971.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19023081" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Central Nervous System/metabolism ; Diabetes Mellitus, Experimental/metabolism ; Hyperplasia ; Insulin/metabolism ; Insulin Resistance ; Insulin-Secreting Cells/*metabolism/pathology ; Liver/*metabolism ; MAP Kinase Kinase 1/*metabolism ; *MAP Kinase Signaling System ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/*metabolism ; Obesity/*metabolism ; Pancreas/innervation ; Recombinant Proteins/metabolism ; Vagus Nerve/cytology/metabolism ; Xenopus
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 8
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    The taste of carbonation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-17
    Description: Carbonated beverages are commonly available and immensely popular, but little is known about the cellular and molecular mechanisms underlying the perception of carbonation in the mouth. In mammals, carbonation elicits both somatosensory and chemosensory responses, including activation of taste neurons. We have identified the cellular and molecular substrates for the taste of carbonation. By targeted genetic ablation and the silencing of synapses in defined populations of taste receptor cells, we demonstrated that the sour-sensing cells act as the taste sensors for carbonation, and showed that carbonic anhydrase 4, a glycosylphosphatidylinositol-anchored enzyme, functions as the principal CO2 taste sensor. Together, these studies reveal the basis of the taste of carbonation as well as the contribution of taste cells in the orosensory response to CO2.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3654389/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3654389/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandrashekar, Jayaram -- Yarmolinsky, David -- von Buchholtz, Lars -- Oka, Yuki -- Sly, William -- Ryba, Nicholas J P -- Zuker, Charles S -- Z01 DE000561-15/Intramural NIH HHS/ -- Z01 DE000561-16/Intramural NIH HHS/ -- ZIA DE000561-17/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):443-5. doi: 10.1126/science.1174601.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Departments of Neurobiology and Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833970" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Benzolamide/pharmacology ; Bicarbonates/metabolism ; Calcium Channels/metabolism ; Carbon Dioxide/*metabolism ; *Carbonated Beverages ; Carbonic Anhydrase IV/antagonists & inhibitors/genetics/*metabolism ; Carbonic Anhydrase Inhibitors/pharmacology ; Carbonic Anhydrases/metabolism ; Chorda Tympani Nerve/physiology ; Gene Expression Profiling ; Mice ; Mice, Transgenic ; Protons ; Receptors, Cell Surface/metabolism ; Taste/*physiology ; Taste Buds/enzymology/*physiology ; *Taste Perception
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 9
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    High salt recruits aversive taste pathways (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-02-15
    Description: In the tongue, distinct classes of taste receptor cells detect the five basic tastes; sweet, sour, bitter, sodium salt and umami. Among these qualities, bitter and sour stimuli are innately aversive, whereas sweet and umami are appetitive and generally attractive to animals. By contrast, salty taste is unique in that increasing salt concentration fundamentally transforms an innately appetitive stimulus into a powerfully aversive one. This appetitive-aversive balance helps to maintain appropriate salt consumption, and represents an important part of fluid and electrolyte homeostasis. We have shown previously that the appetitive responses to NaCl are mediated by taste receptor cells expressing the epithelial sodium channel, ENaC, but the cellular substrate for salt aversion was unknown. Here we examine the cellular and molecular basis for the rejection of high concentrations of salts. We show that high salt recruits the two primary aversive taste pathways by activating the sour- and bitter-taste-sensing cells. We also demonstrate that genetic silencing of these pathways abolishes behavioural aversion to concentrated salt, without impairing salt attraction. Notably, mice devoid of salt-aversion pathways show unimpeded, continuous attraction even to very high concentrations of NaCl. We propose that the 'co-opting' of sour and bitter neural pathways evolved as a means to ensure that high levels of salt reliably trigger robust behavioural rejection, thus preventing its potentially detrimental effects on health.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587117/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587117/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oka, Yuki -- Butnaru, Matthew -- von Buchholtz, Lars -- Ryba, Nicholas J P -- Zuker, Charles S -- ZIA DE000561-18/Intramural NIH HHS/ -- ZIA DE000561-19/Intramural NIH HHS/ -- ZIA DE000561-20/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Feb 28;494(7438):472-5. doi: 10.1038/nature11905. Epub 2013 Feb 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry and Molecular Biophysics, Columbia College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23407495" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Appetite/drug effects/genetics/physiology ; Feeding Behavior/drug effects/physiology ; Gene Silencing ; Mice ; Mice, Knockout ; Mutation/genetics ; Phospholipase C beta/deficiency/genetics/metabolism ; Sodium Chloride, Dietary/administration & dosage/*pharmacology ; TRPM Cation Channels/deficiency/genetics/metabolism ; Taste/*drug effects/genetics/*physiology ; Taste Buds/cytology/*drug effects/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
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    Neuronal pathway from the liver modulates energy expenditure and systemic insulin sensitivity (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: Coordinated control of energy metabolism and glucose homeostasis requires communication between organs and tissues. We identified a neuronal pathway that participates in the cross talk between the liver and adipose tissue. By studying a mouse model, we showed that adenovirus-mediated expression of peroxisome proliferator-activated receptor (PPAR)-g2 in the liver induces acute hepatic steatosis while markedly decreasing peripheral adiposity. These changes were accompanied by increased energy expenditure and improved systemic insulin sensitivity. Hepatic vagotomy and selective afferent blockage of the hepatic vagus revealed that the effects on peripheral tissues involve the afferent vagal nerve. Furthermore, an antidiabetic thiazolidinedione, a PPARg agonist, enhanced this pathway. This neuronal pathway from the liver may function to protect against metabolic perturbation induced by excessive energy storage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uno, Kenji -- Katagiri, Hideki -- Yamada, Tetsuya -- Ishigaki, Yasushi -- Ogihara, Takehide -- Imai, Junta -- Hasegawa, Yutaka -- Gao, Junhong -- Kaneko, Keizo -- Iwasaki, Hiroko -- Ishihara, Hisamitsu -- Sasano, Hironobu -- Inukai, Kouichi -- Mizuguchi, Hiroyuki -- Asano, Tomoichiro -- Shiota, Masakazu -- Nakazato, Masamitsu -- Oka, Yoshitomo -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1656-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778057" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/innervation/*metabolism ; Afferent Pathways/physiology ; Animals ; Blood Glucose/analysis ; Dietary Fats/administration & dosage ; Efferent Pathways/physiology ; *Energy Metabolism ; Fatty Liver/pathology ; Glucose/metabolism ; Glucose Tolerance Test ; Hypoglycemic Agents/pharmacology ; Insulin/blood/*physiology ; Insulin Resistance ; Lipolysis ; Liver/*innervation/*metabolism/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/metabolism ; Oxygen Consumption ; PPAR gamma/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Sympathetic Nervous System/physiology ; Vagotomy ; Vagus Nerve/*physiology ; Weight Gain
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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