<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kempa J</submitter><funding>NCRR NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>Murdock Charitable Trust Foundation</funding><funding>MSU’s office of the Vice President for Research, Economic Development, and Graduate Education at MSU</funding><funding>USPHS</funding><funding>NIH SIG program</funding><funding>National Science Foundation</funding><pagination>815</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9782143</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(12)</volume><pubmed_abstract>Hypoglycemia may be induced by a variety of physiologic and pathologic stimuli and can result in life-threatening consequences if untreated. However, hypoglycemia may also play a role in the purported health benefits of intermittent fasting and caloric restriction. Previously, we demonstrated that systemic administration of ricin toxin induced fatal hypoglycemia in mice. Here, we examine the metabolic landscape of the hypoglycemic state induced in the liver of mice by two different stimuli: systemic ricin administration and fasting. Each stimulus produced the same decrease in blood glucose and weight loss. The polar metabolome was studied using &lt;sup>1&lt;/sup>H NMR, quantifying 59 specific metabolites, and untargeted LC-MS on approximately 5000 features. Results were analyzed by multivariate </pubmed_abstract><journal>Toxins</journal><pubmed_title>Distinct Metabolic States Are Observed in Hypoglycemia Induced in Mice by Ricin Toxin or by Fasting.</pubmed_title><pmcid>PMC9782143</pmcid><funding_grant_id>AI136758(SP)</funding_grant_id><funding_grant_id>R01 AI136758</funding_grant_id><funding_grant_id>S10 RR026659</funding_grant_id><funding_grant_id>R56 AI127398</funding_grant_id><funding_grant_id>NSF-MRI:DBI-1532078</funding_grant_id><funding_grant_id>1S10RR13878</funding_grant_id><funding_grant_id>1S10RR026659</funding_grant_id><funding_grant_id>DK117473</funding_grant_id><funding_grant_id>AI127398</funding_grant_id><funding_grant_id>2015066:MNL</funding_grant_id><funding_grant_id>R01 AI059376</funding_grant_id><funding_grant_id>NSF-MRI:CHE-2018388</funding_grant_id><funding_grant_id>R01DK117473</funding_grant_id><funding_grant_id>R01 DK117473</funding_grant_id><pubmed_authors>Copie V</pubmed_authors><pubmed_authors>Peters T</pubmed_authors><pubmed_authors>Moss CE</pubmed_authors><pubmed_authors>Bothner B</pubmed_authors><pubmed_authors>O'Shea-Stone G</pubmed_authors><pubmed_authors>Tripet B</pubmed_authors><pubmed_authors>Pincus SH</pubmed_authors><pubmed_authors>Marcotte TK</pubmed_authors><pubmed_authors>Kempa J</pubmed_authors><pubmed_authors>Eilers B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Distinct Metabolic States Are Observed in Hypoglycemia Induced in Mice by Ricin Toxin or by Fasting.</name><description>Hypoglycemia may be induced by a variety of physiologic and pathologic stimuli and can result in life-threatening consequences if untreated. However, hypoglycemia may also play a role in the purported health benefits of intermittent fasting and caloric restriction. Previously, we demonstrated that systemic administration of ricin toxin induced fatal hypoglycemia in mice. Here, we examine the metabolic landscape of the hypoglycemic state induced in the liver of mice by two different stimuli: systemic ricin administration and fasting. Each stimulus produced the same decrease in blood glucose and weight loss. The polar metabolome was studied using &lt;sup>1&lt;/sup>H NMR, quantifying 59 specific metabolites, and untargeted LC-MS on approximately 5000 features. Results were analyzed by multivariate </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2025-04-04T21:55:22.976Z</modification><creation>2025-02-19T01:55:55.452Z</creation></dates><accession>S-EPMC9782143</accession><cross_references><pubmed>36548712</pubmed><doi>10.3390/toxins14120815</doi></cross_references></HashMap>