DOI . ORG {
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Detected CMS Systems:
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We began analyzing https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.0030064, but it redirected us to https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.0030064. The analysis below is for the second page.
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Author SummaryIt is known that obesity is linked to type 2 diabetes, however how obesity causes insulin resistance and diabetes is not well understood. Some extremely obese people are not diabetic, while other less obese people develop severe insulin resistance and diabetes. We believe diabetes occurs when adipose tissue becomes “full,” and fat overflows into other organs such as liver, pancreas, and muscle, causing insulin resistance and diabetes. Peroxisome proliferator activated receptor gamma (PPARg) is essential for the development of adipose tissue and control of insulin sensitivity. PPARg2 is the isoform of PPARg regulated by nutrition. Here we investigate the role of PPARg2 under conditions of excess nutrients by removing the PPARg2 isoform in genetically obese mice, the POKO mouse. We report that removing PPARg2 decreases adipose tissue
Title[redir]:
No title found...
Description:
Author SummaryIt is known that obesity is linked to type 2 diabetes, however how obesity causes insulin resistance and diabetes is not well understood. Some extremely obese people are not diabetic, while other less obese people develop severe insulin resistance and diabetes. We believe diabetes occurs when adipose tissue becomes “full,” and fat overflows into other organs such as liver, pancreas, and muscle, causing insulin resistance and diabetes. Peroxisome proliferator activated receptor gamma (PPARg) is essential for the development of adipose tissue and control of insulin sensitivity. PPARg2 is the isoform of PPARg regulated by nutrition. Here we investigate the role of PPARg2 under conditions of excess nutrients by removing the PPARg2 isoform in genetically obese mice, the POKO mouse. We report that removing PPARg2 decreases adipose tissue
Matching Content Categories {📚}
- Science
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Content Management System {📝}
What CMS is doi.org built with?
Doi.org employs WORDPRESS.
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🌍 Impressive Traffic: 500k - 1M visitors per month
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How Does Doi.org Make Money? {💸}
We don't see any clear sign of profit-making.
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Keywords {🔍}
mice, poko, pparg, obob, insulin, tissue, adipose, article, view, google, scholar, compared, resistance, expression, liver, mouse, islets, figure, increased, levels, lipid, analysis, diabetes, decreased, muscle, fat, species, energy, glucose, versus, βcell, gene, body, mass, role, wat, gamma, isoform, data, βcells, obesity, metabolic, skeletal, male, peroxisome, lipidomic, plos, observed, table, receptor,
Topics {✒️}
plos genet 3 cookies plos biology complex diseases dual-energy x-ray absorptiometry digital camera open-access article distributed peroxisome proliferator-activated receptors global energy homeostasis medicine models lack leptin real-time quantitative rt-pcr lipodystrophic models biological systems stress-activated signaling pathways extracellular cuzn-superoxide dismutase impaired β-cell function original author systems diseases ligand-independent activation domain foxo1-pgc-1alpha interaction tissue-specific genetic manipulations facilitating β-cell hyperplasia tailed unpaired t-test liquid chromatography/mass spectrometry adipocyte-beta-cell relationships obesity-related insulin resistance real-time quantitative pcr complex q-tof premier insulin positive β-cells buffer toxic lipids ob/ob skeletal muscle ob/ob background impairs ob/ob mice quickly ob/ob mice aged severe β-cell phenotype ob/ob adipose tissue muscle-specific pparg deletion ppar{gamma}2 impairs poko-mice skeletal muscle β-cell hyperplasia insulin-regulated hepatic gluconeogenesis uk home office poko versus ob/ob ob/ob mice compared pparg2+/− lepob/lep+ mice skeletal muscle lipidomics lipids—antilipotoxic role
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