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TISSUE‐SPECIFIC GENETIC TARGETING OF INOS REVEALS AN UNEXPECTED ROLE OF ADIPOCYTE INOS IN THE DEVELOPMENT OF INSULIN RESISTANCE, DYSLIPIDEMIA AND ALTERED ENERGY METABOLISM IN DIET‐INDUCED OBESE MICE

2018· article· en· W3176614352 on OpenAlexafffundabout
Vanessa Rodrigues Vilela, Gabriel Lachance, Renato Tadeu Nachbar, Carolina Centano‐Baez, Kerstin Bellmann, André Marette

Bibliographic record

VenueThe FASEB Journal · 2018
Typearticle
Languageen
FieldMedicine
TopicAdipokines, Inflammation, and Metabolic Diseases
Canadian institutionsUniversité Laval
FundersCanadian Institutes of Health Research
KeywordsEndocrinologyInsulin resistanceInternal medicineAdipose tissueAdipocyteNitric oxide synthaseBiologyDyslipidemiaLipid metabolismInsulinNitric oxideObesityMedicine

Abstract

fetched live from OpenAlex

Nitric oxide (NO) is synthesized from L‐arginine by NO synthase (NOS) enzymes. The expression of the inducible member of the NOS family, iNOS, is markedly enhanced in adipose, skeletal muscle and liver tissues in response to bacterial endotoxins (LPS), inflammatory cytokines, and diet‐induced obesity. We have previously showed that mice lacking iNOS are protected from insulin resistance induced by high‐fat feeding; acute exposure to LPS or lipid infusion, providing genetic evidence that iNOS is a key inflammatory mediator in these settings. It is believed that in immune cells within adipose tissue of obese animals mainly contribute to iNOS expression and the immunometabolic perturbances of obesity. To clarify the specific role of iNOS induction in adipocytes, muscle and liver in the development of insulin resistance and altered energy metabolism of obese animals, mice containing flox sites flanking Exon 2 of nos2 were created. Myocyte‐specific (MuKO), hepatocyte‐specific (HeKO) and adipocyte‐specific (AdKO) iNOS knockout mice were generated on a C57BL/6J background by crossing mice homozygous for floxed iNOS (nos2 f/f ) with Ckmm‐cre, Alb‐Cre and Adipoq‐Cre, respectively. KO mice and their respective wild‐type controls were fed regular chow or a high‐fat/high sucrose (HFHS) diet for 8 weeks and then extensively phenotyped for metabolic outcomes. We found that AdKO mice were partially protected from HFHS‐diet insulin resistance as compared to WT littermates on the same diet, and that this beneficial effect was associated with increased energy expenditure as measured by indirect calorimetry. These effects were observed despite no differences in body weight gain and adiposity. Adipocyte‐specific iNOS KO was also associated with a reduction in circulating triglyceride levels upon HFHS feeding. However, disrupting iNOS selectively in skeletal muscle and liver did not improve metabolic phenotypes after 2 months of HFHS feeding. Our results reveal an unexpected role of iNOS specifically expressed in adipocytes in the development of systemic insulin resistance, dyslipidemia and altered energy metabolism in diet‐induced obesity, suggesting an important role of adipocyte NO release in the metabolic complications of obesity. The role of muscle and liver iNOS appears limited after 2 months of HFHS diet but studies are underway to document their potential impact after longer‐term feeding experiments. Support or Funding Information Canadian Institutes of Health Research This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.001
Threshold uncertainty score0.003

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0010.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.019
GPT teacher head0.265
Teacher spread0.247 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations1
Published2018
Admission routes3
Has abstractyes

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