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Record W2606374581 · doi:10.1016/j.molmet.2017.04.003

Restoration of Lepr in β cells of Lepr null mice does not prevent hyperinsulinemia and hyperglycemia

2017· article· en· W2606374581 on OpenAlexafffund
Anna M. D'souza, Timothy J. Kieffer

Bibliographic record

VenueMolecular Metabolism · 2017
Typearticle
Languageen
FieldNeuroscience
TopicRegulation of Appetite and Obesity
Canadian institutionsUniversity of British Columbia
FundersNatural Sciences and Engineering Research Council of CanadaCanadian Institutes of Health Research
KeywordsLeptin receptorInternal medicineEndocrinologyLeptinGlucose homeostasisBiologyHyperinsulinemiaAdipose tissueCre recombinaseInsulinInsulin resistanceMedicineTransgeneGeneGenetically modified mouseObesity

Abstract

fetched live from OpenAlex

Objective The adipose-derived hormone leptin plays an important role in regulating body weight and glucose homeostasis. Leptin receptors are expressed in the central nervous system as well as peripheral tissues involved in regulating glucose homeostasis, including insulin-producing β cells of the pancreas. Previous studies assessing the role of leptin receptors in β cells used Cre- loxP to disrupt the leptin receptor gene ( Lepr ) in β cells, but variable results were obtained. Furthermore, recombination of Lepr was observed in the hypothalamus or exocrine pancreas, in addition to the β cells, and Lepr in non-β cells may have compensated for the loss of Lepr in β cells, thus making it difficult to assess the direct effects of Lepr in β cells. To determine the significance of Lepr exclusively in β cells, we chose to selectively restore Lepr in β cells of Lepr null mice ( Lepr loxTB/loxTB ). Materials and methods We used a mouse model in which endogenous expression of Lepr was disrupted by a loxP -flanked transcription blocker ( Lepr loxTB/loxTB ), but was restored by Cre recombinase knocked into the Ins1 gene, which is specifically expressed in β cells ( Ins1 Cre). We bred Lepr loxTB/loxTB and Ins1 Cre mice to generate Lepr loxTB/loxTB and Lepr loxTB/loxTB Ins1 Cre mice, as well as Lepr wt/wt and Lepr wt/wt Ins1 Cre littermate mice. Male and female mice were weighed weekly between 6 and 11 weeks of age and fasting blood glucose was measured during this time. Oral glucose was administered to mice aged 7–12 weeks to assess glucose tolerance and insulin secretion. Relative β and α cell area and islet size were also assessed by immunostaining and analysis of pancreas sections of 12–14 week old mice. Results Male and female Lepr loxTB/loxTB mice, lacking whole-body expression of Lepr , had a phenotype similar to db/db mice characterized by obesity, hyperinsulinemia, glucose intolerance, and impaired glucose stimulated insulin secretion. Despite restoring Lepr in β cells of Lepr loxTB/loxTB mice, fasting insulin levels, blood glucose levels and body weight were comparable between Lepr loxTB/loxTB Ins1 Cre mice and Lepr loxTB/loxTB littermates. Furthermore, glucose tolerance and insulin secretion in male and female Lepr loxTB/loxTB Ins1 Cre mice were similar to that observed in Lepr loxTB/loxTB mice. Analysis of pancreatic insulin positive area revealed that restoration of Lepr in β cells of Lepr loxTB/loxTB mice did not prevent hyperplasia of insulin positive cells nor did it rescue Glut-2 expression. Conclusion Collectively, these data suggest that direct action of leptin on β cells is insufficient to restore normal insulin secretion and glucose tolerance in mice without leptin receptor signaling elsewhere.

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 score0.003
Threshold uncertainty score0.010

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 communication0.0010.000
Open science0.0000.000
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0030.001

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 head0.015
GPT teacher head0.255
Teacher spread0.241 · 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".

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Citations7
Published2017
Admission routes2
Has abstractyes

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