ArticlePhysiological reports2017
Is the FVB/N mouse strain truly resistant to diet-induced obesity?
Article in Physiological reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
- Interactions between Tau Phosphorylation and Endoplasmic Reticulum Stress in Diabetic Nephropathy.Diabetes & metabolism journal · 2026Article
- Chronic High-Fat Diet Does Not Alter Overall Cancer Incidence in Trp53R270H/+ Mice.Cancer research communications · 2026Article
- APOL1 G1 and G2 risk alleles modulate severity of diet-induced obesity in a transgenic mouse model.bioRxiv : the preprint server for biology · 2025Article
- Short-term consumption of the modified standard American diet perturbed the metabolic balance and altered DNA damage in MMTV-PyMT transgenic mice.Breast cancer research : BCR · 2025Article
- Circulating glycerate predicts resilience to fructose-induced hepatic steatosis.Cell metabolism · 2025Article
- Obesity increases genomic instability at DNA repeat-mediated endogenous mutation hotspots.Nature communications · 2024Article
- Genetic Background Strongly Influences the Impact of Carrying the Thr92Ala-DIO2 Polymorphism in the Male Mouse.Endocrinology · 2024Article
- The Impact of Obesity on Diabetes Onset and Neovascularization in Mouse Models of Metabolic Stress.International journal of molecular sciences · 2024Article
- Reduced mitophagy is an early feature of NAFLD and liver-specific PARKIN knockout hastens the onset of steatosis, inflammation and fibrosis.Scientific reports · 2023Article
- Mouse strain-dependent variation in metabolic associated fatty liver disease (MAFLD): a comprehensive resource tool for pre-clinical studies.Scientific reports · 2023Article
- Reduced hepatocyte mitophagy is an early feature of NAFLD pathogenesis and hastens the onset of steatosis, inflammation and fibrosis.Research square · 2023Article
- The double-hit protocol induces HFpEF and impairs myocardial ubiquitin-proteasome system performance in FVB/N mice.Frontiers in physiology · 2023Article
- The placental vasculature is affected by changes in gene expression and glycogen-rich cells in a diet-induced obesity mouse model.PloS one · 2023Article
- FVB/N mouse strain regulatory T cells differ in phenotype and function from the C57BL/6 and BALB/C strains.FASEB bioAdvances · 2022Article
- The role of obesity and bariatric surgery-induced weight loss in breast cancer.Cancer metastasis reviews · 2022Review
- Differential effects of acute versus chronic dietary fructose consumption on metabolic responses in FVB/N mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Non-Obese MKR Mouse Model of Type 2 Diabetes Reveals Skeletal Alterations in Mineralization and Material Properties.JBMR plus · 2022Article
- The Na/K-ATPase α1/Src interaction regulates metabolic reserve and Western diet intolerance.Acta physiologica (Oxford, England) · 2021Article
- Strain-specific differences in muscle CaThe Journal of experimental biology · 2021Article
- Mouse models for V103I and I251L gain of function variants of the human MC4R display decreased adiposity but are not protected against a hypercaloric diet.Molecular metabolism · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C57Bl/6J mice are the gold standard animal model of diet-induced obesity. These animals become obese with higher adiposity, blood fasting glucose, triglycerides, and total cholesterol when fed a high-fat diet (HFD). Conversely, the FVB/N mouse line is thought to be resistant to diet-induced obesity, with low or no weight gain and adiposity in response to a HFD In this study, we investigated whether FVB/N mice are resistant or susceptible to metabolic disorder that is promoted by a HFD Biometric parameters and blood chemistry were analyzed in C57Bl/6J and FVB/N mice that were fed a chow diet or HFD Glucose and insulin sensitivity were assessed by performing the glucose tolerance test and measuring serum insulin/glucose and homeostasis model assessment-insulin resistance. Metabolism-related gene expression was investigated by real-time reverse transcription polymerase chain reaction. Adipocyte morphology and liver steatosis were evaluated using standard histology. FVB/N mice had higher adiposity than C57Bl/6J mice that were fed a chow diet and were glucose intolerant. FVB/N mice that were fed a HFD presented higher insulin resistance and greater liver steatosis. Epididymal white adipose tissue exhibited severe inflammation in FVB/N mice that were fed a HFD The FVB/N mouse strain is suitable for studies of diet-induced obesity, and the apparent lack of a HFD-induced response may reveal several strain-specific events that are triggered by a HFD Further studies of the FVB/N background may shed light on the complex multifactorial symptoms of obesity and metabolic syndrome.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.