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Divergent Compensatory Responses to High Fat Diet Between C57BL6/J and C57BLKs/J Inbred Mouse Strains

ABSTRACT: To assess whether changes in islet gene expression contribute to differences in phenotypes in response to high fat diet or tretament with pioglitazone, Agilent Whole Mouse Genome Oligo Microarrays were performed on RNA isolated from islets of 4 mice per each treatment group for discovery analysis of gene expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE51055 | GEO | 2013/09/21

SECONDARY ACCESSION(S): PRJNA219844

REPOSITORIES: GEO

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Divergent Compensatory Responses to High Fat Diet Between C57BL6/J and C57BLKs/J Inbred Mouse Strains

Project description:To assess whether changes in islet gene expression contribute to differences in phenotypes in response to high fat diet or tretament with pioglitazone, Agilent Whole Mouse Genome Oligo Microarrays were performed on RNA isolated from islets of 4 mice per each treatment group for discovery analysis of gene expression. Male 8 week-old BL6 and BLKS mice were fed normal chow (18% kcal from fat), HFD (42% kcal from fat), or HFD supplemented with the PPAR-Î³ agonist pioglitazone (PIO) (140 mg PIO/kg diet) for 16 weeks.

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Divergent compensatory responses to high-fat diet between C57BL6/J and C57BLKS/J inbred mouse strains.

Project description:Impaired glucose tolerance (IGT) and type 2 diabetes (T2DM) are polygenic disorders with complex pathophysiologies; recapitulating them with mouse models is challenging. Despite 70% genetic homology, C57BL/6J (BL6) and C57BLKS/J (BLKS) inbred mouse strains differ in response to diet- and genetic-induced obesity. We hypothesized these differences would yield insight into IGT and T2DM susceptibility and response to pharmacological therapies. To this end, male 8-wk-old BL6 and BLKS mice were fed normal chow (18% kcal from fat), high-fat diet (HFD; 42% kcal from fat), or HFD supplemented with the PPAR? agonist pioglitazone (PIO; 140 mg PIO/kg diet) for 16 wk. Assessments of body composition, glucose homeostasis, insulin production, and energy metabolism, as well as histological analyses of pancreata were undertaken. BL6 mice gained weight and adiposity in response to HFD, leading to peripheral insulin resistance that was met with increased ?-cell proliferation and insulin production. By contrast, BLKS mice responded to HFD by restricting food intake and increasing activity. These behavioral responses limited weight gain and protected against HFD-induced glucose intolerance, which in this strain was primarily due to ?-cell dysfunction. PIO treatment did not affect HFD-induced weight gain in BL6 mice, and decreased visceral fat mass, whereas in BLKS mice PIO increased total fat mass without improving visceral fat mass. Differences in these responses to HFD and effects of PIO reflect divergent human responses to a Western lifestyle and underscore the careful consideration needed when choosing mouse models of diet-induced obesity and diabetes treatment.

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Project description:To explore the molecular pathways underlying thiazolidinediones effects on pancreatic islets in conditions mimicking normo- and hyperglycemia, apoptosis rate and transcriptional response to Pioglitazone at both physiological and supraphysiological glucose concentrations were evaluated. Adult rat islets were cultured at physiological (5.6 mM) and supraphysiological (23 mM) glucose concentrations in presence of 10 mM Pioglitazone or vehicle. RNA expression profiling was evaluated with the PancChip 13k cDNA microarray after 24-h, and expression results for some selected genes were validated by qRT-PCR.

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Pancreatic islet expression profiling in diabetes prone C57BLKS/J mice vs C57BL6/J mice.

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