Dataset: Col1a1Jrt mouse model on long-term low-fat and high-fat-diet.

Published: 12 August 2021| Version 1 | DOI: 10.17632/np7kpnk9t4.1
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Description

Male and female mice with a dominant severe bone fragility disorder, osteogenesis imperfecta (Col1a1Jrt mouse model), and their wild-type littermates (FVB background) were challenged with a long-term (26 weeks) high-fat diet to evaluate the development of obesity and glucose intolerance. Here we present data for the measurements of body mass, the outcome of glucose homeostasis during the long-term diet, as well as organ weights and bone phenotype at the end of the study. Interpretation of the data and further in-depth analysis can be found in the article “Male but not female mice with severe osteogenesis imperfecta are partially protected from high-fat diet-induced obesity.” by Tauer JT, Boraschi-Diaz I, Al Rifai O, Rauch F, Ferron M, Komarova SV, to be published in Molecular Genetics and Metabolism. The data presented here demonstrate individual mouse outcomes of long-term diet experiments that can be reused for comparative studies of diet-induced changes in wild-type mice on different backgrounds and different mouse models of osteogenesis imperfecta.

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Male and female wild-type (WT, FVB background) and Col1a1Jrt/+ mice (OI) were randomly assigned to treatment with either a high-fat/low-sugar diet (Teklad Custom Diet, #TD.06414) or control low-fat/low-sugar diet (Teklad Custom Diet, #TD.180127) starting at an age of 4 weeks until 30 weeks of age (diet length: 26 weeks). Animals were housed under standard conditions with 12-h alternating light and dark cycle and unrestricted access to water and food. Body mass was recorded weekly using portable compact balance (OHAUS Corporation, Model CS200, Parsippany, US). Glucose tolerance tests were performed every four weeks using ONETOUCH VerioFlex glucometer (LifeScan Europe, Zug, Switzerland). At the end of the study, mice were anesthetized using isoflurane inhalation and terminated by intracardiac puncture followed by cervical dislocation. Soft tissues were isolated, weighted (analytical balance (Denver Instrument GmbH, Model P-114, Goettingen, Germany)) and snap-frozen in liquid nitrogen. Right and left femora were isolated as well, length measured using digital caliper (Starrett, Model EC799A-6/150, Athol, US), and stored at −20 °C in phosphate buffered saline-soaked gauze until testing. Right femurs were collected for ex vivo micro-computed tomography using Skyscan 1272 (Bruker, MA, US) and its corresponding analysis software Skyscan CT Analyser (Version 1.16.1.0, Bruker, MA, US) and three-point bending test using a Materials Testing System Model 5943 (INTRON, Norwood, MA, USA). Further description of used methods, instruments etc. can be found in the article "Data on body mass, glucose tolerance and bone phenotype of mice with osteogenesis imperfecta on long-term low-fat and high-fat diets." by Tauer JT, Boraschi-Diaz I, Komarova SV, to be published in Data in Brief. Interpretation of the data and further in-depth analysis can be found in the article “Male but not female mice with severe osteogenesis imperfecta are partially protected from high-fat diet-induced obesity.” by Tauer JT, Boraschi-Diaz I, Al Rifai O, Rauch F, Ferron M, Komarova SV, to be published in Molecular Genetics and Metabolism.