Dataset: OI/OCN mouse model on long-term low-fat and high-fat-diet.
Description
This study extends previous research suggesting that osteocalcin (OCN), a hormone produced by bone, may play a role in metabolic regulation in osteogenesis imperfecta (OI) mice. Female OI mice tend to develop obesity, hyperglycemia, and glucose intolerance when fed a high-fat diet (HFD), whereas males are protected, possibly because of increased energy expenditure associated with higher serum OCN levels. To determine whether OCN drives these effects, OI mice (Col1a1Jrt/+; FVB background) were crossed with OCN knockout mice (Bglap-/-; C57BL6J background), generating OI/OCN mice on a mixed background. Male and female OI/OCN mice were then challenged with long-term low-fat (LFD) or HFD. We report body mass, body surface temperature, glucose and insulin tolerance, organ weights, and pancreatic insulin levels after 26 weeks of diet. The data show that OCN inactivation partially rescues the metabolic phenotype of OI mice, indicating contributions from both OCN-dependent and OCN-independent mechanisms. Detailed interpretation is available in “Osteocalcin-dependent and -independent metabolic dysregulation in a mouse model of osteogenesis imperfecta” (Tauer JT, Rauch F, Ferron M, Komarova SV, Metabolism). The dataset presented here provides individual outcomes from long-term diet experiments and can be reused for comparative studies of diet-induced changes in wild-type and OI mouse models on mixed backgrounds.
Files
Steps to reproduce
Male and female mice 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 and an Insulin tolerance test once towards the end of the diet study using ONETOUCH VerioFlex glucometer (LifeScan Europe, Zug, Switzerland). One to two days before termination, mice were scanned for adiposity assessment using in vivo micro-computed tomography. 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. 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.
Institutions
- Shriners Hospitals for Children CanadaQC, Montreal
- Johannes Kepler University of LinzUpper Austria, Linz