Dataset: OI/OCN mouse model on long-term low-fat and high-fat-diet.

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.本研究拓展了既往研究结论，即骨源性激素骨钙素（osteocalcin, OCN）可能在成骨不全症（osteogenesis imperfecta, OI）小鼠的代谢调控中发挥作用。雌性成骨不全症小鼠在饲喂高脂饮食（high-fat diet, HFD）时易出现肥胖、高血糖及葡萄糖耐受异常，而雄性小鼠则可免受该影响，这可能与血清OCN水平升高相关的能量消耗增加有关。为明确OCN是否介导上述效应，研究人员将成骨不全症小鼠（Col1a1Jrt/+；FVB背景）与骨钙素敲除小鼠（Bglap-/-；C57BL6J背景）进行杂交，获得混合背景的OI/OCN小鼠。随后对雌雄OI/OCN小鼠分别进行长期低脂饮食（low-fat diet, LFD）或高脂饮食造模。本研究记录了26周饮食干预后的体质量、体表温度、葡萄糖耐受与胰岛素耐受情况、脏器重量及胰腺胰岛素水平。数据显示，OCN失活可部分挽救成骨不全症小鼠的代谢表型，表明该过程同时依赖OCN相关与OCN非相关机制。详细解读可参见"Osteocalcin-dependent and -independent metabolic dysregulation in a mouse model of osteogenesis imperfecta"（Tauer JT, Rauch F, Ferron M, Komarova SV, Metabolism）。本数据集收录了长期饮食干预实验的个体结局数据，可用于混合背景下野生型与成骨不全症小鼠模型饮食诱导代谢变化的比较研究。