Femoral bone structure in Otsuka Long-Evans Tokushima Fatty rats

AbstractObjectivesType 2 diabetes mellitus (T2DM) increases fracture risk despite normal to high levels of bone mineral density. Bone quality is known to affect bone fragility in T2DM. The aim of this study was to clarify the trabecular bone microstructure and cortical bone geometry of the femur in T2DM model rats.MethodsFive-week-old Otsuka Long-Evans Tokushima Fatty (OLETF; n = 5) and Long-Evans Tokushima Otsuka (LETO; n = 5) rats were used. At the age of 18 months, femurs were scanned with micro-computed tomography, and trabecular bone microstructure and cortical bone geometry were analyzed.ResultsTrabecular bone microstructure and cortical bone geometry deteriorated in the femur in OLETF rats. Compared with in LETO rats, in OLETF rats, bone volume fraction, trabecular number and connectivity density decreased, and trabecular space significantly increased. Moreover, in OLETF rats, cortical bone volume and section area decreased, and medullary volume significantly increased.ConclusionsLong-term T2DM leaded to deterioration in trabecular and cortical bone structure. Therefore, OLETF rats may serve as a useful animal model for investigating the relationship between T2DM and bone quality

The Progression of Bone and Muscle Atrophy in Mice Hind Limb with Immobilization

This study investigated the time course of changes of bone and muscle atrophy in mice with immobilization by denervation and fixation. The animals were fifty-two male C57 BL/6J mice, aged 10 weeks old. Eight mice were used as the base line, and the remaining ones were cut at the sciatic nerve of the left hind limb and fixed with a plaster cast. At week 1, 2, 3, and 4 after the operation, a cross-sectional area of the rectus femoris muscles and bone mechanical strength with a three-point bending test of the femur and tibia were measured. The time course of changes of the bone mechanical strength and of the cross-sectional area of the rectus femoris muscles between the intact and experimental limbs in each period compared with the control limbs, was determined. The bone mechanical strength of the femur, tibia, and the cross-sectional area of the rectus femoris muscles of the experimental limbs significantly decreased compared with those of the intact limbs at week 4, 3, 2 and 1 after the operation (p<0.05). Compared with the intact limbs, the bone mechanical strength and the cross-sectional area of the rectus femoris muscles of the experimental limbs declined approximately 10% and 30%, respectively, during the experiment (p<0.05). It was demonstrated that bone and muscle atrophy occurred at an early stage after immobilization by denervation and fixation, and that both types of atrophy progressed simultaneously in the present study

Oxygen therapy may worsen the survival rate in rats with monocrotaline-induced pulmonary arterial hypertension.

Although oxygen therapy rapidly improves arterial oxygen saturation in idiopathic pulmonary arterial hypertension, the effects of chronic administration of oxygen are unknown. The purpose of the present study was to investigate the effects of chronic oxygen therapy on the histological changes and survival rate in rats with idiopathic pulmonary arterial hypertension. Idiopathic pulmonary arterial hypertension was induced by monocrotaline injection. The rats were then randomly assigned to receive or not receive oxygen therapy (O2 group and non-O2 group, respectively). The rats in the O2 group were exposed to a high (90%) oxygen environment from day 17 following injection of monocrotaline, when hypoxemia was first observed. The pulmonary arteriole walls were significantly thicker in monocrotaline-injected rats than in saline-injected rats as vehicle on day 19 and were significantly thicker in the rats that received oxygen therapy than in the rats that did not. Right ventricular inflammations were significantly higher in monocrotaline-injected rats than in saline-injected rats on day 19 and were significantly higher in the rats that received oxygen therapy than in the rats that did not. By day 20 after injection of monocrotaline, the survival rate was significantly lower in the rats that received oxygen therapy than in those that did not. Superoxide dismutase activity in the lungs was higher in monocrotaline-injected rats than in saline-injected rats on day 19 after monocrotaline injection and was also higher in the saline-injected rats that received oxygen therapy than in the saline-injected rats that did not. No interaction was detected between monocrotaline injection and oxygen therapy. These results suggest that chronic oxygen therapy worsens the histological changes and survival rate in idiopathic pulmonary arterial hypertension. The fact that degradation of the histological changes and survival rate was accompanied by increase in superoxide dismutase activity suggests that antioxidant capacity may contribute to the degradation

ラット脊髄の圧迫後における神経細胞損失の経過と範囲

Motor deficits after spinal cord injury arise from damages to the descending spinal pathways and ventral motoneurons (VMN). In contrast to data on damages to the white matter or the descending spinal pathways, few quantitative data on damages to VMN after injury are available currently. The purpose of this study was to examine quantitatively the temporal and spatial pattern of VMN loss after spinal cord compression. Two groups of adult female Wistar rats were used in this study: rats which were subjected to spinal cord compression in short duration with an aneurysm clip (experimental group) and rats which were subjected to a sham-operation (control group). Using serial cross-sections of the spinal cord, VMN were counted up to the 7th day after surgical intervention at 0, 1, 2, and 3 mm rostral and caudal to the lesion epicenter (experimental group) or to the median of the serial sections (control group). At 15 minutes after the compression, VMN were lost only at the epicenter section and no VMN were observed there. By 8 hours, VMN loss had spread to next 1 mm rostral and caudal section to the epicenter. Virtually, no further loss was detected between 8 hours and later time points. This study showed that compression to the adult rat spinal cord in short duration led to VMN loss, which progressed acutely and expanded modestly. Our findings could be used to develop effective treatment and provide a better understanding of VMN loss after spinal cord injury