Chronic Hyperglycemia before Spinal Cord Injury Increases Inflammatory Reaction and Astrogliosis after Injury: Human and Rat Studies.

Traumatic spinal cord injury (SCI) can cause permanent disabilities that seriously reduce quality of life. We evaluated the effects of chronic hyperglycemia before SCI on inflammatory markers and functional recovery after SCI in human patients and a rat model. In the human study, multivariate logistical regression analysis revealed that hemoglobin A1c (HbA1c) values, reflecting average plasma glucose concentration over a 3 month period, at admission were a significant risk factor for poor functional recovery. Moreover, patients with chronic hyperglycemia (HbA1c ≥ 6.5%) had high concentrations of inflammatory biomarkers (interleukin [IL]-6 and IL-8) of cerebrospinal fluid after SCI. Consistent with patient findings, chronic hyperglycemia before SCI in rats was associated with increased inflammatory responses and oxygen-free radicals in the spinal cord and blood, thus resulting in poor functional recovery and histological outcomes. Tight glucose control before SCI decreased the harmful effects of hyperglycemia after SCI in both human and rat studies. Our findings suggest that chronic hyperglycemia before SCI may be a significant prognostic factor with a negative impact on functional and histological outcomes, highlighting the importance of tight glucose control before SCI.

Relationships between vitamin D and paraspinal muscle: human data and experimental rat model analysis.

BACKGROUND CONTEXT: Vitamin D deficiency (VDD) has been closely linked with skeletal muscle atrophy in many studies, but to date no study has focused on the paraspinal muscle. PURPOSE: To verify paraspinal muscle changes according to serum vitamin D level. STUDY DESIGN: A cross-sectional study of patients who visited our hospital and an in vivo animal study. METHODS: We measured serum vitamin D concentration in 91 elderly women and stratified them according to their vitamin D status in three groups, control, vitamin D insufficiency, and VDD, and obtained magnetic resonance imaging data of the lumbar spine and evaluated the quality and quantity of the paraspinal muscles. Additionally, we designed experimental rat models for VDD and VDD replacement. Then, we analyzed the microcomputed tomography data and histologic data of paraspinal muscles, and the histologic data and reverse transcription-quantitative polymerase chain reaction data of intramyonuclear vitamin D receptor (VDR) in paraspinal muscle through comparison with control rats (n=25, each group). This work was supported by a Biomedical Research Institute grant ($40,000), Kyungpook National University Hospital (2014). RESULTS: In the human studies, a significant decrease was noted in the overall paraspinal muscularity (p<.05) and increase in fatty infiltration in the VDD group as compared with the other groups (p<.05). In the rat experiment, a decrease was noted in paraspinal muscle fiber size and VDR concentration and VDR gene expression level, and total muscle volume of the VDD rats as compared with the control rats (p<.05). Vitamin D replacement after VDD could partially restore the muscle volume, muscle fiber size, and intramyonuclear VDR concentration levels (p<.05) of the paraspinal muscles. CONCLUSIONS: VDD induces paraspinal muscle atrophy and decreases the intramyonuclear VDR concentration and VDR gene expression level in these muscles. Vitamin D replacement contributes to the recovery from atrophy and restoration of intramyonuclear VDR concentration in VDD status.