Objective The aims of this study were to evaluate the morbidity of osteoporosis and the relationship between bone mineral density ( BMD ) and bone metabolic markers in the patients with spine degeneration disease needing surgery, at the same time to observe the influence of type 2 diabetes mellitus on bone metabolism and BMD.Methods This retrospective analysis included 139 patients suffered by spine degeneration disease needing surgery from the October 2013 to October 2014 in Beijing Jishuitan Hospital. Lumbar BMD was measured by quantitative computed tomography ( QCT) before surgery.Serum N-terminal propeptide of type I procollagen ( PINP) , βC-terminal cross-linked telopeptide of type I collagen (β-CTX), osteocalcin (OC) , 25-hydroxyvitamin D[25(OH)D], parathyroid hormone (PTH), calcium and phosphorus were quantified simultaneously.The relationship between the results of lumbar BMD measured by QCT and bone metabolic markers was analyzed by partial correlation.The differences of bone metabolic markers among three groups classified according to BMD were performed by one-way ANOVA and analysis of covariance.The influence factors of lumbar BMD measured by QCT were analyzed by multifactor linear regression.T-test was used to analyze the differences of BMD and bone metabolic markers between two groups with and without type 2 diabetes mellitus.Results The average age of 139 patients was(62.74 ± 6.83) years old.Lumbar BMD revealed that the percentage of osteoporosis, osteopenia and normal BMD were 40.2%(56/139) , 43.8% (61/139) and 16% (22/139) separately.The percentage was 47%(66/139) in subjects with 25(OH)D below 30 nmol/L.The percentage of subjects with the concentrations of 25 ( OH ) D between 30-50 nmol/L was 40% ( 55/139 ) , while the percentage of subjects with the concentrations of 25(OH)D between 50-125 nmol/L was only 13% (18/139).Partial correlation analysis revealed that lumbar BMD measured by QCT was negatively correlated with PINP ( r=-0.352, P<0.01) ,β-CTX ( r=-0.356, P<0.01 ) and OC ( r=-0.276, P=0.001 ) with gender and type 2 diabetes mellitus as covariates.Along with the age of patients increasing and BMD reducing, the levels of PINP,β-CTX and OC increased gradually and the differences were statistically significant ( F=11.575, P<0.01;F=11.550, P<0.01; F=9.738, P<0.01).Multiple linear regression analysis revealed that age and PINP were the main factors that influenced the change of BMD in the patients with spine degeneration disease needing surgery (β=-1.863, t=-5.425, P<0.01;β=-0.393, t=-2.061, P=0.041) .Subjects were divided into diabetes group and non-diabetes group according to the clinical diagnosis and whether having abnormal serum glucose.The levels of PINP (36.56 ±14.56 versus 49.51 ±16.68μg/L) ,β-CTX (0.39 ±0.20 versus 0.52 ±0.21 μg/L) and OC (14.21 ±5.13 versus 20.74 ±6.84 μg/L) in serum between two groups had significant differences (t=3.648, P<0.01;t=2.754, P<0.01;t=4.573, P<0.01) .Conclusions There was prevalence of osteoporosis, osteopenia and vitamin D deficiency in the patients with spine degeneration disease needing surgery.The patients with high level of PINP and age were more prone to appear lower BMD which increasing the risk of osteoporosis.The patients combined with type 2 diabetes mellitus had suppressed bone markers which maybe the risk factor, independent of BMD, increasing fracture risk.

Metabolic dysfunction-associated fatty liver disease （MAFLD） is a common chronic liver disease with the pathological feature of lipid accumulation in the liver， and it is closely associated with liver metabolic disorders. The latest research has shown that the pathogenesis of MAFLD is associated with the abnormal expression of specific genes， especially the fat mass and obesity-associated （FTO） gene. The abnormal activity of the FTO gene may lead to an imbalance in liver lipid metabolism， which manifests as the increase in fatty acid synthesis and the reduction in fatty acid oxidation， thereby promoting liver fat deposition and inflammatory response. Therefore， regulating the expression or activity of the FTO gene is considered one of the potential strategies for the treatment of MAFLD. At present， drug research targeting the function of the FTO gene has achieved preliminary results， and inhibition of the activity of the FTO gene can help to regulate liver lipid metabolism and alleviate liver inflammatory injury. This article reviews the mechanism of action of the FTO gene in the development and progression of MAFLD， summarizes the advances in drug research on the FTO gene and related metabolic pathways in recent years， and analyzes their application prospect in research and treatment.