Middle-aged premenopausal women with type 1 diabetes have lower bone mineral density and calcaneal quantitative ultrasound than nondiabetic women

OBJECTIVE: To determine whether middle-aged premenopausal women with type 1 diabetes had more self-reported fractures and lower bone mineral density (BMD) compared with nondiabetic women. RESEARCH DESIGN AND METHODS: Participants were premenopausal women aged 35-55 years with type 1 diabetes (n = 67; 32.2 +/- 5.3 years duration) and without diabetes (n = 237). Total hip, femoral neck, whole-body, and spine BMD were measured by dual X-ray absorptiometry. Calcaneal broadband ultrasound attenuation (BUA) was assessed with quantitative ultrasound. RESULTS: Women with type 1 diabetes were more likely to report a fracture after age 20 years compared with nondiabetic women (33.3 vs. 22.6%; age-adjusted odds ratio 1.89 [95% CI 1.02-3.49]). Type 1 diabetes was associated with lower total hip BMD (0.890 vs. 0.961 g/cm2; P < 0.001), femoral neck BMD (0.797 vs. 0.847 g/cm2; P = 0.001), whole-body BMD (1.132 vs. 1.165 g/cm2; P < 0.01), and lower calcaneal BUA (71.6 vs. 84.9 dB/MHz; P < 0.001) after multivariate adjustment. BMD was 3-8% lower in type 1 diabetic compared with control women and calcaneal BUA was 15% lower. Spine BMD and biomarkers of bone remodeling were not significantly different between groups. In the type 1 diabetic women, reduced monofilament detection and blindness were both associated with lower BMD. CONCLUSIONS: Lower BMD in premenopausal women with type 1 diabetes may substantially increase their risk of developing osteoporosis after menopause. Type 1 diabetic women should be targeted for osteoporosis screening and possible fracture prevention as they transition through menopause.     

老年2型糖尿病患者骨密度与血清胰岛素水平和BMI关系的临床观察

目的研究老年2型糖尿病(DM)患者骨密度的改变及探讨其与胰岛素水平的关系。方法应用DEXA测定38例老年2型DM患者和26例老年健康对照组L2-4及股骨近端骨密度(BMD)并测定2型DM患者血清胰岛素(Ins)及体重指数(BM I)。结果①2型糖尿病中男、女W ard`s区、男性腰椎、女性股骨颈BMD均显著低于正常对照组(P<0.05);男性股骨颈、女性腰椎的BMD低于正常对照组,但无统计学意义(P>0.05)。②将DM患者分成骨质疏松组(OP组)和非骨质疏松组(非OP组),比较两组的血Ins水平和BM I,发现非OP组空腹及餐后2 h Ins水平和BM I明显高于OP组(P<0.05)。结论①老年2型DM患者较易发生OP。②肥胖和血中高胰岛素水平对骨密度有一定保护作用。     

Does low bone mineral density start in post-teenage years in women with type 1 diabetes?

OBJECTIVE: Type 1 diabetes has been associated with decreased bone mineral density (BMD). However, the natural history and etiopathogenesis of osteoporosis in type 1 diabetes are not clear. The aims of this study were to assess BMD in a cohort of young women with type 1 diabetes compared with nondiabetic control subjects and to evaluate the possible association of BMD with diabetes duration, HbA(1c), and biomarkers of bone metabolism. RESEARCH DESIGN AND METHODS: BMD was measured by dual-energy X-ray absortiometry scan in 39 teenage (age 13-19 years) and 33 post-teenage females (age 20-37 years) with type 1 diabetes and 91 female age-matched control subjects. Serum osteocalcin, IGF-I, IGF binding protein-3 (IGFBP-3), HbA(1c), and urine N-telopeptides were measured. RESULTS: After adjustment for age and BMI, BMD values were significantly lower at the femoral neck and lateral spine in women with type 1 diabetes older than age 20 years compared with control subjects but not in the case subjects younger than age 20 years, nor at the anterio-posterior spine, wrist, or whole body. No association was found between BMD and diabetes duration or glycemic control. IGF-I, IGFBP-3, osteocalcin, and N-telopeptides were similar in diabetic subjects and control subjects. CONCLUSIONS: This study indicates that women with type 1 diabetes exhibit BMD differences early in life with significant differences already present in the post-teenage years. Lower hip BMD in these young women may explain, in part, the higher incidence of hip fracture experienced in postmenopausal women with type 1 diabetes.     

Young women with type 1 diabetes have lower bone mineral density that persists over time

OBJECTIVE—Individuals with type 1 diabetes have decreased bone mineral density (BMD), yet the natural history and pathogenesis of osteopenia are unclear. We have previously shown that women with type 1 diabetes (aged 13–35 years) have lower BMD than community age-matched nondiabetic control subjects. We here report 2-year follow-up BMD data in this cohort to determine the natural history of BMD in young women with and without diabetes.RESEARCH DESIGN AND METHODS—BMD was measured by dual-energy X-ray absorptiometry at baseline and 2 years later in 63 women with type 1 diabetes and in 85 age-matched community control subjects. A1C, IGF-1, IGF binding protein-3, serum osteocalcin, and urine N-teleopeptide were measured at follow-up.RESULTS—After adjusting for age, BMI, and oral contraceptive use, BMD at year 2 continued to be lower in women ≥20 years of age with type 1 diabetes compared with control subjects at the total hip, femoral neck, and whole body. Lower BMD values were observed in cases <20 years of age compared with control subjects; however, the differences were not statistically significant. Lower BMD did not correlate with diabetes control, growth factors, or metabolic bone markers.CONCLUSIONS—This study confirms our previous findings that young women with type 1 diabetes have lower BMD than control subjects and that these differences persist over time, particularly in women ≥20 years of age. Persistence of low BMD as well as failure to accrue bone density after age 20 years may contribute to the increased incidence of osteoporotic hip fractures seen in postmenopausal women with type 1 diabetes.Type 1 diabetes is an autoimmune disorder resulting in loss of pancreatic insulin-producing β-cells that presents in childhood or early adulthood. Along with increased risk of complications including retinopathy, nephropathy, neuropathy, and cardiovascular events, adults with type 1 diabetes have decreased bone mineral density (BMD) compared with control subjects (1,2). In fact, osteoporosis is the most significant metabolic bone disease in individuals with diabetes (3). Patients with diabetes are at risk for osteoporosis and its complications, including hip fracture (4,5).Recent studies demonstrate that diabetes is associated with alterations in bone health in children and adolescents. Prepubertal and pubertal patients with type 1 diabetes (aged <15 years) have decreased bone mass measured both by duel-energy X-ray absorptiometry (DEXA) scan and quantitative ultrasound (6–8). These observations suggest that adverse effects on bone health may occur early after the diabetes diagnosis. Understanding the natural history of BMD changes in young adults with type 1 diabetes may elucidate how the disease progresses and provide opportunities for prevention of significant bone loss and, presumably, fracture.We demonstrated previously that premenopausal women (aged 20–35 years) with type 1 diabetes have lower BMD at the femoral neck and lateral spine than nondiabetic control subjects (7). This difference was not associated with diabetes duration, metabolic control, or biochemical markers of bone formation, a finding supported by previous work (9,10). Few studies have followed young women longitudinally to assess whether bone mineral acquisition or turnover play a role in the natural history of low BMD in diabetes. The aim of this study was to address the natural history of bone metabolism in type 1 diabetes by performing a follow-up DEXA 2 years after baseline enrollment to determine whether differences persist over time.     

胰岛素治疗对2型糖尿病患者骨代谢的影响

目的探讨胰岛素治疗对2型糖尿病患者骨代谢的影响及可能机制。方法收集547例2型糖尿病患者(口服降糖药188例:B组,应用胰岛素349例:C组)临床资料,测定骨密度(BMD)、空腹血糖、糖化血红蛋白、血钙、血磷、碱性磷酸酶,并对两组患者上述指标进行比较;另设健康对照组(A组)282例,与2型糖尿病患者骨密度进行比较。结果 (1)与健康对照组相比,2型糖尿病患者骨密度降低(P<0.05);(2)C组与B组相比,两组间骨密度无统计学差异,C组男女间比较,男性骨密度高于女性(P<0.05);(3)B组和C组血钙、血磷、血碱性磷酸酶无统计学差异,C组HbA1c明显低于B组(P<0.05);(4)2型糖尿病患者的骨密度与病程、年龄负相关,与体重正相关。结论女性、高龄、病程长、低体重是糖尿病合并骨质疏松的危险因素,胰岛素治疗对2型糖尿病患者骨代谢无明显影响。     

甲状旁腺素、维生素D受体、雌激素受体基因多态对糖尿病患者骨密度的影响

目的探讨甲状旁腺素(PTH)基因多态与中国北方汉族人糖尿病患者骨密度的关系。分析维生素D受体(VDR)、雌激素受体(ER)基因多态性对PTH基因多态性与骨密度、骨量减少及骨质疏松关系的影响。方法运用PCR-RFLP技术检测1型糖尿病(T1DM)组54例、2型糖尿病(T2DM)组104例、健康对照(CON)组102例的中国北方汉族人PTH基因多态性。结果甲状旁腺素基因型和等位基因分布频率在T1DM组、T2DM组与CON组间差异无统计学意义(P0.05);DM患者Bb/bb基因型者发生骨量减少/骨质疏松的相对危险度增加(OR=2.8684)。联合VDR基因多态分析,Bbaa基因型组糖尿病患者并发骨量减少/骨质疏松的相对危险度增高(OR=4.3125);联合ER基因多态分析,bPxx基因型骨量减少/骨质疏松的相对危险度也增高(OR=4.0);联合分析PTH、VDR、ER基因型,同时存在3个或4个易感基因型者伴有骨量减少或骨质疏松,相对危险度增加(OR=5.5385)。结论糖尿病患者PTH基因多态性(BST B1位点)可能是预测骨量减少、骨质疏松易感性的遗传标志。联合VDR、ER基因多态有助于识别DM患者发生骨质疏松的高危人群。     

Effect of alendronate on bone mineral density and biochemical markers of bone turnover in type 2 diabetic women: the fracture intervention trial

OBJECTIVE: Alendronate sodium (ALN) increases bone mineral density (BMD) in heterogeneous populations of postmenopausal women, but its effect is unknown in women with type 2 diabetes. The objective of this project was to compare changes in BMD during 3 years of ALN treatment versus placebo in diabetic women. RESEARCH DESIGN AND METHODS: We used data from the Fracture Intervention Trial, a randomized blinded placebo-controlled trial conducted at 11 centers in which 6458 women aged 54-81 years with a femoral neck BMD of or=200 mg/dl. RESULTS: In diabetic women, 3 years of ALN treatment was associated with increased BMD at all sites studied, including 6.6% at the lumbar spine and 2.4% at the hip, whereas women in the placebo group experienced a decrease in BMD at all sites except the lumbar spine. The safety/tolerability of ALN was similar to placebo, except for abdominal pain, which was more likely in the ALN group. CONCLUSIONS: ALN increased BMD relative to placebo in older women with type 2 diabetes and was generally well tolerated as a treatment for osteoporosis. Increases in BMD with ALN therapy compared with placebo were similar between women with and without diabetes.     

2型糖尿病女性患者骨密度与骨转换率的相关性

目的探讨2型糖尿病(T2DM)女性患者骨密度与骨转换及骨重建的相关性。方法回顾性分析纳入在南方医科大学第三附属医院内分泌科住院的201例T2DM女性患者住院期间的临床数据,采用双能X线骨密度仪,测量骨密度,包括腰椎、左侧股骨颈和髋部总体,将纳入对象分为骨量正常组85例(T>-1)、骨量减少组87例(-2.5 < T < -1)和骨质疏松组29例(T < -2.5),检测骨钙素N端中分子片段和β-Ⅰ型胶原C-末端交联分别评估骨形成和骨吸收。根据骨形成和骨吸收的T值分别计算骨转换率和骨重建率,比较T2DM患者骨质疏松组和骨量正常组患者的的骨转换率T值以及骨重建率T值的差异,并评估T2DM女性患者骨转换率T值和骨重建率T值与骨密度之间的相关性。结果T2DM女性患者骨质疏松组的骨转换率T值与T2DM女性患者骨量正常组的骨转换率T值差异有统计学意义(P=0.041),T2DM女性患者骨转换率T值与髋部骨密度负相关(r=-0.14,P =0.049)。校正糖化血红蛋白后,T2DM女性患者骨转换T值与髋部仍呈骨密度负相关(r=-0.144,P=0.043)。结论在T2DM女性患者中,随着骨转换率的增高,患者骨密度越低,并发低创伤性骨折的风险也会随之增高。      

Oxidation, type 2 diabetes, and coronary heart disease: a complex interaction: findings from a population-based study

OBJECTIVE—The purpose of this study was to analyze the interrelationship among oxidation, myocardial infarction (MI), and type 2 diabetes in a population-based case-control study of MI.RESEARCH DESIGN AND METHODS—Participants were 1,709 individuals from western New York: 257 women and men with incident MI and 1,452 healthy control subjects (aged 35–70 years). Lipid peroxidation was measured by plasma levels of thiobarbituric acid reactive substances (TBARS). History of type 2 diabetes was determined by self-reported history of medical diagnosis.RESULTS—In multivariate analyses, there was no significant difference in TBARS levels between case and control subjects in both sexes. In subgroup analyses by diabetes status, diabetic subjects, regardless of MI status, exhibited significantly higher TBARS values than nondiabetic subjects. For diabetic women, TBARS values were 1.84 and 1.83 nmol/ml for case and control subjects, respectively. Values for nondiabetic women were 1.29 and 1.31 nmol/ml, respectively. In diabetic men, values were 1.65 and 1.97 nmol/ml for case and control subjects, respectively. Values for nondiabetic men were 1.36 and 1.36 nmol/ml, respectively.CONCLUSIONS—Whereas type 2 diabetes may be an important correlate of lipid peroxidation, clinical coronary heart disease may not.Oxidation has been hypothesized to be one of the plausible pathogenic mechanisms underlying the associations between coronary heart disease (CHD) and abnormalities in glucose and insulin metabolism (1). Although several studies have demonstrated the presence of increased oxidative stress in either CHD or type 2 diabetes individually, very little is known about the interrelationship among oxidation, clinical atherosclerosis, and type 2 diabetes in the general population. Thus, the current analysis attempts to examine this complex interaction using data from a population-based case-control study of myocardial infarction (MI) among residents of two western New York counties.     

Increased plasma-soluble tumor necrosis factor-alpha receptor 2 level in lean nondiabetic offspring of type 2 diabetic subjects

OBJECTIVE: Tumor necrosis factor-alpha (TNF-alpha) is one of the proposed mediators of insulin resistance, upregulated in human obesity. Insulin resistance, however, might precede the development of obesity, especially in subjects with a family history of type 2 diabetes. Therefore, the aim of the present study was to assess plasma levels of TNF-alpha and soluble forms of its receptors (soluble TNF-alpha receptors 1 [sTNFR1] and 2 [sTNFR2]) and to evaluate the relationship of the TNF-alpha system with insulin resistance in lean, nondiabetic offspring of type 2 diabetic patients. RESEARCH DESIGN AND METHODS: We compared 20 lean offspring (BMI <25 kg/m(2), 8 men and 12 women) of type 2 diabetic patients with 20 lean subjects with no family history of diabetes, matched for age, sex, and BMI (control group). Anthropometry and blood biochemical parameters were measured, and insulin sensitivity was evaluated with the euglycemic-hyperinsulinemic clamp technique. RESULTS: Both men and women in the offspring group were markedly more insulin-resistant and had higher plasma levels of sTNFR2 (all P < 0.05). TNF-alpha, sTNFR1, and other examined parameters did not differ between the studied groups. Both TNF-alpha receptors were related to waist-to-hip ratio (WHR), fat-free mass (FFM), plasma total cholesterol, HDL cholesterol, LDL cholesterol, and nonesterified fatty acids (NEFAs). sTNFR2, but not sTNFR1, was also associated with insulin sensitivity (r = -0.49, P = 0.001). This relationship remained significant after adjustment for WHR, FFM, plasma insulin, and NEFA. CONCLUSIONS: TNF-alpha system might be involved in modulating insulin action before the onset of obesity in subjects at high risk for type 2 diabetes.     

Low Serum Level of the Endogenous Secretory Receptor for Advanced Glycation End Products (esRAGE) Is a Risk Factor for Prevalent Vertebral Fractures Independent of Bone Mineral Density in Patients With Type 2 Diabetes

OBJECTIVE

Patients with type 2 diabetes are known to have an increased risk for fracture compared with non–type 2 diabetic control subjects, despite having higher bone mineral density (BMD). We previously showed that serum pentosidine, one of the advanced glycation end products (AGEs), was associated with prevalent vertebral fractures (VFs) in those with type 2 diabetes. The involvement of the endogenous secretory receptor for AGEs (esRAGE) in VFs in those with type 2 diabetes, however, is still unknown.

RESEARCH DESIGN AND METHODS

We compared parameters including esRAGE, pentosidine, and BMD in Japanese type 2 diabetic patients (137 men >50 years old and 140 postmenopausal women) with and without VFs.

RESULTS

The esRAGE-to-pentosidine ratio in type 2 diabetic patients with VFs was significantly lower than in those without VFs (men: 7.1 ± 2.8 vs. 9.4 ± 6.2, P = 0.013, respectively; women: 4.7 ± 2.7 vs. 8.2 ± 5.4, P < 0.001, respectively). Multivariate logistic regression analysis adjusted for age, BMI, A1C, serum creatinine, duration of diabetes, therapeutic agents, diabetes complications, osteoporotic risk factors, and lumbar BMD identified the serum esRAGE level and esRAGE-to-pentosidine ratio as factors associated with the presence of VFs, independent of BMD in men (odds ratio [OR] 0.46 [95% CI 0.25–0.84], P = 0.012; and OR 0.34 [0.15–0.76], P = 0.009, respectively) and in women (OR 0.32 [0.16–0.67], P = 0.002; and OR 0.14 [0.04–0.43], P = 0.001, respectively).

CONCLUSIONS

These results show that serum esRAGE level and esRAGE-to-pentosidine ratio are more useful than BMD for assessing the risk of VFs in type 2 diabetic patients.The association between diabetes and osteoporosis has been investigated in many studies because these two disorders affect a large proportion of the elderly population. Recent meta-analyses of accumulating studies have shown that patients with type 2 diabetes have an increased risk for hip fracture compared with non–type 2 diabetic control subjects, despite their higher bone mineral density (BMD) (1,2). We have also shown that patients with type 2 diabetes have an increased risk for vertebral fractures (VFs) and that BMD at any site fails to assess the risk of VF (3). Because bone strength reflects integration of bone density and bone quality (4), these findings suggest that bone quality may be more important than bone density in defining bone strength in type 2 diabetic patients.Bone quality is known to be determined by bone architecture, turnover, accumulation of microdamage, mineralization, and properties of bone matrix proteins such as collagen (4). In diabetic patients, advanced glycation end products (AGEs) are generated by sequential nonenzymatic glycosylation of protein amino groups (5). Pentosidine is one of the well-known AGEs, and its bone content in spontaneous diabetic rats has been shown to increase concurrently with the onset of diabetes, resulting in impaired mechanical properties of the bone despite normal BMD (6). We have shown clinically that the serum pentosidine level is associated with the presence of VFs in postmenopausal diabetic women independent of BMD (7). These findings suggest that AGEs, including pentosidine, may act as causative factors for poor bone quality in type 2 diabetic patients.The receptor for AGEs (RAGE) belongs to the immunoglobulin superfamily of cell surface receptors and is capable of interacting with multiple ligands, including AGEs (8). When transgenic mice overexpressing human RAGE in vascular cells were crossbred with a transgenic line that develops insulin-dependent diabetes shortly after birth, a more progressive histological change of diabetic nephropathy was observed compared with controls (9), confirming that RAGE is associated with the development of diabetes complications. Endogenous secretory RAGE (esRAGE), a splice variant of one of the naturally occurring secretory forms, is known to carry all the extracellular domains but lacks the transmembrane and cytoplasmic domains (10). Secreted esRAGE in the extracellular space is thought to act as a decoy receptor that binds AGEs and results in reducing the activity of intercellular signal pathways via RAGE (10). Indeed, administration of a genetically engineered murine-soluble RAGE suppressed the development of diabetic atherosclerosis in a dose-dependent manner in streptozotocin-induced apoE-null diabetic mice (11). Recently, RAGE-knockout mice have been shown to increase BMD and biomechanical bone strength by decreasing osteoclast formation as well as serum levels of interleukin-6 and pyridinoline (12). We have also shown that the combination of high glucose with AGEs inhibits osteoblastic mineralization through glucose-induced increases in the expression of RAGE in vitro (13). These experimental findings suggest that enhanced RAGE activity may also be clinically linked to reduced bone strength in diabetic patients. Given the neutralizing nature of esRAGE, it is possible that the ratio of serum esRAGE-to-AGE levels could be linked to clinical bone problems, such as fractures, more prominently than either parameter alone.To examine this issue, we compared serum levels of esRAGE and pentosidine as well as the esRAGE-to-pentosidine ratio between type 2 diabetic patients with and without VFs and evaluated the usefulness of these markers for assessing the risk of VFs in the population.     

Elevated hip fracture risk in type 1 diabetic patients: a population-based cohort study in Sweden

OBJECTIVE: Patients with type 1 diabetes often have low bone mineral density, but epidemiological data on fracture risk are sparse and imprecise, particularly for men. RESEARCH DESIGN AND METHODS: In the Swedish Inpatient Register, we identified a population-based cohort of 24,605 patients (12,551 men and 12,054 women) who were hospitalized for diabetes before age 31 years during 1975 through 1998. Follow-up for hip fracture was accomplished through cross-linkage in the Inpatient Register until the end of 1998. Censoring information was obtained from the registers of Death and Migration. Using the Kaplan-Meier method, we calculated the cumulative probability of getting a hip fracture. Standardized hospitalization ratios and their 95% CIs estimated relative risks with the age-, sex-, and calendar period-matched Swedish general population as reference. RESULTS: In total, 70 and 51 first hip fractures were ascertained in men and women, respectively, corresponding to a cumulative probability (both sexes) of 65.8/1,000 until age 65 years. Markedly elevated risks were observed in both men and women (standardized hospitalization ratios = 7.6 [95% CI 5.9-9.6] and 9.8 [7.3-12.9], respectively), increasing with follow-up time. Ophthalmic, nephropathic, neurological, and cardiovascular complications were indicators of particularly high risks. CONCLUSIONS: Both male and female type 1 diabetic patients are at increased risk for hip fracture. Although optimal preventive measures still need to be defined, the co-occurrence with other diabetes complications suggests that tighter metabolic control might reduce the risk.     

男性2型糖尿病患者病程与骨密度和骨代谢指标关系的研究

目的　评价男性 2型糖尿病患者病程与骨密度和骨代谢指标的变化的关系。方法　同时测定2 4例正常人和 6 2例男性 2型糖尿病患者的骨密度 (BMD)、血骨钙素 (BGP)、骨型特异性碱性磷酸酶 (BAP)、Ⅰ型胶原氨基末端肽 (NTx)、甲状旁腺素 (PTH)、血钙、血磷和血浆白蛋白。根据病程将糖尿病分为Ⅰ组 :病程 <5年 ,31例 ;Ⅱ组 :病程 5～ 10年 ,2 0例 ;Ⅲ组 :病程 >10年 ,11例。结果　与正常对照组 (K组 )比较 ,Ⅰ组和Ⅱ组患者BMD、BGP、BAP、PTH和NTx差异无显著意义 (P >0 0 5 ) ;Ⅲ组糖尿病BMD明显下降 ,P <0 0 5 ;BGP、BAP、NTx和PTH显著增高 ,P <0 0 1。结论　病程 (大于 10年 )是男性 2型糖尿病患者骨质疏松症的重要危险因素。     

血清骨钙素水平与绝经后女性2型糖尿病患者骨密度的关系

目的:探讨血清骨钙素水平与绝经后女性2型糖尿病(type 2 diabetes,T2DM)患者骨密度(bone minaral density,BMD)间的关系。方法:本研究为回顾性分析,共纳入505例绝经后女性,其中T2DM住院患者305例,非糖尿病对照者200例,采用双能X线骨密度仪(DXA)检测腰椎(第2至第4腰椎)、股骨颈和全髋的BMD,同时检测血清骨钙素(osteocalcin,OC)水平。结果:与正常对照组相比,T2DM组患者的血清OC水平显著降低(P<0.05),腰椎、股骨颈、全髋的BMD及体质量指数显著增高(P<0.01)均呈显著负相关;校正年龄、体质量指数和糖尿病病程后,血清OC水平与腰椎及全髋的BMD间仍存在明显的负相关。结论:血清OC水平与绝经后女性T2DM患者腰椎及全髋的BMD密切相关,随着OC水平的升高,BMD呈下降趋势,提示血清OC水平可作为早期筛查绝经后女性T2DM患者骨质疏松的生化指标,结合血清OC水平和BMD能更好地预测绝经后女性T2DM患者的骨质疏松和骨折的风险。     

老年男性2型糖尿病及糖尿病肾病患者的骨密度及骨代谢变化

目的: 探讨老年男性2型糖尿病和糖尿病肾病患者的骨密度及骨代谢以及影响因素。方法: 用DEXA测定了131 例60岁以上的男性2型糖尿病患者(正常蛋白尿组73例,微量白蛋白尿组30例,临床蛋白尿或肾功能不全者组28 例)和49 例对照组的腰椎与股骨近端骨密度,并检测生化及骨代谢指标。结果: 男性2 型糖尿病患者的骨密度和糖尿病病程有关,随着病程的延长,糖尿病患者的骨密度降低加重。临床蛋白尿或肾功能不全者组的2 型糖尿病患者的骨密度显著降低(P<0.05或P<0.01),微量白蛋白尿期的骨密度也呈下降趋势。结论: 男性2 型糖尿病患者的骨量丢失程度与糖尿病病程及肾脏功能有关,肾脏功能下降是加重男性2型糖尿病患者骨质疏松的重要因素。     

Leisure time physical activity is associated with poor glycemic control in type 1 diabetic women: the FinnDiane study

OBJECTIVE: We studied the association between leisure time physical activity (LTPA) and glycemic control, insulin dose, and estimated glucose disposal rate (eGDR) in type 1 diabetes. RESEARCH DESIGN AND METHODS: This is a cross-sectional study of 1,030 type 1 diabetic patients participating in the Finnish Diabetic Nephropathy Study, a nationwide multicenter study. LTPA was assessed by a validated 12-month questionnaire and expressed in metabolic equivalent (MET) units. Patients were grouped as sedentary (LTPA <10 MET h/week, n = 247), moderately active (LTPA 10-40 MET h/week, n = 568), and active (LTPA >40 MET h/week, n = 215). Outcome measures were HbA(1c), insulin dose, and eGDR (estimate of insulin sensitivity based on waist-to-hip ratio, hypertension, and HbA(1c)). RESULTS: LTPA correlated with HbA(1c) in women (r = -0.12, P = 0.007) but not in men (r = -0.03, P = 0.592). Sedentary women had higher HbA(1c) than moderately active and active women: 8.8 +/- 1.4% vs. 8.3 +/- 1.4% vs. 8.3 +/- 1.4% (P = 0.004), whereas HbA(1c) in men was 8.4 +/- 1.3% vs. 8.2 +/- 1.4% vs. 8.2 +/- 1.3% (P = 0.774), respectively. In men, insulin doses were 0.74 +/- 0.21 vs. 0.71 +/- 0.20 vs. 0.68 +/- 0.23 IU . kg(-1) . 24 h(-1) (P = 0.003). In both sexes, sedentary patients had lower eGDRs than active patients [median (interquartile range) 5.5 (4.0-8.2) vs. 6.8 (4.7-8.8) vs. 6.7 (4.6-8.6) mg . kg(-1) . min(-1); P < 0.01 for sedentary vs. others]. Age, obesity, smoking, insulin dose, social class, diabetic nephropathy, or cardiovascular disease did not explain the results. CONCLUSIONS: Low levels of LTPA were associated with poor glycemic control in type 1 diabetic women. Men seem to use less insulin when physically active. Increased LTPA levels were associated with increased estimated insulin sensitivity. Longitudinal studies are needed to further clarify the effects of LTPA on type 1 diabetes.     

骨钙素在2型糖尿病合并骨代谢异常患者中的表达水平

目的探讨骨钙素(OC)在2型糖尿病合并骨代谢异常患者中的表达情况。方法选取2017年5月至2018年11月辽宁省沈阳市第四人民医院收治的120例2型糖尿病患者为研究对象,根据骨密度结果分为2型糖尿病合并骨量正常组、2型糖尿病合并骨量异常组(骨量减少及骨质疏松者),每组60例,选取同期健康体检者60例纳入健康对照组。全部受试者均于清晨空腹采集静脉血检测OC、血钙(Ca)、血磷(P)、碱性磷酸酶(ALP)、糖化血红蛋白(HbA1c)等水平,并计算胰岛素抵抗指数(HOMA-IR)及胰岛β细胞功能指数(HOMA-β)。结果3组研究对象血Ca、血P及ALP水平比较,差异无统计学意义(P>0.05)。与健康对照组比较,2型糖尿病合并骨量异常组及2型糖尿病合并骨量正常组OC水平明显降低,差异有统计学意义(P<0.05)。同时2型糖尿病合并骨量异常组OC水平明显低于2型糖尿病合并骨量正常组,差异有统计学意义(P<0.05)。OC水平与HbA1c及HOMA-IR呈负相关(r=-0.67,P=0.004;r=-0.56,P=0.035),与HOMA-β呈正相关(r=0.46,P=0.024)。结论血糖代谢与骨代谢密切相关,2型糖尿病患者易合并骨代谢异常,骨形成下降是骨代谢特点之一,OC可作为2型糖尿病患者骨代谢异常发生、发展的参考因子。     

胰岛素样生长因子-I与2型糖尿病患者骨密度关系的研究

目的:探讨胰岛素样生长因子-I(IGF-I)在2型糖尿病患者骨质疏松(OP)发病中的作用与机制。方法:用双能x线骨密度仪分别测定2型糖尿病患者骨密度值(BMD);用酶联免疫的方法测定受试者血清IGF-I的水平,并与正常对照组比较。结果:2型糖尿病组骨密度低于对照组(P<0.01);血清IGF-I水平低于对照组(P<0.01);糖尿病患者骨密度值与血清IGF-I水平显著正相关(P<0.01)。结论:2型糖尿病组OP发病率增高,与IGF-I水平降低导致骨形成减少有关。     

Bone mineral density: serum markers of bone turnover and their relationships in peritoneal dialysis.

BACKGROUND: The usefulness of bone mass measurements and bone turnover markers to estimate the risk of fracture and the type of underlying renal osteodystrophy are not well established in patients on peritoneal dialysis (PD). OBJECTIVE: To assess bone mass using total and regional bone densitometry in a group of patients on PD and to determine if serum markers of bone turnover identify patients with low bone mass. METHODS: Bone densitometry was studied by dual-energy x-ray absorptiometry (DEXA), and bone turnover using several serum markers, in 65 patients on PD. Bone mass was classified as normal, osteopenic, or osteoporotic according to World Health Organization criteria based on bone mineral density (BMD) T scores. RESULTS: T scores in the osteopenia range were present at the lumbar spine (LS) in 44.6% (45% of men and 44.4% of women) of patients and at the femoral neck (FN) in 56.9% (55% of men and 58% of women). T scores in the osteoporosis range were present at the LS in 13.8% of patients (10% of men and 15.5% of women) and at the FN in 21.5% (30% of men and 17.7% of women). Patients with BMD T scores in the osteoporosis range at both regions had increased serum intact parathyroid hormone (iPTH) levels compared to patients in the osteopenic/normal range. Bone mineral content in the whole skeleton (TBMC) correlated negatively with iPTH (r = -0.34) and with total time on dialysis (r = -0.26); in multivariate analysis, only iPTH correlated negatively with TBMC (B = -0.26, p = 0.03). No correlations were found between the other bone markers and BMD T scores at the FN or LS. There were no significant differences in absolute BMD or BMD T scores at the LS or FN between patients with and patients without fractures. CONCLUSIONS: BMD T scores in the osteopenia/osteoporosis range were observed at the LS in 58.4% of these patients on PD and at the FN in 78.4%. TBMC correlated negatively with iPTH. There were no correlations between markers of bone turnover and bone mass measurements at the two skeletal regions, although patients with BMD T scores in the osteoporosis range had increased serum iPTH levels. Bone mass measurements were not different between patients with and patients without fractures.