Correlation between serum 25-hydroxyvitamin D levels and quadriceps muscle strength in elderly cretans

Vitamin D deficiency is associated with osteomalacic myopathy, and muscle weakness related to vitamin D deficiency has been implicated as a possible risk factor for falls in the elderly. This study investigated the possible correlation between serum 25-hydroxyvitamin D (25[OH]D) concentration and quadriceps muscle strength in ambulatory community dwelling Cretan men (n=13) and women (n=35) aged > or = 65 years. Quadriceps muscle strength was measured isometrically using Cybex 6000 apparatus. The mean serum 25(OH)D concentration was significantly higher in men than in women (76.00 versus 49.11 nmol/l, respectively). Serum 25(OH)D values were < 50 nmol/l in 15% of men and in 60% of women. Serum 25(OH)D concentration correlated positively with quadriceps muscle strength. In conclusion, vitamin D deficiency was common in the study participants despite the high levels of sunlight in Crete. Serum 25(OH)D levels were positively correlated with muscle strength.     

Vitamin D status is associated with bone mineral density and functional exercise capacity in patients with chronic obstructive pulmonary disease

Background. Chronic obstructive pulmonary disease (COPD) is associated with several extrapulmonary effects that contribute to the severity of the disease. Vitamin D is suggested to play a role in COPD and its related extrapulmonary effects. Aims. To determine the prevalence of vitamin D deficiency and its relation with bone density, muscle strength, and exercise capacity in patients with COPD. Methods. Our cross-sectional study included patients with moderate to very severe COPD. We collected data on lung function, body composition, bone density, quadriceps muscle strength, 6-minute walking distance, and plasma 25-hydroxyvitamin D (25(OH)D) concentration. Vitamin D deficiency was defined as plasma 25(OH)D concentration below 50 nmol/L. Results. In total, 151 COPD patients were included; 87 patients (58%) had vitamin D deficiency. Plasma 25(OH)D concentration was positively associated with bone density (P =?0.005) and 6-minute walking distance (P <?0.001) after adjustment for potential confounders. Plasma 25(OH)D concentration was not associated with quadriceps muscle strength. Conclusions. The majority of COPD patients had vitamin D deficiency. Plasma 25(OH)D concentration was positively associated with bone density and exercise capacity. Intervention studies are necessary to determine whether vitamin D supplementation is of benefit in the prevention or treatment of osteoporosis and poor exercise capacity in patients with COPD.     

Vitamin D metabolism and parathyroid function in man.

1. The metabolism of an intravenous pulse dose of double-isotope-labelled cholecalciferol has been studied in control subjects with widely differing states of vitamin D nutrition and in patients with primary disorders of parathyroid function. 2. The formation of labelled 1,25-dihydroxy-cholecalciferol [1,25-(OH)2D3] and labelled 24,25-dihydroxycholecalciferol [24,25-(OH)2D3] has been related to the prevailing concentrations in serum of 25-hydroxycholecalciferol [25-(OH)D3], immunoreactive parathyroid hormonel, calcium and orthophosphate (Pi). 3. In control subjects with relative vitamin D deficiency [serum 25-(OH)2D3 was related inversely to the serum 25-(OH)D3 and serum calcium, and directly to serum immunoreactive parathyroid hormone. No formation of 1,25-(OH)2D3 was detectable to form labelled 24,25(OH)2D3 preferentially. 4. No control subject produced significant amounts of both labelled 1,25-(OH)2D3 and labelled 24,25-(OH)2D3 simultaneously. 5. All subjects with primary hyperparathyroidism produced significant amounts of labelled 1,25-(OH)2D3 and labelled 24,25-(OH)2D3 simultaneously; the renal turnover of 25-(OH)D3 was apparently greater than in nutritionally matched controls. Serum labelled 1,25-(OH)2D3 in this disease was not correlated with serum 25-(OH)D3, immunoreactive parathyroid hormone, calcium or Pi. Production of labelled 24,25-(OH)2D3 was inappropriately high for the prevailing nutritional state. 6. The indirectly estimated their concentration of 1,25-(OH)2D3 showed only a fourfold variation in control subjects (45-180 pmol/l), compatible with its having a regulated hormonal function. 7. The data suggest that the production of 1,25-(OH)2D3 from a pulse dose of cholecalciferol is normally regulated, directly or indirectly, by the parathyroid hormone.     

Muscle weakness and foot deformities in diabetes: relationship to neuropathy and foot ulceration in caucasian diabetic men

OBJECTIVE: To examine the relationships among muscle weakness, foot deformities, and peroneal and tibial nerve conduction velocity in diabetic and nondiabetic men. RESEARCH DESIGN AND METHODS: A neuropathic and foot evaluation was undertaken in 10 nondiabetic control subjects (group C) and in 36 consecutive diabetic patients attending Diabetes Centre clinics, including 10 diabetic control subjects (group D), 15 diabetic neuropathic patients (group DN), and 11 diabetic patients with a history of ulceration (group DU). Neuropathy was defined as a peroneal motor nerve conduction <40 m/s. Muscle weakness was assessed in seven intrinsic and seven extrinsic muscles of the foot using a semiquantitative score (max score per muscle = 3). Foot deformities were assessed using a foot deformity score (max score = 3). A higher score indicated increased muscle weakness or more severe foot deformities. Muscle weakness and foot deformities were assessed without prior knowledge of patient and neuropathy status. RESULTS: Peroneal and tibial nerve conduction velocity were associated with weakness in muscles innervated by, respectively, the peroneal and tibial nerve (r = -0.70 and r = -0.51, P < 0.01) and foot deformities (r = -0.60 and r = -0.59, P < 0.001). The DN and DU groups had more weakness in intrinsic and extrinsic muscles compared with the C and D groups. Muscles innervated by the tibial nerve had a greater proportional muscle weakness than those innervated by the peroneal nerve in the DN and DU groups. The DN and DU patients had more foot deformities (median food deformity score [interquartile range]) (3 [2-3] and 2 [2-3]) compared with D and C patients (0 [0-0.75] and 0 [0-0]). CONCLUSIONS: Important relationships have been shown between motor nerve conduction deficit and muscle weakness; however, it is still not clear whether abnormal nerve function, leading to a decrease in muscle strength, could be responsible for the development of foot deformities.     

Plasma levels of vitamin D metabolites in diphosphonate-treated rats

1. Protein-binding assays have been used to measure plasma 1,25-dihydroxy-vitamin D [1,25-(OH)2D] as well as 25-hydroxy-vitamin D [25-(OH)D] in rats given 10 mg of phosphorus (P) day(-1) kg(-1) as ethane-1-hydroxy-1,1-diphosphonate (EHDP). 2. In control animals given a normal laboratory chow plasma 25-(OH)D and 1,25-(OH)2D were about 40 nmol/l and 300 pmol/l respectively. 3. EHDP produced a decrease of plasma 1,25-(OH)2D to below 50 pmol/l in 2 days. 4. Both in control and in EHDP-treated rats plasma 1,25-(OH)2D increased when dietary calcium (Ca) was restricted to 0.1%, or dietary P to 0.2%, indicating that the well-known stimulatory effect of Ca or P deprivation was at least partially effective in EHDP-treated rats. 5. In response to an increase of the oral supply of vitamin D3 to 65 nmol/day the plasma level of 25-(OH)D rose in both control and EHDP groups. Plasma 1,25-(OH)2D was not increased above the normal value in control rats. In EHDP-treated rats, however, plasma 1,25-(OH)2D rose to a level equal to that in controls, suggesting that the effect of EHDP on plasma 1,25-(OH)2D can be overcome at high precursor concentration.     

血清维生素D水平对维持性血液透析患者下肢肌力减退的预测作用

目的探讨维持性血液透析(MHD)患者血清维生素D水平对下肢肌力减退的预测作用。 方法横断面研究设计，选择2018年9月至10月于战略支援部队特色医学中心血液净化中心的95例MHD患者，检测其血清25-羟维生素D₃[25(OH)D₃]水平，采用5次站立-坐下实验(5-STS)评价其下肢肌力。根据5-STS完成时间将MHD患者分为下肢肌力正常组(n＝85)与减退组(n＝10)，比较两组患者人口学特征、实验室指标。采用多因素Logistic回归分析下肢肌力减退的影响因素，绘制受试者工作特征(ROC)曲线分析上述因素预测MHD患者发生下肢肌力减退的特异度和敏感度。 结果95例MHD患者血清25(OH)D₃水平为11.00~99.50 nmol/L，中位数31.23(19.90~43.30)nmol/L；5-STS完成时间为3.55 s~18.71 s，中位数9.81(7.12，12.43)s，下肢肌力减退者10例(10.53%)。多因素Logistic回归分析显示，血清25(OH)D₃是MHD患者下肢肌力减退的保护性因素[OR＝0.761，95%CI(0.592~0.978)，P＝0.033]。进一步ROC曲线分析显示，25(OH)D₃对应的ROC曲线下面积为0.815，其预测MHD患者发生下肢肌力减退的敏感度为80.00%，特异度为80.00%。 结论MHD患者血清25(OH)D₃水平普遍较低，下肢肌力减退者更为明显；血清维生素D水平对MHD患者是否存在下肢肌力减退具有较好的预测价值。     

Abnormal vitamin D metabolism in patients with cirrhosis.

To assess the role of hepatic function and alcohol on vitamin D metabolism, serum 25-hydroxyvitamin D (25-OHD) levels were measured in 20 healthy nonalcoholic control subjects, 31 "inactive" cirrhotics whose alcoholism was in remission, 8 alcoholic cirrhotics, and 15 alcoholics with normal liver function. Cirrhosis but not alcoholism, was assoicated with low serum 25-OHD levels. The aminopyrine breath test (ABT) was performed because aminopyrine, like vitamin D3, is metabolized by hepatic microsomes; the ABT correlated highly (r = 0.74, rho less than 0.01) with serum 25-OHD in the inactive cirrhotics. After an intravenous injection of 120 mug vitamin D3, serum 25-OHD rose significantly within 24 hr in 6 healthy controls and 2 patients with celiac disease but not in 6 inactive cirrhotics. The data suggest impaired 25-hydroxylation of vitamin-D impaired in patients with cirrhosis, related predominantly to the degree of hepatic dysfunction.     

Low Plasma 25-Hydroxyvitamin D and Serum Calcium Levels in Institutionalized Epileptic Subjects: Associated Risk Factors, Consequences and Response to Treatment with Vitamin D

In a survey of 108 subjects with a history of epilepsy in ahospital for the mentally handicapped, administration of bothphenobarbitone and phenytoin was associated with low serum calciumand plasma 25-hydroxyvitamin D (25-(OH)D) levels in female subjectsonly. Intake of phenytoin (as mg/kg body weight) in female subjectsexceeded that in males by 22 per cent, whilst the intake ofphenobarbitone was 37 per cent higher. The doses of phenobarbitoneand phenytoin were each inversely related to plasma 25-(OH)Dconcentration, but anticonvulsant drug dosage did not correlatewith the magnitude of the decline of plasma 25-(OH)D concentrationin winter (November-February). No influence of sodium valproatewas detected on serum calcium or on plasma 25-(OH)D levels. Limited exposure to ultraviolet irradiation (UVR) or oral administrationof vitamin D restored plasma 25-(OH)D to normal levels and healedosteomalacia in a subject with tuberous sclerosis. In this subject,fit frequency declined in response to UVR and to a lesser extentin response to oral vitamin D, despite the attainment of similarlevels of serum calcium and of plasma 25-(OH)D. Serum calciumlevels in the other 108 subjects were lower in those experiencingthe most frequent fits, but serum calcium could not be restoredto levels found in subjects not receiving anticonvulsant drugsunless supraphysiological doses of vitamin D were given. Vitamin D deficiency in the epileptic population receiving drugswas assessed by the response of alkaline phosphatase to vitaminD administration. A consistent fall of serum alkaline phosphatasewas found only if the initial level exceeded 175 per cent ofthe normal value established by reference to a population notreceiving phenobarbitone or phenytoin. By this criterion fiveout of 45 subjects (11 per cent), aged nine to 36 years werevitamin D deficient.     

老年糖尿病患者维生素D与握力和肌肉质量相关性研究

目的研究老年2型糖尿病(type 2 diabetes mellitus,T2DM)患者维生素D水平与肌肉质量和握力的相关性。方法选取2016年5月至2018年1月入住宣武医院内分泌科年龄≥60岁的2型糖尿病患者201例进行前瞻性研究,根据25羟维生素D[25-hydroxyvitamin D,25(OH)D]水平分为维生素D缺乏组[25(OH)D<20μg/L]140例和非缺乏组[20μg/L≤25)(OH)D<70μg/L]61例,测定患者握力、步速及上下肢肌肉质量。并进行体格检查和实验室检查。结果两组患者实验室各项指标比较差异均无统计学意义(P均>0.05)。维生素D非缺乏组患者的握力、上肢及下肢肌肉含量显著高于缺乏组[(33.49±9.43)kg与(29.59±10.30)kg、(4.99±1.09)kg与(4.57±1.11)kg、(15.69±3.10)kg与(14.54±3.03)kg,P值分别为0.010、0.015、0.017]。多因素Logistic回归分析显示维生素D缺乏与握力减低及下肢肌肉质量下降独立相关(OR=1.286,95%CI:1.197~1.346,P<0.01;OR=1.231,95%CI:1.102~1.283,P<0.05)。结论维生素D缺乏是老年2型糖尿病患者握力减低及下肢肌肉质量下降的危险因素。     

Vitamin D from skin: contribution to vitamin D status compared with oral vitamin D in normal and anticonvulsant-treated subjects

1. The plasma 25-hydroxycholecalciferol [25-(OH)D3] response to measured u.v. irradiation applied thrice weekly for 10 weeks was investigated in normal and in anticonvulsant-treated subjects. 2. Levels of plasma 25-(OH)D3 achieved after u.v. irradiation were similar in both normal and anticonvulsant-treated subjects, suggesting that hepatic microsomal enzyme induction does not lead to low plasma 25-(OH)D3 concentrations. 3. Cholecalciferol was present in plasma of normal subjects in a very low concentrations (less than 5.0 nmol/l) and did not increase until plasma 25-(OH)D3 levels exceeded 62.5 nmol/l. 4. Cholecalciferol occurred in significant concentrations in plasma during whole body u.v. irradiation or during oral dosage of 62.5 nmol (100 i.u) or more daily. 5. Plasma 25-(OH)D3 concentrations reached a steady state after 5-6 weeks of u.v. irradiation or of oral intake within the usual intake range. 6. Cholecalciferol synthesis in skin calculated from the steady-state equation was 0.0015 +/- 0.0008 nmol/mJ. 7. Cholecalciferol synthesis in skin was also calculated from the oral dosage required to yield the same plasma 25-(OH)D3 concentration as u.v. irradiation and was 0.0024 +/- 0.0018 nmol/mJ. 8. Rates of cholecalciferol synthesis calculated from these data suggest that many of the population of England receive insufficient u.v. irradiation to maintain vitamin D status throughout the year.     

The biliary excretion of 25-hydroxy-[3H] vitamin D3 in the Gunn rat

1. The biliary excretion of 25-hydroxy-[3H]-vitamin D3 (25-(OH)-[3H]D3)-derived materials after the intravenous administration of 25-(OH)-[3H]D3 (1.25 nmol/100 g body weight) was studied during a period of 3 h in homozygous (icteric) and heterozygous (anicteric) Gunn rats. 2. The heterozygous rats excreted significantly more 25-(OH)-[3H]D3-derived materials than the homozygous Gunn rats (7.2 +/- 1.5% vs 3.1 +/- 0.5% of the administered dose, P < 0.025). 3. The lower biliary excretion of 25-(OH)-[3H]-D3-derived material in homozygous compared with heterozygous Gunn rats was not due to differences in the plasma 25-(OH)-[3H]D3 concentrations nor was it due to differences in the uptake of 25-(OH)-[3H]D3 by the liver since similar liver/plasma concentration ratios were observed in both groups of animals; it seemed, however, to be due to differences in the biliary transfer of 25-(OH)-[3H]-D3, as indicated by a lower bile/liver concentration ratio in homozygous than in heterozygous rats (1.39 +/- 0.23 vs 0.49 +/- 0.06, P < 0.05). 4. Moreover, samples of bile obtained from homozygous rats contained no beta-glucuronidase-sensitive 25-(OH)-[3H]D3-derived materials but contained significantly more intact 25-(OH)-[3H]-D3 than samples obtained from heterozygous Gunn rats (P < 0.05). After hydrolysis of bile obtained from homozygous and heterozygous Gunn rats with the enzyme beta-glucuronidase, the total amount of intact 25-(OH)-[3H]D3 recovered was found to be similar in the two groups of rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Muscle strength in healthy white and Asian subjects: the relationship of quadriceps maximum voluntary contraction to age, sex, body build and vitamin D

1. The maximum voluntary isometric contraction (MVC) of the dominant quadriceps muscle was measured in 136 healthy White and 172 healthy Hindu Asian subjects resident in London, using a specially designed chair equipped with a force measuring load cell. 2. Males were stronger than females, and for both sexes MVC declined with age. From age 20 to 60 the annual decline in MVC ranged from 0.56% in White males to 1.5% in female Asians. 3. White subjects were stronger than Asian subjects even after correcting for the effect of age, height, weight and sex in a multi-factorial analysis. 4. Only in males did MVC correlate with height and weight. Asian women were more obese than any other group, and showed an increase in body mass index with age. 5. Twenty-two per cent of Asian subjects had marked vitamin D deficiency (plasma 25-hydroxycholecalciferol less than 10 nmol/1). There was no correlation between MVC, and plasma 25-hydroxycholecalciferol.     

Resurrection of vitamin D deficiency and rickets

The epidemic scourge of rickets in the 19th century was caused by vitamin D deficiency due to inadequate sun exposure and resulted in growth retardation, muscle weakness, skeletal deformities, hypocalcemia, tetany, and seizures. The encouragement of sensible sun exposure and the fortification of milk with vitamin D resulted in almost complete eradication of the disease. Vitamin D (where D represents D2 or D3) is biologically inert and metabolized in the liver to 25-hydroxyvitamin D [25(OH)D], the major circulating form of vitamin D that is used to determine vitamin D status. 25(OH)D is activated in the kidneys to 1,25-dihydroxyvitamin D [1,25(OH)2D], which regulates calcium, phosphorus, and bone metabolism. Vitamin D deficiency has again become an epidemic in children, and rickets has become a global health issue. In addition to vitamin D deficiency, calcium deficiency and acquired and inherited disorders of vitamin D, calcium, and phosphorus metabolism cause rickets. This review summarizes the role of vitamin D in the prevention of rickets and its importance in the overall health and welfare of infants and children.     

Calcium malabsorption in elderly women with vertebral fractures: evidence for resistance to the action of vitamin D metabolites on the bowel

Radio-calcium absorption, plasma 25-hydroxyvitamin D [25-(OH)D] and 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations were measured in 19 elderly women with, and 21 without, vertebral fractures, before and after treatment with 25-hydroxyvitamin D3 [25-(OH)D3], to establish whether malabsorption of calcium in elderly women with vertebral fractures has a cause different from that in elderly women without vertebral fractures. Malabsorption of calcium and low plasma 25-(OH)D and 1,25-(OH)2D concentrations were common in both groups of women but there was no significant difference in these variables between the two groups. After treatment with 40 micrograms of 25-(OH)D3 daily for 7 days, there was a significant increase in plasma 25-(OH)D and 1,25-(OH)2D in both groups of women, but radio-calcium absorption increased significantly only in the group without vertebral fractures. Elderly women with vertebral fractures have malabsorption of calcium which is resistant to the action of vitamin D metabolites at concentrations which correct calcium malabsorption in elderly women without vertebral fractures.     

Assessment in vitro and in vivo of muscle degradation in chronic skeletal muscle myopathy of alcoholism

1. Muscle protein breakdown in vivo has been studied by measurements of urinary 3-methyl-histidine/creatinine ratios. No differences were found between control subjects and chronic alcoholics either with or without proximal muscle wasting or cirrhosis. 2. Calculation of muscle turnover rates, with the correction of Afting et al. (1981, Biochemical Journal, 200, 449-452) for non-skeletal muscle contributions of 3-methylhistidine and creatinine, showed lower values for alcoholics compared with controls. 3. Tissue activities of a neutral protease, assayed by a novel, rapid and sensitive fluorimetric method, were similar in patients and controls. The activity did not vary with severity of atrophy or the presence of cirrhosis. 4. No evidence was therefore obtained to suggest that alcoholic myopathy is due to increased muscle breakdown.     

血清25-(OH)D3与自身免疫性甲状腺疾病体液免疫的相关性

目的:探讨自身免疫性甲状腺疾病(AITD)患者血清中25-(OH)D3与健康人群有无差异,及25-(OH)D3与AITD患者体液免疫紊乱之间的关系.方法:选取Graves病(GD)50例、桥本甲状腺炎(HT)30例,健康人20例,检测样本血清25-(OH)D3、甲状腺自身抗体(TSAb、TGAb、TPOAb)及甲状腺功能,并对25-(OH)D3水平与其他检测指标进行相关分析.结果:GD组及HT组25-(OH)D3均显著低于对照组,GD组25-(OH)D3与TSAb、FT3、FT4呈负相关,与TSH呈正相关;HT组25-(OH)D3与TGAb、TPOAb、TSH呈负相关,与FT3、FT4呈正相关.结论:AITD患者存在低25-(OH)D3血症,与患者的体液免疫紊乱密切相关.     

Increased muscular fatigue in patients with neurogenic muscle weakness: quantification and pathophysiology

The strength of maximum voluntary contraction (MVC) and muscular fatigue measured from ankle dorsiflexors and knee extensors of 15 patients with neurogenic muscle weakness was compared with those of 20 healthy subjects. Muscle weakness, defined as the failure to generate the expected force, was determined by two methods: (1) manual muscle testing and (2) measurement of MVC using a force transducer. Muscle strength was then quantified as the MVC in Newtons (N)/kg body weight. The percent decrease in both MVC (the Fatigue Index [FI]), and rectified-integrated electromyogram (RIEMG) at the end of 60sec of sustained MVC were computed. There were three main findings. (1) Muscle strength was significantly (p less than 0.001) reduced in both muscles of the patient group: in ankle dorsiflexors, means = 1.62 +/- 0.7N/kg vs 4.8 +/- 0.5N/kg; in knee extensors, means = 3.2 +/- 1.8N/kg vs 7.8 +/- 1.5N/kg. (2) Fatigue was significantly greater (p less than 0.01) in the patient group: for ankle dorsiflexors, means = 50 +/- 15% vs 34 +/- 13%; and for knee extensors, means = 62 +/- 17% vs 46 +/- 15%. There was a negative correlation between muscle strength and FI of only the knee extensors of the patients (r = -0.88, p less than 0.001). (3) The mean decline in RIEMG of the two muscles combined was also significantly greater (p less than 0.001) in the patient group (means = 48 +/- 16% vs 2 +/- 11%).(ABSTRACT TRUNCATED AT 250 WORDS)     

中国北方地区老年人冬季维生素D缺乏与骨量丢失

背景：中国北方地区老年人维生素D营养状态存在季节变化,冬春季维生素D缺乏严重。目的：分析沈阳市老年人冬季维生素D缺乏对骨量丢失的影响。方法：随机选择沈阳市60岁以上汉族健康老年人100名,于2000-03检测受试者血浆中25羟维生素D、甲状旁腺激素、钙和磷,清晨空腹2h尿中脱氧吡啶、钙、磷、肌酐,2000-03/2005-03两次检测髋部骨密度。结果与结论：基线时,血浆25羟维生素D浓度为（31.0±12.30）nmol/L,40%受试者低于25nmol/L;血浆甲状旁腺激素水平为（29.4±11.5）ng/L,血浆25羟维生素D浓度低于25nmol/L者甲状旁腺激素水平为（34.6±13.5）ng/L,血浆25羟维生素D浓度与甲状旁腺激素呈负相关（r=-0.479,P〈0.0001）。5年后股骨颈骨丢失率为（3.05±4.07）%,大转子为（1.46±5.02）%,经体质量和身高变化率校正后,股骨颈骨丢失率与基线血浆25羟维生素D浓度呈负相关（r=-2.3,P=0.02）,股骨颈骨丢失率基线血浆25羟维生素D浓度≤25nmol/L者高于浓度〉25nmol/L者103%（F=7.2062,P=0.0085）。其他检测指标与骨丢失无显著相关性。说明老年人群冬季维生素D缺乏严重,维生素D缺乏促进骨量丢失,影响骨健康。     

A high prevalence of prediabetes and vitamin D deficiency are more closely associated in women: results of a cross-sectional study

ObjectiveMany studies have shown that vitamin D deficiency is associated with insulin resistance and metabolic syndrome. However, few studies have shown independent associations between vitamin D deficiency and the metabolic characteristics of prediabetes. We aimed to evaluate the relationship between serum vitamin D concentration and metabolic risk factors in adults with prediabetes.MethodsWe enrolled 161 patients aged 25 to 75 years in a cross-sectional study and collected clinical and biochemical data, including 25-hydroxyvitamin D (25[OH]D) status and fasting glucose concentration. Vitamin D status was defined as follows: deficiency (25[OH]D <49.9 ng/mL), insufficiency (49.9 to 74.9 nmol/L) or sufficiency (>74.9 nmol/L). Prediabetes was defined using fasting plasma glucose concentrations of 5.55 to 6.49 mmol/L.ResultsThe prevalences of vitamin D deficiency and insufficiency were 49.7% and 24.8%, respectively. Participants with vitamin D deficiency had a higher prevalence of prediabetes than those without (53.8% vs. 32.1%), and there was a significant relationship between female sex and vitamin D status (odds ratio: 1.382; 95% confidence interval: 0.335–5.693).ConclusionVitamin D deficiency is more closely associated with a high prevalence of prediabetes in women than in men. Further studies are needed to elucidate the explanation for this association.     

Effect of vitamin D deficiency on sarcoplasmic reticulum function and troponin C concentration of rabbit skeletal muscle.

1. Weanling rabbits were made rachitic either by a vitamin D-deficient diet or by parenteral administration of ethane 1-hydroxy-1,1-diphosphonate (EHDP) in amounts sufficient in other species to block the formation of 1,25-dihydroxycholecalciferol [1,25-(OH)2D3]. 2. The uptake of calcium into the isolated sarcoplasmic reticulum from mixed striated quadriceps muscle, and the amount of troponin C (the calcium-binding component of the troponin complex) in relation to other proteins from the same muscle, were measured. 3. In muscle from animals made rachitic by a dietary deficiency of vitamin D, the rate of uptake of calcium by the sarcoplasmic reticulum and the troponin C concentration were both significantly less (P less than 0.02) than in control littermates. In EHDP-treated animals no significant differences from controls were found. 4. These results show that dietary deficiency of vitamin D in such animals can affect muscle physiology. Since no changes are found in animals made rachitic with EHDP, who presumably have a selective deficiency of 1,25-(OH)2D3, it is possible that the effect of vitamin D on muscle is mediated through metabolites other than 1,25-(OH)2D3 such as 25-hydroxycholecalciferol.