c-peptide and Vitamin-D-Deficiency

Gestational Diabetes Mellitus (GDM) and vitamin D deficiency are related to insulin resistance and impaired beta cell function, with heightened risk for future development of diabetes. We evaluated the impact of vitamin D supplementation on markers of glucose metabolism and cardio metabolic risk in Asian women with former GDM and hypovitaminosis D. In this double blind, randomized controlled trial, 26 participants were randomized to receive either daily 4000 IU vitamin D3 or placebo capsules. 75 g Oral Glucose Tolerance Test (OGTT) and biochemistry profiles were performed at baseline and 6 month visits. Mathematical models, using serial glucose, insulin and C peptide measurements from OGTT, were employed to calculate insulin sensitivity and beta cell function. Thirty three (76%) women with former GDM screened had vitamin D level of <50 nmol/L at baseline. Supplementation, when compared with placebo, resulted in increased vitamin D level (+51.1 nmol/L vs 0.2 nmol/L, p<0.001) and increased fasting insulin (+20% vs 18%, p = 0.034). The vitamin D group also demonstrated a 30% improvement in disposition index and an absolute 0.2% (2 mmol/mol) reduction in HbA1c. There was no clear change in insulin sensitivity or markers of cardio metabolic risk. This study highlighted high prevalence of vitamin D deficiency among Asian women with former GDM. Six months supplementation with 4000 IU of vitamin D3 safely restored the vitamin D level, improved basal pancreatic beta-cell function and ameliorated the metabolic state. There was no effect on markers of cardio metabolic risk. Further mechanistic studies exploring the role of vitamin D supplementation on glucose homeostasis among different ethnicities may be needed to better inform future recommendations for these women with former GDM at high risk of both hypovitaminosis D and future diabetes.

Topics: Adult; Asian People; Biomarkers; Blood Glucose; C-Peptide; Diabetes, Gestational; Female; Humans; Insulin; Metabolic Syndrome; Pregnancy; Vitamin D; Vitamin D Deficiency; Vitamins

Vitamin D insufficiency is common in subjects with type 2 diabetes. Observational studies suggest that vitamin D plays a role in the pathogenesis of type 2 diabetes. However, results of intervention studies have been inconsistent. We investigated the effects of improving vitamin D status on insulin sensitivity, insulin secretion, and inflammatory markers in patients with type 2 diabetes.. A double blind, randomized, placebo controlled trial was conducted. Sixteen patients with type 2 diabetes and hypovitaminosis D were recruited. Eight patients received colecalciferol and (280 μg daily for 2 weeks, 140 μg daily for 10 weeks) and 8 patients received identical placebo tablets for 12 weeks. Before and after intervention, patients underwent IVGTT, hyperinsulinemic euglycemic clamp, assessment of baseline high-frequency insulin pulsatility, glucose-entrained insulin pulsatility, DXA scans, 24-hour-ambulatory blood pressure monitorings, and fasting blood samples.. Serum-25(OH) vitamin D and serum-1,25(OH)₂ vitamin D increased significantly after 12 weeks in the intervention group (p=0.01, p=0.004). Serum-25(OH) vitamin D was also significantly higher in the vitamin D group compared to the placebo group (p=0.02) after intervention. Although no significant changes in insulin sensitivity, inflammation, blood pressure, lipid profile, or HbA1c were found, we observed borderline (p between 0.05 and 0.10) improvements of insulin secretion, in terms of c-peptide levels, first phase incremental AUC insulin and insulin secretory burst mass.. Improvement in vitamin D status does not improve insulin resistance, blood pressure, inflammation or HbA1c, but might increase insulin secretion in patients with established type 2 diabetes.

Topics: Aged; Biomarkers; C-Peptide; Calcifediol; Calcitriol; Cholecalciferol; Denmark; Diabetes Mellitus, Type 2; Dietary Supplements; Double-Blind Method; Female; Humans; Inflammation Mediators; Insulin; Insulin Resistance; Insulin Secretion; Insulin-Secreting Cells; Kinetics; Male; Middle Aged; Seasons; Severity of Illness Index; Vitamin D Deficiency

To examine whether combined vitamin D and calcium supplementation improves insulin sensitivity, insulin secretion, β-cell function, inflammation and metabolic markers.. 6-month randomized, placebo-controlled trial.. Ninety-five adults with serum 25-hydroxyvitamin D [25(OH)D] ≤55 nmol/L at risk of type 2 diabetes (with prediabetes or an AUSDRISK score ≥15) were randomized. Analyses included participants who completed the baseline and final visits (treatment n = 35; placebo n = 45).. Daily calcium carbonate (1,200 mg) and cholecalciferol [2,000-6,000 IU to target 25(OH)D >75 nmol/L] or matching placebos for 6 months.. Insulin sensitivity (HOMA2%S, Matsuda index), insulin secretion (insulinogenic index, area under the curve (AUC) for C-peptide) and β-cell function (Matsuda index x AUC for C-peptide) derived from a 75 g 2-h OGTT; anthropometry; blood pressure; lipid profile; hs-CRP; TNF-α; IL-6; adiponectin; total and undercarboxylated osteocalcin.. Participants were middle-aged adults (mean age 54 years; 69% Europid) at risk of type 2 diabetes (48% with prediabetes). Compliance was >80% for calcium and vitamin D. Mean serum 25(OH)D concentration increased from 48 to 95 nmol/L in the treatment group (91% achieved >75 nmol/L), but remained unchanged in controls. There were no significant changes in insulin sensitivity, insulin secretion and β-cell function, or in inflammatory and metabolic markers between or within the groups, before or after adjustment for potential confounders including waist circumference and season of recruitment. In a post hoc analysis restricted to participants with prediabetes, a significant beneficial effect of vitamin D and calcium supplementation on insulin sensitivity (HOMA%S and Matsuda) was observed.. Daily vitamin D and calcium supplementation for 6 months may not change OGTT-derived measures of insulin sensitivity, insulin secretion and β-cell function in multi-ethnic adults with low vitamin D status at risk of type 2 diabetes. However, in participants with prediabetes, supplementation with vitamin D and calcium may improve insulin sensitivity.. Australian New Zealand Clinical Trials Registry ACTRN12609000043235.

Topics: Adiponectin; Adult; Aged; Blood Glucose; C-Peptide; C-Reactive Protein; Calcium, Dietary; Cholecalciferol; Diabetes Mellitus, Type 2; Dietary Supplements; Female; Humans; Insulin; Insulin Resistance; Insulin-Secreting Cells; Interleukin-6; Male; Middle Aged; Osteocalcin; Pilot Projects; Prediabetic State; Tumor Necrosis Factor-alpha; Vitamin D Deficiency

Vitamin D insufficiency has been associated with impaired pancreatic beta-cell function. We aimed to determine if high dose oral vitamin D3 (D) improves beta-cell function and glycaemia in type 2 diabetes.. Fifty adults with type 2 diabetes diagnosed less than 12 months, with normal baseline serum 25-OH D (25D), were randomised to 6000 IU D (n=26) or placebo (n=24) daily for 6 months. Beta-cell function was measured by glucagon-stimulated serum C-peptide (delta C-peptide [DCP], nmol/l). Secondary outcome measures were fasting plasma glucose (FPG), post-prandial blood glucose (PPG), HbA1c and insulin resistance (HOMA-IR).. In the D group, median serum 25D (nmol/l) increased from 59 to 150 (3 months) and 128 (6 months) and median serum 1,25D (pmol/l) from 135 to 200 and 190. After 3 months, change in DCP from baseline in D (+0.04) and placebo (-0.08) was not different (P=0.112). However, change in FPG (mmol/l) was significantly lower in D (-0.40) compared to placebo (+0.1) (P=0.007), as was the change in PPG in D (-0.30) compared to placebo (+0.8) (P=0.005). Change in HbA1c (%) between D (-0.20) and placebo (-0.10) was not different (P=0.459). At 6 months, changes from baseline in DCP, FPG, PPG and HbA1c were not different between groups.. Oral D3 supplementation in type 2 diabetes was associated with transient improvement in glycaemia, but without a measurable change in beta-cell function this effect is unlikely to be biologically significant. High dose D3 therefore appears to offer little or no therapeutic benefit in type 2 diabetes.

Topics: Adult; Biomarkers; Blood Glucose; C-Peptide; Diabetes Mellitus, Type 2; Dose-Response Relationship, Drug; Double-Blind Method; Female; Follow-Up Studies; Humans; Hypoglycemic Agents; Insulin; Male; Middle Aged; Time Factors; Vitamin D; Vitamin D Deficiency

Women with polycystic ovary syndrome (PCOS) frequently suffer from metabolic disturbances, in particular from insulin resistance. Accumulating evidence suggests that vitamin D deficiency may contribute to the development of insulin resistance. Hence, we aimed to examine the effect of vitamin D supplementation on metabolic and endocrine parameters in PCOS women.. Fifty-seven PCOS women were included in the study. PCOS women received 20,000 IU cholecalciferol weekly for 24 weeks. Anthropometric measures, oral glucose tolerance test, and blood analyses of endocrine parameters were performed at baseline and after 12 weeks (V2) and 24 weeks (V3).. Forty-six PCOS women finished the study. 25-hydroxyvitamin D [25(OH)D] levels significantly increased from 28.0±11.0 ng/ml at baseline to 51.3±17.3 and 52.4±21.5 at V2 and V3, respectively (p<0.001). We observed a significant decrease of fasting and stimulated glucose (V3, p<0.05) and C-peptide levels (V2 and 3, p<0.001) after vitamin D treatment. Moreover, triglyceride and estradiol levels significantly decreased at V3 (p=0.001) and V2 (p=0.022), respectively, whereas total cholesterol (V2, p=0.008) and LDL cholesterol levels (V2, p=0.005; V3, p=0.026) significantly increased after vitamin D treatment. There were no changes in androgens. At V2, 14 out of 46 PCOS women previously affected by menstrual disturbances (30.4%) reported improvement of menstrual frequency; at V3, 23 out of 46 women (50.0%), who were oligo- or amenorrheic at baseline reported improvement.. Our results suggest that vitamin D treatment might improve glucose metabolism and menstrual frequency in PCOS women. Further randomized controlled trails are warranted to confirm our findings.

Topics: Administration, Oral; Adolescent; Adult; Blood Glucose; C-Peptide; Cholecalciferol; Cholesterol; Cholesterol, LDL; Female; Humans; Menstruation; Menstruation Disturbances; Pilot Projects; Polycystic Ovary Syndrome; Prospective Studies; Vitamin D Deficiency

To estimate vitamin D levelsin children with type 1 diabetes, and to evaluate itsrole in the pathogenesis and progress of the disease.. The cross-sectional study was conducted at the Paediatric Department of Kafrelsheikh University Hospital, Egypt, from November 2019 to August 2021, and comprised children of either gender aged 3-18 years who were either inpatients or visiting the paediatric outpatient clinic. The subjects were enrolled into 3 groups. Those with newly diagnosed type 1 diabetes were in group A, those with established type 1 diabetes were in group B, and healthy children matched for age and gender and randomly selected were in the control group C. Glycated haemoglobin, serum fasting C-peptide, and serum vitamin D levels were evaluated using quantitative colorimetric determination, an automated analyser, and enzyme-linked immunosorbent assay, respectively. Data was analysed using SPSS 25.. Of the 80 subjects, 30(37.5%) were in group A; 17(56.7%) boys and 13(43.3%) girls with mean age 7.77±2.95 years. In group B, there were 30(37.5%) subjects; 14(46.7%) boys and 16(53.3%) girls with mean age 9.6±3.62 years. There were 20(25%) subjects in group C; 10(50%) boys and as many girls with mean age 8.38±2.68 years (p>0.05). Glycated haemoglobin,serum fasting C-peptide and serum vitamin D wassignificantly different between the control group and the treatment groups (p<0.05). Between the treatment groups, group B had better markers than group A (p<0.05).. Serum vitamin D deficiency may play a role in the pathogenesis and insulin sensitivity in cases of type 1 diabetes.

Topics: Adolescent; Blood Glucose; C-Peptide; Child; Child, Preschool; Cross-Sectional Studies; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Female; Glycated Hemoglobin; Humans; Male; Vitamin D; Vitamin D Deficiency

To estimate the associations of cord meta-inflammatory markers with neurodevelopment, including the potential impact of cord blood vitamin D levels.. The prospective cohort study comprised 7198 participants based on the Maternal & Infants Health in Hefei study. Cord blood C-peptide, high-sensitive C-reactive protein (hsCRP), high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, total cholesterol, triglycerides and 25(OH)D levels were measured. The Gesell Developmental Schedules were used to assess neurodevelopmental outcomes in offspring.. After adjusting potential confounders, per quartile increase in cord blood 25(OH)D concentrations was associated with a decreased risk of neurodevelopmental delay [hazard ratios (HR) 0.65 (95% CI 0.57, 0.74)]. Conversely, significant positive associations with cord blood serum C-peptide levels above the 90th percentile [HR 2.38 (95% CI 1.81, 3.13)] and higher levels of cord hsCRP (per quartile increase) [HR 1.18 (95% CI 1.01, 1.37)] with neurodevelopmental delay were observed. These associations could vary by quartiles of cord blood 25(OH)D levels: the adjusted HRs in neurodevelopmental delay comparing children with vs without hyperinsulinemia were 1.28 (95% CI: 1.03, 1.59) for quartiles 1 (lowest), and 1.06 (95% CI: 0.78, 1.44) for quartile 4 (highest).. Immune activation and metabolic abnormalities in fetal circulation were associated with neurodevelopmental delay in offspring, which could be attenuated by higher cord blood 25(OH)D levels in a dose-response manner.

Topics: C-Peptide; C-Reactive Protein; Child; Cholesterol; Cohort Studies; Fetal Blood; Humans; Infant; Inflammation; Prospective Studies; Vitamin D; Vitamin D Deficiency; Vitamins

Vitamin D3 (vit. D3) deficiency is considered as one of the main factors involved in the development of type 2 diabetes (T2D). We assessed insulin resistance (IR), β-cell functional activity and metabolic profile according to 25(OH) vit. D3 status in patients with T2D.. The study included 109 patients with T2D, divided in 3 groups: group 1 (N.=11) with normal levels of vit. D3 (>30 ng/mL); group 2 (N.=38) with vit. D3 insufficiency (21-29 ng/mL); and group 3 (N.=60) with vit. D3 deficiency (<20 ng/mL). IR and β-cell functional activity were assessed as change in C-peptide concentration and homeostasis model assessment-estimated (HOMA) β-cell function which was calculated using HOMA2 calculator.. Patients with vit. D3 deficiency presented significantly higher C-peptide concentration compared to other groups. HOMA2 (3.29±1.89 vs. 2.12±0.71; P=0.049) and hemoglobin (H8b)A1c (9.11±1.63 vs. 7.75±1.06; P=0.016) levels changed significantly only in patients with vit. D3 deficiency compared to diabetics with normal vit. D3 levels. Furthermore, in univariate Pearson's correlation analysis, we observed significant association between vit. D3 levels and C-peptide, insulin sensitivity, HOMA2, triglyceride-glucose index, HbA1c and Body Mass Index, only in the vit. D3 deficiency group. In multivariate logistic regression analysis, poor glycemic control, as defined by HbA1c levels, was independent from metformin use while high density lipoprotein-cholesterol levels were associated with vit. D3 deficiency.. Our study demonstrated that vit. D3 deficiency in patients with T2D was associated with more severe IR, poor glycemic control and obesity compared to normal status or vit. D3 insufficiency.

Topics: Adolescent; Adult; Aged; Body Mass Index; C-Peptide; Cholecalciferol; Cross-Sectional Studies; Diabetes Mellitus, Type 2; Ergocalciferols; Female; Glycemic Control; Humans; Hypoglycemic Agents; Insulin Resistance; Male; Metformin; Middle Aged; Obesity; Vitamin D Deficiency; Young Adult

We aimed to assess Vitamin D levels in patients with Type 1 Diabetes (T1D) and to investigate the correlation between vitamin D and metabolic imbalance.. For our study, we selected thirty-one patients with T1D without complications and fifty-seven healthy controls. Diabetic patients were diagnosed using the criteria of the World Health Organization/American Diabetes Association. Vitamin D, Parathyroid Hormone (PTH), insulin and C peptide assay were performed using chimilunescence. Glucose level, lipid profile, glycated haemoglobin (HbA1c) and ionogram were also analysed.. Vitamin D, HbA1c and Gly levels were found to be significant in T1D patients than in controls (P<0.5). However, for PTH, no significant difference was observed (P > 0. 05) and the results show a non-significant difference of total cholesterol potassium, sodium, phosphor and calcium concentration averages.. Our results indicate that the deficiency of VD is associated with an increased risk of T1DM in Algerian population.

Topics: Adult; Algeria; Biomarkers; Blood Glucose; C-Peptide; Case-Control Studies; Diabetes Mellitus, Type 1; Energy Metabolism; Female; Glycated Hemoglobin; Humans; Insulin; Male; Parathyroid Hormone; Risk Factors; Vitamin D; Vitamin D Deficiency; Young Adult

To measure total 25-hydroxyvitamin D levels in women in mid-pregnancy who participated in the Belfast centre of the Hyperglycaemia and Adverse Pregnancy Outcome (HAPO) observational study, and to investigate the associations between levels of 25-hydroxyvitamin D and markers of gestational diabetes mellitus and lipid biomarkers.. A total of 1585 pregnant women had serum samples available for measurement. Participants were recruited from the Royal Jubilee Maternity Hospital, Belfast, Northern Ireland, at 24-32 weeks' gestation, as part of the HAPO study. 25-hydroxyvitamin D concentrations were measured using liquid chromatography tandem mass spectrometry. Glucose, C-peptide and lipid levels were previously analysed in a central laboratory. Statistical analysis was performed.. The median (interquartile range) 25-hydroxyvitamin D concentration during pregnancy was 38.6 (24.1-60.7) nmol/l, with 65.8% of women being vitamin D-deficient (≤50 nmol/l). In regression analysis, the association between maternal 25-hydroxyvitamin D and fasting plasma glucose levels approached significance [regression coefficient -0.017 (95% CI -0.034 to 0.001); P=0.06], and a significant positive association was observed between maternal 25-hydroxyvitamin D and β-cell function [1.013 (95% CI 1.001 to 1.024); P=0.031]. Maternal 25-hydroxyvitamin D level was positively associated with HDL [0.047 (95% CI 0.021 to 0.073) P≤ 0.001] and total cholesterol [0.085 (95% CI 0.002 to 0.167); P=0.044] in regression analysis.. These results indicate a high prevalence of vitamin D deficiency during pregnancy, which requires identification and treatment; however, only weak associations were observed between 25-hydroxyvitamin D level and markers of glucose and insulin metabolism. This would suggest that these are of doubtful clinical significance.

Topics: 25-Hydroxyvitamin D 2; Adolescent; Adult; Blood Glucose; C-Peptide; Calcifediol; Cholesterol; Chromatography, Liquid; Diabetes, Gestational; Diet; Female; Humans; Northern Ireland; Pregnancy; Pregnancy Complications; Pregnancy Trimester, Second; Pregnancy Trimester, Third; Tandem Mass Spectrometry; Vitamin D; Vitamin D Deficiency; White People; Young Adult

Neonatal body fat is an important indicator of foetal energy supply and growth with potential importance for long-term health. In this study, we wanted to explore seasonal variation of 25-hydroxy-vitamin D (25(OH)D) in maternal and umbilical cord plasma (UCP) to examine whether maternal and foetal 25(OH)D levels were associated with maternal BMI and neonatal fat mass (FM), and to explore the relationship among maternal and neonatal 25(OH)D levels, maternal glucose/insulin levels and UCP C-peptide.. An observational, prospective study of determinants of foetal growth and birth weight in healthy pregnant women. Total body composition in 202 newborns was measured by dual-energy X-ray absorptiometry. Circulating levels of biomarkers were assessed in mothers at gestational weeks 14-16 and 30-32 and UCP.. The mean 25(OH)D concentration in UCP was significantly lower than in maternal circulation (31 vs 45 nmol/l, P<0.001). Maternal and UCP 25(OH)D levels varied significantly with season. No significant association between maternal BMI (weeks 14-16) and UCP 25(OH)D concentration was found. We found a strong positive association between maternal 25(OH)D and UCP 25(OH)D (P<0.001). There was no significant linear association between maternal BMI (weeks 14-16) and maternal 25(OH)D. We found no association between maternal 25(OH)D levels and glucose/insulin levels, nor with maternal or UCP 25(OH)D on UCP C-peptide levels. Finally, neonatal total body FM was positively associated with UCP 25(OH)D, P=0.02.. We demonstrated seasonal variation in maternal and neonatal 25(OH)D levels at northern latitudes. UCP, but not maternal, 25(OH)D was a significant predictor of neonatal total FM. Maternal BMI and metabolic parameters such as glucose, insulin and UCP C-peptide levels were not associated with 25(OH)D in mothers or offspring.

Topics: Absorptiometry, Photon; Adiposity; Adult; Blood Glucose; Body Composition; Body Mass Index; C-Peptide; Female; Fetal Blood; Fetal Development; Humans; Infant, Newborn; Insulin; Linear Models; Male; Norway; Obesity; Pregnancy; Prospective Studies; Seasons; Vitamin D; Vitamin D Deficiency

We investigated whether improving 25-hydroxyvitamin D status in young type 1A diabetic patients reduces reactivity of peripheral blood mononuclear cells against islet autoantigens and associates with beta-cell functional changes.. Eight patients with 25-hydroxyvitamin D deficiency (<20 ng/ml), out of 15 consecutive young type 1A diabetic subjects received 25-hydroxyvitamin D3 to achieve and maintain levels above 50 ng/ml for up to one year. Peripheral blood mononuclear cell reactivity (Interferon-γ spots) against beta-cell autoantigens (glutamic acid decarboxylase 65-kD isoform, proinsulin and tyrosine phosphatase-like protein IA-2) and C-peptide during mixed meal were assessed before and after 25-hydroxyvitamin D3 replenishment.. Target 25-hydroxyvitamin D blood levels were safely reached and maintained. Peripheral blood mononuclear cell reactivity against glutamic acid decarboxylase 65-kD isoform (3.8 ± 4.0 vs. 45 ± 16) and proinsulin (3.5 ± 3.2 vs. 75 ± 51) decreased significantly (p < 0.001 and p < 0.02) upon 25-hydroxyvitamin D3 replenishment, which was correlated with 25-hydroxyvitamin D concentrations. C-peptide values remained stable after one year of treatment.. Safely restored and maintained 25-hydroxyvitamin D levels associated with reduced peripheral blood mononuclear cell reactivity against beta-cell autoantigens with no significant decrease of beta-cell function in this cohort of patients.

Topics: Adolescent; Autoantigens; C-Peptide; Calcifediol; Child; Diabetes Mellitus, Type 1; Female; Glutamate Decarboxylase; Humans; Insulin-Secreting Cells; Interferon-gamma; Leukocytes, Mononuclear; Male; Proinsulin; Vitamin D Deficiency

Vitamin D deficiency has been related to diabetes, hypertension, hyperlipidemia and peripheral vascular disease. In this study, we aimed to investigate the role of vitamin D status in non-alcoholic fatty liver disease.. We included 211 consecutive subjects to examine the presence of non-alcoholic fatty liver disease. Of these subjects, 57 did not have non-alcoholic fatty liver disease and 154 had non-alcoholic fatty liver disease.. The non-alcoholic fatty liver disease group had significantly higher fasting blood glucose (p = 0.005), uric acid (p = 0.001), aspartate aminotransferase (p<0.001), alanine aminotransferase (p<0.001), γ-glutamyltransferase (p<0.0001), alkaline phosphatase (p = 0.028), HbA1c (p<0.001), ferritin (p<0.001), insulin (p = 0.016), C-peptide (p = 0.001), HOMA-IR (p = 0.003), total cholesterol (p = 0.001), triglyceride (p = 0.001) and white blood cell (p = 0.04) levels. In contrast, the non-alcoholic fatty liver disease group had significantly lower 25(OH)D levels (12.3±8.9 ng/dl, p<0.001) compared with those of the control group (20±13.6 ng/dl).. In this study, we found lower serum 25(OH)D levels in patients with non-alcoholic fatty liver disease than in subjects without non-alcoholic fatty liver disease. To establish causality between vitamin D and non-alcoholic fatty liver disease, further interventional studies with a long-term follow-up are needed.

Topics: Adult; Albuminuria; Blood Glucose; C-Peptide; Creatinine; Fasting; Female; Humans; Insulin; Male; Middle Aged; Non-alcoholic Fatty Liver Disease; Outpatients; Regression Analysis; Seasons; Vitamin D; Vitamin D Deficiency

Vitamin D deficiency reduces insulin secretion and still occurs in East London Asians in whom the prevalence of diabetes mellitus is at least four times that of Caucasians. Vitamin D status was assessed in 44 of 65 non-diabetic subjects 'at risk' of diabetes (spot blood glucose level >6.0 mmol/l <2 h post cibum, or>4.6 mmol/l >2 h post cibum on two separate occasions) and in 15 of 60 age and sex-matched 'low-risk' control subjects who attended for oral glucose tolerance test (OGTT) after screening of 877 omnivorous subjects not known to have diabetes. It was found that 95% of at-risk and 80% of low-risk subjects were vitamin D deficient (serum 25-hydroxy-vitamin D <11 ng/ml). Diabetes was present in 16, impaired glucose tolerance in 12 and normoglycaemia in 19 at-risk subjects, imparied glucose tolerance in 2, and normoglycaemia in 13 low-risk subjects. Correlation of 30-min OGTT blood glucose, specific insulin and C-peptide levels with 25-hydroxy-vitamin D concentrations in 44 at-risk subjects were -0.31 (p=0.04), 0.59 (p=0.0001) and 0.44 (p=0.006). In 15 'not-at-risk' subjects 30-min OGTT specific insulin and C-peptide levels correlated with 25-hydroxy-vitamin D, r=0.39 (p=0.04) and 0.16 (p=0.43), respectively. Serum alkaline phosphatase concentration was higher in at-risk than not-at-risk subjects (59.6 vs 46.5 IU/l, p=0.012); corrected calcium concentrations were comparable (2.38 vs 2.39 mmol/l, p=0.7). Following treatment with 100,000 IU vitamin D by i.m. injection, specific insulin, C-peptide [30 min on OGTT] and 25-hydroxy-vitamin D concentrations had risen 8-12 weeks later [mean +/- DS] from 57 +/- 62 to 96.2 +/- 82.4 mU/l [p=0.0017], 1.0 +/- 0.4 to 1.7 +/- 0.8 pmol/ml [p=0.001] and 3.6 +/- 1.8 to 13.5 +/- 7.4 ng/ml [p=0.0001], (but not to low-risk group values of 179 +/- mU/l, 2.7 +/- 1.14 pmol/ml and 8.16 +/- 6.4 ng/ml), respectively. Both total serum alkaline phosphatase and corrected calcium concentrations rose following vitamin D treatment in the at-risk subjects by 11.1 +/- 8.22 (from 44 to 55 IU/l) and 0.15 +/- 0.18, (2.43 to 2.57 mmol/l), respectively (p=0.004). Abnormal glucose tolerance was unchanged by vitamin D treatment. The value of early and sustained repletion with vitamin D in diabetes prophylaxis should be examined in communities where vitamin D depletion is common.

Topics: Asian People; Bangladesh; Blood Glucose; C-Peptide; Calcifediol; Calcitriol; Diabetes Mellitus; Glucose Intolerance; Humans; Insulin; Insulin Secretion; London; Prevalence; Proinsulin; Reference Values; Regression Analysis; Risk Factors; Statistics, Nonparametric; Vitamin D Deficiency; White People

The regulatory functions of vitamins are described with particular reference to their importance in the metabolic processes of ageing. Although clear hypovitaminosis is uncommon, slight vitamin deficiencies are often encountered in the clinical practice. They cause a speed up of the organism deterioration. The nutritional requirement and the effect of vitamin A, B1, B6, B12, are rapidly reviewed. More attention is paid to the data about vitamin C, D and E. Vitamin C deficiency in elderly, especially in the hospitalized ones; whereas a high content of ascorbic acid in necessary in order to extend the life length and to achieve a good self-sufficiency. Also the deficiency of vitamin D and of its metabolites is frequent in the aged due to both a lower uptake and a scarce exposure to the sunlight. Low levels of vitamin D cause a worsening of bone tissue and consequent demineralization (osteomalacia and osteoporosis). Some aspects of ageing can be prevented by the supply of vitamin E, particularly the impaired bone trophism. The anti-oxidant power of tocopherol could also interfere some pathogenetic processes of ageing.

Topics: Adolescent; Adult; Aged; Aging; Ascorbic Acid; Ascorbic Acid Deficiency; C-Peptide; Calcifediol; Child; Child, Preschool; Humans; Hydroxycholecalciferols; Insulin; Middle Aged; Osteomalacia; Osteoporosis; Prediabetic State; Vitamin D Deficiency; Vitamin E