A randomised controlled trial of high dose vitamin D in recent-onset type 2 diabetes

AimsVitamin 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.MethodsFifty 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).ResultsIn 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.ConclusionOral 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.     

Association of the ENPP1 K121Q polymorphism with type 2 diabetes and obesity in the Moroccan population

AimThe ectonucleotide pyrophosphatase/phosphodiesterase 1 enzyme (ENPP1), which downregulates insulin signaling by inhibiting insulin-receptor tyrosine kinase activity, is encoded by the ENPP1 gene. A common functional ENPP1 K121Q polymorphism has been suggested to contribute to insulin resistance, obesity and type 2 diabetes (T2D) in various ethnic groups. For this reason, we assessed the association between the ENPP1 K121Q polymorphism in T2D and obesity phenotypes in the Moroccan population.MethodsUsing LightCycler^® technology, we genotyped the ENPP1 K121Q polymorphism in 503 subjects with T2D and 412 normoglycaemic individuals.ResultsThere was no evidence of an association between ENPP1 K121Q and T2D in either an additive (P = 0.99) or recessive mode of inheritance (P = 0.47). However, the Q121 variant was significantly more frequent in obese than in non-obese subjects after adjusting for age, gender and T2D status. We observed genetic heterogeneity between obese and non-obese T2D patients (P = 0.02). The K121Q polymorphism was associated with T2D in the presence of obesity in both additive (1.55 [95% CI 1.16–2.07]; P = 0.003) and recessive (2.31 [95% CI 1.34–3.97]; P = 0.002) modes of inheritance.ConclusionAlthough there was no evidence of an association between the ENPP1 K121Q variant and the general phenotype of T2D, we did find an association with adult obesity and T2D. The Q121 allele frequency in Morocco is 37.3%, placing it between European Caucasians (15%) and Black Africans (79%). This study is the first to report an association between K121Q and metabolic diseases in the Moroccan population.     

T-cadherin gene variants are associated with type 2 diabetes and the Fatty Liver Index in the French population

AimAdiponectin is an adipocyte-secreted protein associated with insulin sensitivity. T-cadherin is a receptor for high and medium molecular weight adiponectin. In GWAS, T-cadherin gene (CDH13) polymorphisms are associated with circulating adiponectin levels. This study investigated the associations between genetic variants of CDH13 and type 2 diabetes (T2D), and its related parameters, in a Caucasian population.MethodsTwo polymorphisms of CDH13 (rs11646213 and rs3865188) were genotyped in two French cohorts, a general population from the D.E.S.I.R. study (n = 5212) and people with T2D in the DIABHYCAR study (n = 3123). Baseline adiponectin levels were measured in D.E.S.I.R. participants who were normoglycaemic at baseline, but hyperglycaemic after 3 years (n = 230), and in controls who remained normoglycaemic (n = 226) throughout.ResultsIn a cross-sectional analysis, CDH13 genotype distributions differed between those with and without T2D, with T2D odds ratios (OR) of 1.11 (95% CI: 1.04–1.18; P = 0.001) and 0.92 (95% CI: 0.87–0.98; P = 0.01) for rs11646213 and rs3865188, respectively. The rs11646213 variant, associated with a higher OR for T2D, was also associated with higher BMI (P = 0.03) and HbA_1c (P = 0.006), and lower plasma adiponectin levels (P = 0.03) in the D.E.S.I.R. participants. Conversely, the rs3865188 variant, associated with a lower OR for T2D, was also associated with lower BMI (P = 0.03), HbA_1c (P = 0.02) and Fatty Liver Index (FLI; P ≤ 0.01), and higher plasma adiponectin levels (P = 0.002). Associations with HbA_1c, FLI and adiponectin levels persisted after adjusting for BMI.ConclusionCDH13 polymorphisms are associated with prevalent T2D in this French population study. The association may be mediated through effects on BMI and/or plasma adiponectin.     

Indirect comparison of efficacy and safety of insulin glargine/lixisenatide and insulin degludec/insulin aspart in type 2 diabetes patients not controlled on basal insulin

BackgroundFixed-dose combinations of insulin glargine/lixisenatide (IGlarLixi) or insulin degludec/insulin aspart (IDegAsp) constitute treatment intensification in type 2 diabetes mellitus (T2D).ObjectivesCompare efficacy and safety of IGlarLixi and IDegAsp (as intensification from basal insulin), by indirect comparison of phase III trials, in the absence of head-to-head trials.Study eligibility criteriaStudies comparing treatment intensification by once-daily IDegAsp or IGlarLixi to basal insulin. Data were extracted from two trials (BOOST: Intensify-Basal and LixiLan-L) retained for analysis.Synthesis methodsTreatments were compared in terms of estimated treatment difference (ETD) in glycated haemoglobin (HbA1c), fasting and postprandial plasma glucose (FPG and PPG) change from baseline; in addition to hypoglycaemia incidence and weight changes.ResultsIn a fixed-effect model examining HbA1c control, IGlarLixi was more effective than IDegAsp in reducing HbA1c (ETD 0.53%, P < 0.0001]), PPG (ETD 2.65%, P < 0.0001), and body weight (ETD 1.73 kg, P < 0.0001). Patients on IGlarLixi were more likely to achieve HbA1c < 7% than patients on IDegAsp (odds ratio [OR] = 0.40, P < 0.0001), with lower incidence of hypoglycaemia (OR = 1.33, P < 0.001).LimitationsLimited number of studies; different baseline HbA1c and FPG.ConclusionOnce-daily IGlarLixi is more efficient than once-daily IDegAsp in controlling HbA1c and PPG and associates with greater weight loss and lower hypoglycaemia incidence.     

Race/ethnicity and measures of glycaemia in the year after diagnosis among youth with type 1 and type 2 diabetes mellitus

AimsTo assess associations between race/ethnicity, glycated hemoglobin (HbA1c), and glycemic control among youth with type 1 (T1D) or type 2 diabetes (T2D).MethodsThe study sample was youth < 20 years old from the SEARCH California Center diagnosed from 2002 to 2009 who remained insured for at least one year. HbA1c at one year was from clinical data; HbA1c at diagnosis was from clinical data (81%) or imputed (19%). Multivariable logistic and linear regression models were used to examine associations between race/ethnicity and poor glycemic control (≥ 9.5%), HbA1c at one-year, and change in HbA1c.ResultsThe study included 1162 Hispanic (52.3%), non-Hispanic White (NHW, 28.4%), African American (15.1%) and Asian/Pacific Islander (4.1%) youth. Among T1D youth (n = 789), Hispanics were 1.60 times as likely (95% CI 1.01–2.53) to have poor control at one year compared to NHWs, after adjustments. Among T2D youth (n = 373), only African American youth were significantly more likely (OR = 4.85; 95% CI 1.49–15.77) to have poor control at one year, after adjustments. HbA1c at one year and change in HbA1c did not differ by race/ethnicity.ConclusionPoor glycemic control was evident one year after diagnosis in some minority youth with T1D or T2D in an integrated managed health care setting.     

Decreased A20 mRNA and protein expression in peripheral blood mononuclear cells in patients with type 2 diabetes and latent autoimmune diabetes in adults

AimsA20 is a negative regulator of nuclear factor kappa B activation and the central gatekeeper in inflammation and immunity. While its role in type 1 diabetes has been widely studied, its expression level in immune cells from type 2 diabetes (T2D) and latent autoimmune diabetes in adult (LADA) patients remains unclear. This study aimed to clarify whether the expression of A20 is altered in patients with T2D or LADA.MethodsQuantitative real-time polymerase chain reaction and western blotting were utilized to determine the expression of A20 mRNA and protein respectively in peripheral blood mononuclear cells (PBMCs) from patients with T2D (n = 36) or LADA (n = 17) and sex- and age-matched healthy controls (n = 34).ResultsThe mRNA and protein expression of A20 in PBMCs from T2D and LADA patients was significantly decreased compared with healthy controls (P < 0.05). Furthermore, A20 mRNA and protein expression was significantly lower in newly diagnosed T2D patients (≤1 year since diagnosis) than in patients with a long T2D duration (>1 year since diagnosis) (P < 0.05).ConclusionsOur results suggest that decreased expression of A20 in PBMCs may be involved in the pathogenesis of diabetes, and targeting A20 may offer a potential therapeutic tool in the treatment of diabetes.     

Family history of type 1 and type 2 diabetes and risk of latent autoimmune diabetes in adults (LADA)

BackgroundA family history of diabetes (FHD) is a strong predictor of diabetes risk, yet has rarely been investigated in latent autoimmune diabetes in adults (LADA). This study therefore investigated the risk of LADA and type 2 diabetes (T2D) in relation to FHD, taking into account the type of diabetes in relatives.MethodsData from a population-based study were used, including incident cases of LADA [glutamic acid decarboxylase antibody (GADA)-positive, n = 378] and T2D (GADA-negative, n = 1199), and their matched controls (n = 1484). First-degree relatives with disease onset at age < 40 years and taking insulin treatment were classified as type 1 diabetes (T1D) or, if otherwise, as T2D. Odds ratios (ORs) were adjusted for age, gender, BMI, education and smoking. Cases were genotyped for high- and low-risk HLA genotypes.ResultsBoth FHD–T1D (OR: 5.8; 95% CI: 3.2–10.3) and FHD–T2D (OR: 1.9; 95% CI: 1.5–2.5) were associated with an increased risk of LADA, whereas the risk of T2D was associated with FHD–T2D (OR: 2.7; 95% CI: 2.2–3.3), but not FHD–T1D. In LADA patients, FHD–T1D vs FHD–T2D was associated with higher GADA but lower C-peptide levels, lower prevalence of low-risk HLA genotypes (5.0% vs 28.6%, respectively; P = 0.038) and a tendency for higher prevalence of high-risk genotypes (90.0% vs 69.1%, respectively; P = 0.0576).ConclusionThe risk of LADA is substantially increased with FHD–T1D but also, albeit significantly less so, with FHD–T2D. This supports the idea of LADA as a mix of both T1D and T2D, but suggests that the genes related to T1D have greater impact. LADA patients with FHD–T1D had more T1D-like features, emphasizing the heterogeneity of LADA.     

Exercise ameliorates serum MMP-9 and TIMP-2 levels in patients with type 2 diabetes

AimThis study assessed the impact of regular exercise on inflammatory markers (high-sensitivity C-reactive protein [hsCRP], fibrinogen), and matrix metalloproteinases (MMPs) and their inhibitors (TIMPs), in patients with type 2 diabetes mellitus (T2DM).PatientsFifty overweight patients with T2DM were randomly assigned to two groups: (A) an exercise group (EXG, n = 25), with self-controlled exercise for at least 150 min/week and one additional supervised exercise session/week; and (B) a control group (COG, n = 25), with no exercise instructions. All participants were taking oral antidiabetic drugs, and none had diabetic complications. Clinical parameters, exercise capacity (VO_2peak), ventilatory threshold (VT), insulinresistance indices (fasting insulin, HOMA-IR, HOMA%S), hsCRP, fibrinogen, MMP-2, MMP-9, TIMP-1 and TIMP-2 were assessed at baseline and after 16 weeks.ResultsNo significant changes were found in body mass index, waist/hip ratio, insulin-resistance indices, MMP-2 and TIMP-1 throughout the study in either group (P > 0.05). Compared with controls, the EXG showed a significant decrease in systolic and mean blood pressure, total and LDL cholesterol, and HbA_1c (P < 0.05). Also, exercise significantly suppressed levels of fibrinogen (P = 0.047), hsCRP (P = 0.041) and MMP-9 (P = 0.028), and the MMP-9-to-TIMP-1 ratio (P = 0.038), whereas VO_2peak (P = 0.011), VT (P = 0.008) and plasma TIMP-2 levels (P = 0.022) were considerably upregulated in the EXG vs. COG. Standard multiple-regression analyses revealed that MMP-9 changes were independently associated with fibrinogen and HbA_1c changes, while fibrinogen changes independently predicted TIMP-2 alterations with exercise.ConclusionMostly self-controlled exercise of moderate intensity ameliorated serum levels of pro- and anti-atherogenic markers in patients with T2DM, with no effects on body weight. These data offer further insight into the cardioprotective mechanisms of exercise in patients with T2DM.     

Association of adiponectin with dietary factors and cardiovascular risk factors in type 2 diabetes mellitus patients

Background and aimAdiponectin, is an adipose tissue-specific adipokine, that circulates in human plasma at high levels, although lower levels are noted with insulin resistance and atherosclerosis. We investigated the relationship of adiponectin concentrations with dietary factors and some of the cardiovascular risk factors in patients with T2DM.Methods and resultsTotally 107 patients with T2DM were recruited from the out patients clinic of Shariati Hospital, Tehran, Iran. Patients were evaluated for laboratory and anthropometric measurements including serum adiponectin, fasting insulin, FPG, OGTT, HbA1c, HOMA-IR, hsCRP, weight, height, BMI and WHR. Nutrients intakes were obtained via 24-h recall from each patient in three successive days. Nutrients and data analysis were done using FPII and SPSS version 13 softwares. The mean of log 10-transformed serum adiponectin concentration was 0.79 ± 0.27 μg/ml. The univariate linear regression analysis could not show any significant relation between the log of serum adiponectin and dietary factors. In multivariate linear regression after multiple adjustment, the log of serum adiponectin was independently associated with WHR (P = 0.02, t = ?2.33), HDL-C (P = 0.050, t = 2.03) and markedly but not significantly with age of patients (P = 0.058, t = 1.92).ConclusionsOur findings showed that WHR, one of the important cardiovascular risk factors, can modulate independently adiponectin levels of T2DM patients in inverse manner. Also, the age of patients and HDL-C levels have marked positive effect on circulating levels of this adipocytokine. Thus, adiponectin might be a useful biomarker to prevent developing CVD in type 2 diabetes.     

Insulin glargine versus insulin degludec in patients failing on oral therapy in type 2 diabetes: A retrospective real world comparative data from India

ObjectiveTo compare the changes in various glycemic parameters in insulin-naïve type 2 diabetes mellitus (DM) patients who were initiated on insulin glargine or insulin degludec in a real world setting.MethodsRetrospective data were analyzed in consecutive type 2 DM patients in a real world setting, who failed oral therapy (at least 2 oral anti-diabetic drugs) and were initiated with either insulin glargine or insulin degludec. The parameters assessed were the changes in HbA1c, fasting plasma glucose, body weight, dose of Insulin and the total number of patient reported hypoglycemic episodes up to 6 months after initiation.ResultAt baseline, insulin glargine and insulin degludec groups were similar in terms of gender, age, weight, HbA1c and duration of diabetes. After 6 months follow up the change in HbA1c (−1.09 versus −1.45 P = 0.124), change in FPG (−72.81 mg/dl [−4mmol/L] versus −75.88 mg/dl [−4.2 mmol/L] P = 0.755), and the change in body weight (+1.65 versus +0.85 P = 0.082) were similar in glargine and degludec groups, respectively. Patients in insulin degludec group experienced significantly lesser patient reported hypoglycemic episodes (12 versus 40) and required significantly lesser dose (25.68 Units versus 18.61 Units per day; P = 0.002) compared to insulin glargine. 41% of the patients reached HbA1C target of ≤7% with insulin glargine compared to 69% with insulin degludec within the specified time period.ConclusionResults from this real world analysis suggest that among type 2 DM patients who were initiated on insulin degludec as compared to insulin glargine may be associated with significantly lesser patient reported hypoglycemic episodes and lesser dose of insulin while achieving similar glycemic control. This study is however limited by the retrospective nature of the data collection.     

The consumption of bread enriched with betaglucan reduces LDL-cholesterol and improves insulin resistance in patients with type 2 diabetes

AimPrevious studies have shown that the water-soluble dietary fibre betaglucan, a natural component of oats, reduces cholesterol and postprandial hyperglycaemia. The aim of the present study was to investigate the effect of betaglucan-enriched bread consumption on the lipid profile and glucose homoeostasis of patients with type 2 diabetes (T2D).MethodsWe conducted a randomized, double-blind study in which 46 patients with T2D and LDL-C greater than 3.37 mmol/l (130 mg/dl) were randomized to incorporate into their diet, for 3 weeks, either bread enriched with betaglucan (providing 3 g/day of betaglucan) or white bread without betaglucan.ResultsThe consumption of bread containing betaglucan led to significant reductions (vs the control group) in LDL-C of 0.66 mmol/l (15.79%) versus 0.11 mmol/l (2.71%) (P = 0.009), in total cholesterol of 0.80 mmol/l (12.80%) versus 0.12 mmol/l (1.88%) (P = 0.006), in Fasting plasma insulin (FPI) of 3.23 μU/ml versus an increase of 3.77 μU/ml (P = 0.03) and in Homa-IR (Homoeostasis model assessment–insulin resistance) by 2.08 versus an increase of 1.33 (P = 0.04).ConclusionsBetaglucan enriched bread may contribute to the improvement of the lipid profile and insulin resistance in patients with T2D.     

Increased intestinal permeability as a risk factor for type 2 diabetes

AimRelationships between the intestinal microbiota, intestinal permeability and inflammation in the context of risk for obesity-associated disease continue to be of interest. The aim of the study was to examine the associations between intestinal permeability and type 2 diabetes (T2D).MethodsA total of 130 individuals with T2D (age: 57.5 ± 6.2 years (mean ± SD); BMI: 30.4 ± 3.2; 45% female) and 161 individuals without T2D (age: 37.4 ± 12.5 years; BMI: 25.1 ± 3.9; 65% female) were included in the study. Assessment of intestinal permeability included measurement of circulating lipopolysaccharide (LPS), LPS-binding protein (LBP) and intestinal fatty acid binding protein (iFABP) concentrations, which were used for calculation of a derived permeability risk score (PRS). Associations between permeability measures and T2D status were assessed using logistic regression models.ResultsLBP (∼34%, P < 0.001), iFABP (∼46%, P < 0.001) and the PRS (∼24% P < 0.001) were all significantly higher in the T2D affected individuals. Individuals with a PRS in the upper tertile were 5.07 times more likely (CI: 1.72–14.95; P = 0.003) to have T2D when models were adjusted for age, sex and BMI. There was a trend towards improved prediction when including the PRS in models containing age, sex and BMI (AUC: 0.954 versus 0.962; P = 0.06).ConclusionThese data demonstrate differences in measures of intestinal permeability between individuals with and without T2D. The utility of using intestinal permeability measures as a tool for predicting T2D risk in at risk individuals should be further investigated.     

Reductions in systolic blood pressure with liraglutide in patients with type 2 diabetes: Insights from a patient-level pooled analysis of six randomized clinical trials

AimsTo quantify the effect of liraglutide on systolic blood pressure (SBP) and pulse in patients with type 2 diabetes (T2D), and assess the influence of covariates on observed SBP reductions.MethodsA patient-level pooled analysis of six phase 3, randomized trials was conducted.ResultsThe analysis included 2792 randomized patients. In the intention-to-treat population (n = 2783), mean [± SE] SBP reductions from baseline with liraglutide 1.2 mg (2.7 [0.8] mmHg) and 1.8 mg (2.9 [0.7] mmHg) once daily were significantly greater than with placebo (0.5 [0.9] mmHg; P = 0.0029 and P = 0.0004, respectively) after 26 weeks, and were evident after 2 weeks. Liraglutide was also associated with significantly greater SBP reductions than glimepiride and, at a dose of 1.8 mg, insulin glargine and rosiglitazone. SBP reductions with liraglutide weakly correlated with weight loss (Pearson’s correlation coefficient: 0.08–0.12; P ≤ 0.0148). No dependence of these reductions on concomitant antihypertensive medications was detected (P = 0.1304). Liraglutide 1.2 and 1.8 mg were associated with mean increases in pulse of 3 beats per minute (bpm), versus a 1 bpm increase with placebo (P < 0.0001 for each dose versus placebo).ConclusionsLiraglutide reduces SBP in patients with T2D, including those receiving concomitant antihypertensive medication.     

Studying progression from glucose intolerance to type 2 diabetes in obese children

AimIdentification of metabolic and genetic factors capable to mediate progression from normal glucose tolerance (NGT) through impaired glucose tolerance (IGT) to type 2 diabetes (T2D) in childhood obesity.Patients and methodsThree groups of obese children with NGT (n = 54), IGT (n = 35), and T2D (n = 62) were evaluated. A control group of non-obese normal children (n = 210) was also studied. In obese patients, an oral glucose tolerance test (OGTT) was performed. Insulin resistance (IR) was assessed using HOMA-IR index. Insulin sensitivity (IS) was assessed according to the Matsuda formula. Genomic DNA from obese and control children was genotyped for genetic variants of PPARG, ADIPOQ, ADIPOR1, FTO, TCF7L2, and KCNJ11 using a real-time PCR strategy. The unpaired Student's t-test and Kruskal–Wallis one-way test were used to compare quantitative data in two and more groups. To assess the extent to which the various genetic variants were associated with pathology, ORs (odds ratios) and 95% CI (confidence interval) were estimated.ResultsIn T2D children, HOMA-IR value (7.5 ± 3.1) was significantly (P < 0.001) higher than that in IGT (4.21 ± 2.25) and NGT (4.1 ± 2.4) subjects. The Matsuda IS index was significantly increased in normoglycemic patients compared to IGT individuals (2.8 ± 1.75 vs. 2.33 ± 1.2, P < 0.05). The Pro12Ala polymorphism of PPARG was significantly associated with obesity (OR = 1.74, 95% CI = 1.19–2.55, P = 0.004) and T2D in obesity (OR = 2.01, 95% CI = 1.24–3.26, P = 0.004).ConclusionIR is a major risk factor that mediates progression from NGT to clinical T2D in Russian obese children. This progression may be genetically influenced by the Pro12Ala variant of PPARG.     

Association of myocardial dysfunction with vitamin D deficiency in patients with type 2 diabetes mellitus

AimsThe underlying mechanism of myocardial dysfunction in patients with type 2 diabetes mellitus (T2DM) is unclear. Nonetheless recent studies have revealed that vitamin D (vit-D) deficiency, which is prevalent in such patients, is associated with adverse cardiovascular events. We hypothesized that vit-D deficiency in patients with T2DM may contribute to left ventricular (LV) dysfunction.MethodsWe studied 95 patients (62 ± 9 years, 58% female) with T2DM. None had any history of coronary artery disease and all underwent detailed transthoracic echocardiography, including speckle tracking derived strains. Plasma level of 25-hydoxyvitamin D (25-OHD) was also measured.ResultsVitamin D deficiency was evident in 60 (63%) patients. The LV dimension, LVEF and diastolic grade were similar between those with and without deficiency although an impaired global longitudinal strain was present in the former. Importantly, 25-OHD was negatively associated with global longitudinal strain(R = − 0.21, P = 0.046) and positively with body-mass index (BMI; R = 0.26, P = 0.01). Both vit-D deficiency and BMI were associated with impaired global LV longitudinal strain, independent of T2DM disease characteristics.ConclusionsIn patients with T2DM and no history of coronary artery disease, vit-D deficiency is independently associated with impaired global longitudinal strain. This suggests that vit-D deficiency may contribute to the development of myocardial dysfunction in these patients.     

Does insulin resistance in type 2 diabetes alter vitamin D status?

AimsData on changes of vitamin D due to insulin resistance are conflicting. We assessed vitamin D concentrations and parameters of glycemia and mineral homeostasis in patients with insulin resistant type 2 diabetes and in matched normal controls.MethodsSixty-nine patients with type 2 diabetes and 60 matched normal control subjects were studied. After an overnight fast, blood was collected for measuring the parameters of glycemia (glucose, insulin and HbA1c), mineral profile (corrected calcium, phosphate and alkaline phosphatase), total 25(OH) vitamin D and parathyroid hormone (PTH) levels.ResultsPatients had significantly elevated fasting glucose (P = 0.0001), insulin (P = 0.0003) and HbA1c (P = 0.0005) than the controls had. They had significantly raised calculated insulin resistance compared with control subjects (P = 0.0001). Patients and controls had similar levels of serum corrected calcium and ALP, whereas serum phosphate was significantly lower in the patients compared with controls (P = 0.001).Patients and controls had similar levels of 25(OH)D, but the levels of 25(OH)D in both were in the deficiency range. Intact PTH was similar in the patients and controls. Levels of 25(OH)D did not demonstrate any relation with fasting insulin, insulin resistance, or HbA1c, but correlated negatively with intact PTH (r = ?0.4, P = 0.02).ConclusionThis study demonstrated prevalent vitamin D deficiency in insulin resistant type 2 diabetic and normal subjects. Insulin resistance did not influence the status of vitamin D.     

Association of fructosamine to indices of dyslipidemia in older adults with type 2 diabetes

AimsTo evaluate the association of serum fructosamine values to lipid profiles and to other indices of glycemia both at baseline and over time in adults with type 2 diabetes (T2DM).MethodsForty adults aged 45 or older with T2DM, not taking insulin, and an HbA1c of 6–10% were enrolled in a randomized controlled trial regarding the effects of an 8-week yoga program on glycemia and related cardiovascular disease risk indices in adults with T2DM. Fasting blood was drawn to assess glycemia (HbA1c, glucose, and fructosamine) and dyslipidemia (LDL, HDL, total cholesterol, cholesterol:HDL ratio, LDL:HDL ratio, and triglycerides) pre and post-intervention. Because the relation of fructosamine to other indices of glycemia and to lipid profiles did not differ between treatment groups either at baseline or over time, groups were pooled for analysis.ResultsBaseline fructosamine values were significantly correlated with HbA1c (r = 0.77, P < 0.0001), glucose (r = 0.72, P < 0.0001), LDL:HDL ratio (r = 0.46, P = 0.01), cholesterol:HDL ratio (r = 0.55, P = 0.002), and triglycerides (r = 0.39, P = 0.032), but not to other lipid indices at baseline. Change in fructosamine over 8 weeks was significantly correlated with change in HbA1c (r = 0.63, P = 0.0001), glucose (r = 0.39, P = 0.029), cholesterol (r = 0.65, P < 0.0001), LDL (r = 0.55, P = 0.001), LDL:HDL ratio (r = 0.53, P = 0.003), and cholesterol:HDL ratio (r = 0.52, P = 0.002), and was more strongly related to change in lipid values than were other indices of glycemia.ConclusionsFructosamine was significantly correlated with measures of dyslipidemia and glycemia both at baseline and over time, and may represent a relatively sensitive and low cost index of short to medium term change in both glycemia and certain lipid profiles. However, findings from this small pilot study should be interpreted with caution, and warrant replication in larger prospective studies.     

Glycemic control among patients with type 2 diabetes at a primary health care center in Oman

AimsTo determine the status of blood sugar control by using fasting blood sugar (FBS) of ≤6.1 mmol/l and glycosyted hemoglobin A1c (HbAc1) of <7% as indictors of glycemic control and to assess the influence of demographic, blood pressure (BP) and lipid characteristics on glycemic control.MethodsThis retrospective study included all Omani patients with type 2 diabetes (N = 177) attended a primary health care center in Al-Dakhiliya region, Oman.ResultsThe overall mean age of the cohort was 53 ± 12 years (range: 24–91) with females representing 60% (n = 106) of the study sample. The study found that only 9.6% (n = 17) and 35% (n = 62) of the patients attained optimal FBS and HbAc1 levels, respectively. Higher HbA1c was significantly associated with higher diastolic BP (84 versus 80 mm Hg; p = 0.006), higher total cholesterol (5.2 versus 4.7 mmol/l; p = 0.002) and higher low-density lipoprotein cholesterol (3.8 versus 3.0 mmol/l; p = 0.034).ConclusionsThe results demonstrated poor glycemic control in Oman type 2 diabetic patients comparable to local and global studies especially in those hypertensive and dyslipidemic patients. Implementation of early and aggressive management of diabetes mellitus at the primary care setting is warranted.     

Risk of type 2 diabetes and cumulative excess weight exposure in the Framingham Offspring Study

AimMid-life obesity is associated with T2D risk. However, less is known about the cumulative effect of obesity during adulthood.MethodsFramingham Offspring Study participants who had an examination at 35 ± 2 years and were initially free of T2D were included in this study (N = 1026). A cumulative excess weight (CEW) score (year*kg/m²) was calculated until T2D diagnostic or the end of follow-up.ResultsEighty-four individuals (8.2%) developed T2D over 20 ± 6 years. Mean CEW scores were 118.0 ± 114.6 year*kg/m² in individuals who developed T2D and 30.2 ± 91.4 year*kg/m² in those who did not develop T2D (P < 0.01). T2D risk was doubled for each standard deviation increase in the CEW score (OR = 1.99 [1.64-2.40]; P < 0.001). However, CEW score was only significantly associated with T2D incidence for participants with a baseline BMI < 25 kg/m² (OR = 2.13 [1.36–3.36]; P < 0.001).ConclusionsAccumulating weight between the mid-thirties to the mid-fifties increases the risk of developing T2D. However, BMI in mid-thirties remains a stronger predictor of T2D risk.