MATERIALS AND METHODS: This was an investigator-initiated, single-center, randomized, controlled, clinical trial in patients with T2DM and DKD, comparing 12-weeks of low carbohydrate diet (<20g daily intake) versus standard low protein (0.8g/kg/day) and low salt diet. Patients in the VLCBD group underwent 2-weekly monitoring including their 3-day food diaries. In addition, Dual-energy x-ray absorptiometry (DEXA) was performed to estimate body fat percentages.
RESULTS: The study population (n = 30) had a median age of 57 years old and a BMI of 30.68kg/m2. Both groups showed similar total calorie intake, i.e. 739.33 (IQR288.48) vs 789.92 (IQR522.4) kcal, by the end of the study. The VLCBD group showed significantly lower daily carbohydrate intake 27 (IQR25) g vs 89.33 (IQR77.4) g, p<0.001, significantly higher protein intake per day 44.08 (IQR21.98) g vs 29.63 (IQR16.35) g, p<0.05 and no difference in in daily fat intake. Both groups showed no worsening of serum creatinine at study end, with consistent declines in HbA1c (1.3(1.1) vs 0.7(1.25) %) and fasting blood glucose (1.5(3.37) vs 1.3(5.7) mmol/L). The VLCBD group showed significant reductions in total daily insulin dose (39(22) vs 0 IU, p<0.001), increased LDL-C and HDL-C, decline in IL-6 levels; with contrasting results in the control group. This was associated with significant weight reduction (-4.0(3.9) vs 0.2(4.2) kg, p = <0.001) and improvements in body fat percentages. WC was significantly reduced in the VLCBD group, even after adjustments to age, HbA1c, weight and creatinine changes. Both dietary interventions were well received with no reported adverse events.
CONCLUSION: This study demonstrated that dietary intervention of very low carbohydrate diet in patients with underlying diabetic kidney disease was safe and associated with significant improvements in glycemic control, anthropometric measurements including weight, abdominal adiposity and IL-6. Renal outcomes remained unchanged. These findings would strengthen the importance of this dietary intervention as part of the management of patients with diabetic kidney disease.
METHODS: Genetic analysis was performed in 42 patients with MODY aged 1 month to 18 years among a cohort of 759 patients with diabetes, identified with the following four clinical criteria: age of diagnosis ≤18 years; negative pancreatic autoantibodies; family history of diabetes; or persistently detectable C-peptide; or diabetes associated with extrapancreatic features. GCK gene mutations were first screened by Sanger sequencing. GCK mutation-negative patients were further analyzed by WES.
RESULTS: Mutations were identified in 24 patients: 20 mutations in GCK, 1 in HNF4A, 1 in INS, 1 in ABCC8, and a 17q12 microdeletion. Four previously unpublished novel GCK mutations: c.1108G>C in exon 9, and c.1339C>T, c.1288_1290delCTG, and c.1340_1343delGGGGinsCTGGTCT in exon 10 were detected. WES identified a novel missense mutation c.311A>G in exon 3 in the INS gene, and copy number variation analysis detected a 1.4 Mb microdeletion in the long arm of the chromosome 17q12 region. Compared with mutation-negative subjects, the mutation-positive subjects had lower hemoglobin A1c and initial blood glucose levels.
CONCLUSIONS: Most MODY cases in this study were due to GCK mutations, which is in contrast to previous reports in Chinese patients. Diabetes associated with extrapancreatic features should be a clinical criterion for MODY genetic analysis. Mutational analysis by WES provided a precise diagnosis of MODY subtypes. Moreover, WES can be useful for detecting large deletions in coding regions in addition to point mutations.
FINDINGS: A total of 274 venous blood was collected from normal healthy adults during the community screening programmes. The performance of POC devices, Afinion and Quo-test were compared to central laboratory HPLC method; Adams A1c HA 8160. Both POC devices showed good correlation to HA 8160 with r = 0.94 (p < 0.001) and r = 0.95 (p < 0.001) for Afinion and Quo-test respectively. The means difference were statistically higher between POC and HA 8160 with 0.23% (95% CI 0.19-0.26, p < 0.001) and 0.29% (95% CI 0.24-0.34, p < 0.001) for Afinion and Quo-test respectively.
CONCLUSIONS: Both POC devices could be considered in health clinics for diabetes management but not to be used for the diagnostic purposes.
MATERIAL AND METHODS: This was a five-year retrospective open cohort study using secondary data from the National Diabetes Registry. The study setting was all public health clinics (n = 47) in the state of Negeri Sembilan, Malaysia. Time to treatment intensification was defined as the number of years from the index year until the addition of another oral antidiabetic drug or initiation of insulin. Life table survival analysis based on best-worst case scenarios was used to determine the time to treatment intensification. Discrete-time proportional hazards model was fitted for the factors associated with treatment intensification.
RESULTS: The mean follow-up duration was 2.6 (SD 1.1) years. Of 7,646 patients, the median time to treatment intensification was 1.29 years (15.5 months), 1.58 years (19.0 months) and 2.32 years (27.8 months) under the best-, average- and worst-case scenarios respectively. The proportion of patients with treatment intensification was 45.4% (95% CI: 44.2-46.5), of which 34.6% occurred only after one year. Younger adults, overweight, obesity, use of antiplatelet medications and poorer HbA1c were positively associated with treatment intensification. Patients treated with more oral antidiabetics were less likely to have treatment intensification.
CONCLUSION: Clinical inertia is present in the management of T2D patients in Malaysian public health clinics. We recommend further studies in lower- and middle-income countries to explore its causes so that targeted strategies can be developed to address this issue.
METHODS: This is a controlled, intervention based study. It was run on three phases: before, during, and after Ramadan on 262 type 2 diabetes patients. The intervention group (n = 140) received RFEP on medications doses & timing adjustment before and after Ramadan, while the control group (n = 122) received standard care.
RESULTS: The dose of insulin glargine was reduced from 42.51 ± 22.16 at the baseline to 40.11 ± 18.51-units during Ramadan (p = 0.002) in the intervention group while it remained the same in the control group before Ramadan and during Ramadan (38.51 ± 18.63 and 38.14 ± 18.46, P = 0.428, respectively). The hypoglycemia score was 14.2 ± (8.5) pre-Ramadan in the intervention and reduced to 6.36 ± 6.17 during Ramadan (p
METHODS: A randomized, double-blind, placebo-controlled trial was performed in a university hospital. Women with GDMA1 were recruited at 16-30 weeks of pregnancy and randomized to oral metformin 500 mg twice daily or identical placebo tablets to delivery. Level of HbA1c was taken at recruitment and at 36 weeks of pregnancy. The primary outcome was the change in level of HbA1c at recruitment and 36 weeks of pregnancy.
RESULTS: Data from 106 participants were analyzed. The level of HbA1c during pregnancy increased significantly with a mean increase of 0.20% ± 0.31% (P
METHODS: Patients who were 10 to less than 17 years of age were randomly assigned, in a 1:1 ratio, to receive subcutaneous liraglutide (up to 1.8 mg per day) or placebo for a 26-week double-blind period, followed by a 26-week open-label extension period. Inclusion criteria were a body-mass index greater than the 85th percentile and a glycated hemoglobin level between 7.0 and 11.0% if the patients were being treated with diet and exercise alone or between 6.5 and 11.0% if they were being treated with metformin (with or without insulin). All the patients received metformin during the trial. The primary end point was the change from baseline in the glycated hemoglobin level after 26 weeks. Secondary end points included the change in fasting plasma glucose level. Safety was assessed throughout the course of the trial.
RESULTS: Of 135 patients who underwent randomization, 134 received at least one dose of liraglutide (66 patients) or placebo (68 patients). Demographic characteristics were similar in the two groups (mean age, 14.6 years). At the 26-week analysis of the primary efficacy end point, the mean glycated hemoglobin level had decreased by 0.64 percentage points with liraglutide and increased by 0.42 percentage points with placebo, for an estimated treatment difference of -1.06 percentage points (P<0.001); the difference increased to -1.30 percentage points by 52 weeks. The fasting plasma glucose level had decreased at both time points in the liraglutide group but had increased in the placebo group. The number of patients who reported adverse events was similar in the two groups (56 [84.8%] with liraglutide and 55 [80.9%] with placebo), but the overall rates of adverse events and gastrointestinal adverse events were higher with liraglutide.
CONCLUSIONS: In children and adolescents with type 2 diabetes, liraglutide, at a dose of up to 1.8 mg per day (added to metformin, with or without basal insulin), was efficacious in improving glycemic control over 52 weeks. This efficacy came at the cost of an increased frequency of gastrointestinal adverse events. (Funded by Novo Nordisk; Ellipse ClinicalTrials.gov number, NCT01541215.).