METHODS: We randomized 108 overweight and obese patients with T2D (46 M/62F; age 60 ± 10 years; HbA1c 8.07 ± 1.05%; weight 101.4 ± 21.1 kg and BMI 35.2 ± 7.7 kg/m2) into three groups. Group A met with RDN to develop an individualized eating plan. Group B met with RDN and followed a structured meal plan. Group C did similar to group B and received weekly phone support by RDN.
RESULTS: After 16 weeks, all three groups had a significant reduction of their energy intake compared to baseline. HbA1c did not change from baseline in group A, but decreased significantly in groups B (- 0.66%, 95% CI -1.03 to - 0.30) and C (- 0.61%, 95% CI -1.0 to - 0.23) (p value for difference among groups over time
MATERIALS AND METHODS: This was a retrospective study conducted at nephrology unit of a tertiary hospital in Kedah. All diabetic ESRD patients who fulfilled the inclusion criteria were identified and recruited for analysis.
RESULTS: The mean duration of DM to ESRD was found to be 14.37 ± 4.42 years. Mean duration for the onset of diabetic nephropathy was 8.73 ± 3.37 years. There was a relative short duration from diabetic nephropathy to ESRD noted, which was 5.63 ± 2.06 years. The mean duration of DM to ESRD for patients receiving RAAS blocker was found to be 18.23 ± 2.38 years as compared to 11.41 ± 2.94 years for those who did not (95% CI: -0.64 to -2.46). For different type of RAAS blockers, namely ACE inhibitor and angiotensin receptor blocker (ARB), there was no significant difference observed pertaining to mean duration of DM to ESRD; 17.89 ± 1.97 years for ACEi and 19.00 ± 4.16 years for ARB (95% CI: -4.74 to 2.52).
DISCUSSION: Time frame from diabetic nephropathy to ESRF among Malaysian population was shorter as compared to findings from other countries with an average period of 15 to 25 years. RAAS blockers should be initiated early in diabetic patients.
METHODS: We studied 101 patients with pre-operative diabetes and albuminuria [defined as urine albumin:creatinine ratio (uACR) > 30 mg/g] who underwent bariatric surgery at an academic center from 2005 to 2014.
RESULTS: Fifty-seven patients (56%) were female with a mean age of 53 (± 11) years. The mean pre-operative BMI and glycated hemoglobin (HbA1c) were 43.1 (± 7.6) kg/m2 and 8.4 (± 1.8)%, respectively. The median pre-operative uACR was 80.0 (45.0-231.0) mg/g. Bariatric procedures included Roux-en-Y gastric bypass (n = 75, 74%) and sleeve gastrectomy (n = 26, 26%). The mean follow-up period was 61 (± 29) months. At last follow-up, the mean BMI was 33.8 (± 8.3) kg/m2. The overall glycemic control improved after bariatric surgery. At last follow-up, 73% had good glycemic control (HbA1c type 2 diabetes. Our data showed almost an 80% improvement in albuminuria at the short- and long-term period after bariatric surgery.
MATERIALS & METHODS: A total of 50 participants with T2DM with peripheral neuropathy were included. Age group of 30-75 years were selected for the study. Participants with a known history of neurological disease, locomotor disability, and pregnancy were excluded from the study. Demographic details of the participants like duration of diabetes mellitus, age, Fasting Blood Glucose, Fasting Insulin, HOMA-IR, Glycated Haemoglobin (HBA1c), Neuropathy and Blood pressure values were noted. We measured Basal Metabolic Rate (BMR) by using Mifflin-St Jeor predictive equation in T2DM with peripheral neuropathy.
RESULTS: The mean age of the participants is 60.16 ± 10.62. The mean duration of T2DM 13.44 ± 11.92. In the present study we found a statistical significant correlation between BMR and HOMA IR (r = 0.913*; p = 0.000), BMR & Fasting blood sugar (FBS) (r = 0.281*; p = 0.048), BMR and Visceral fat (VF) (r = 0.332*; p = 0.018).
CONCLUSION: Basal metabolic rate is correlated to Homa-IR, visceral fat, fasting blood sugar and musculoskeletal mass among T2DM with peripheral neuropathy.
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.
CASE PRESENTATION: The present report describes a case of F. philomiragia bacteraemia first reported in Malaysia and Asian in a 60-year-old patient with underlying end-stage renal disease (ESRF) and diabetes mellitus. He presented with Acute Pulmonary Oedema with Non-ST-Elevation Myocardial Infarction (NSTEMI) in our hospital. He was intubated in view of persistent type I respiratory failure and persistent desaturation despite post haemodialysis. Blood investigation indicated the presence of ongoing infection and inflammation. The aerobic blood culture growth of F. philomiragia was identified using the matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometry (Score value: 2.16) and confirmed by 16S Ribosomal DNA (16S rDNA) sequencing. He was discharged well on day 26 of admission, after completing one week of piperacillin/tazobactam and two weeks of doxycycline.
CONCLUSION: Clinical suspicion should be raised if patients with known risk factors are presenting with pneumonia or pulmonary nodules especially as these are the most common manifestations of F. philomiragia infection. Early diagnosis via accurate laboratory identification of the organism through MALDI-TOF mass spectrometry and molecular technique such as 16S rDNA sequencing are vital for prompt treatment that results in better outcomes for the afflicted patients.
OBJECTIVES: To investigate the anti-atherosclerotic activity of a C. nutans leaf methanol extract (CNME) in a type 2 diabetic (T2D) rat model induced by a high-fat diet (HFD) and low-dose streptozotocin.
MATERIALS AND METHODS: Sixty male Sprague-Dawley rats were divided into five groups: non-diabetic fed a standard diet (C), C + CNME (500 mg/kg, orally), diabetic fed an HFD (DM), DM + CNME (500 mg/kg), and DM + Metformin (DM + Met; 300 mg/kg). Treatment with oral CNME and metformin was administered for 4 weeks. Fasting blood glucose (FBG), serum lipid profile, atherogenic index (AI), aortic tissue superoxide dismutase levels (SOD), malondialdehyde (MDA), and tumour necrosis factor-alpha (TNF-α) were measured. The rats' aortas were stained for histological analysis and intima-media thickness (IMT), a marker of subclinical atherosclerosis.
RESULTS: The CNME-treated diabetic rats had reduced serum total cholesterol (43.74%; p = 0.0031), triglycerides (80.91%; p = 0.0003), low-density lipoprotein cholesterol (56.64%; p = 0.0008), AI (51.32%; p
OBJECTIVES: To determine the prevalence and characteristics of NAFLD in individuals with metabolically healthy obesity.
SETTING: A tertiary, academic, referral hospital.
METHODS: All patients who underwent bariatric surgery with intraoperative liver biopsy from 2008 to 2015 were identified. Patients with preoperative hypertension, dyslipidemia, or prediabetes/diabetes were excluded to identify a cohort of metabolically healthy obesity patients. Liver biopsy reports were reviewed to determine the prevalence of NAFLD.
RESULTS: A total of 270 patients (7.0% of the total bariatric surgery patients) met the strict inclusion criteria for metabolically healthy obesity. The average age was 38 ± 10 years and the average body mass index was 47 ± 7 kg/m2. Abnormal alanine aminotransferase (>45 U/L) and asparate aminotransferase levels (>40 U/L) were observed in 28 (10.4%) and 18 (6.7%) patients, respectively. A total of 96 (35.5%) patients had NAFLD with NALFD Activity Scores 0 to 2 (n = 61), 3 to 4 (n = 25), and 5 to 8 (n = 10). A total of 62 (23%) patients had lobular inflammation, 23 (8.5%) had hepatocyte ballooning, 22 (8.2%) had steatohepatitis, and 12 (4.4%) had liver fibrosis.
CONCLUSION: Even with the use of strict criteria to eliminate all patients with any metabolic problems, a significant proportion of metabolically healthy patients had unsuspected NAFLD. The need and clinical utility of routine screening of obese patients for fatty liver disease and the role of bariatric surgery in the management of NAFLD warrants further investigation.
MATERIALS AND METHODS: A total of 100 type 2 diabetes participants with stage 3-4 CKD were recruited. Blood for glycated hemoglobin (HbA1c ), serum 25(OH)D, renal and lipid profiles were drawn at enrollment. Correlation and regression analyses were carried out to assess the relationship of serum 25(OH)D, HbA1c and other metabolic traits.
RESULTS: A total of 30, 42, and 28% of participants were in CKD stage 3a, 3b and 4, respectively. The proportions of participants based on ethnicity were 51% Malay, 24% Chinese and 25% Indian. The mean (±SD) age and body mass index were 60.5 ± 9.0 years and 28.3 ± 5.9 kg/m2 , whereas mean HbA1c and serum 25(OH)D were 7.9 ± 1.6% and 37.1 ± 22.2 nmol/L. HbA1c was negatively correlated with serum 25(OH)D (rs = -0.314, P = 0.002), but positively correlated with body mass index (rs = 0.272, P = 0.006) and serum low-density lipoprotein cholesterol (P = 0.006). There was a significant negative correlation between serum 25(OH)D and total daily dose of insulin prescribed (rs = -0.257, P = 0.042). Regression analyses showed that every 10-nmol/L decline in serum 25(OH)D was associated with a 0.2% increase in HbA1c .
CONCLUSIONS: Lower serum 25(OH)D was associated with poorer glycemic control and higher insulin use among multi-ethnic Asians with type 2 diabetes and stage 3-4 CKD.