METHODS: This was a cross-sectional, single-center study involving adults with established COPD (n = 186) divided into those with or without hospital admissions for acute exacerbation. Oral glucose tolerance test (OGTT) was performed in patients with no known history of dysglycemia.
RESULTS: There were 16 patients who had overt diabetes, and 32 had prediabetes following the OGTT. Forty percent had histories of hospital admissions for COPD exacerbations. Both groups demonstrated similar 2-h post prandial glucose, glycated hemoglobin (HbA1c) and fasting blood glucose. The incidences of newly diagnosed dysglycemia were higher in both groups (40.8% vs 34.6%, p = 0.57). Cumulative days of admission (≥6 days/year) and weight (≥65 kg) were identified as predictors for dysglycemia within the study population.
DISCUSSION: This study demonstrated a high number of overt and newly diagnosed dysglycemia among COPD patients who had no previous history of abnormal glucose. Recent acute exacerbations of COPD could have a negative impact on glycemia, although the results did not attain statistical significance. However, there is a need for adequate screening for dysglycemia, particularly among those with frequent acute exacerbations of their condition.
Methods: In this study, type 2 diabetes model mice were induced by streptozotocin and high-fat diet (HFD) and used to evaluate the antihyperglycemic and anti-inflammatory effects of FFP. Mice were fed with HFD and challenged with 30 mg/kg body weight (BW) of streptozotocin for 1 month followed by 6 weeks of supplementation with 0.1 and 1.0 g/kg BW of FFP. Metformin was used as positive control treatment.
Results: Xeniji™-supplemented hyperglycemic mice were recorded with lower glucose level after 6 weeks of duration. This effect was contributed by the improvement of insulin sensitivity in the hyperglycemic mice indicated by the oral glucose tolerance test, insulin tolerance test, and end point insulin level. In addition, gene expression study has shown that the antihyperglycemic effect of FFP is related to the improvement of lipid and glucose metabolism in the mice. Furthermore, both 0.1 and 1 g/kg BW of FFP was able to reduce hyperglycemia-related inflammation indicated by the reduction of proinflammatory cytokines, NF-kB and iNOS gene expression and nitric oxide level.
Conclusion: FFP potentially demonstrated in vivo antihyperglycemic and anti-inflammatory effects on HFD and streptozotocin-induced diabetic mice.
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: Twenty healthy subjects were enrolled in a randomized, 3-way, blinded cross-over trial. The study was registered under ClinicalTrials.gov Identifier no. NCT00123456. At each test day, the subjects received one of three meals comprising 30 g of starch with 5 g of LD or UP or an energy-adjusted control meal containing pea protein. Fasting and postprandial blood glucose, insulin, C-peptide and glucagon-like peptide-1 (GLP-1) concentrations were measured. Subjective appetite sensations were scored using visual analogue scales (VAS).
RESULTS: Linear mixed model (LMM) analysis showed a lower blood glucose, insulin and C-peptide response following the intake of LD and UP, after correction for body weight. Participants weighing ≤ 63 kg had a reduced glucose response compared to control meal between 40 and 90 min both following LD and UP meals. Furthermore, LMM analysis for C-peptide showed a significantly lower response after intake of LD. Compared to the control meal, GLP-1 response was higher after the LD meal, both before and after the body weight adjustment. The VAS scores showed a decreased appetite sensation after intake of the seaweeds. Ad-libitum food intake was not different three hours after the seaweed meals compared to control.
CONCLUSIONS: Concomitant ingestion of brown seaweeds may help improving postprandial glycaemic and appetite control in healthy and normal weight adults, depending on the dose per body weight.
CLINICAL TRIAL REGISTRY NUMBER: Clinicaltrials.gov (ID# NCT02608372).
METHOD: This cross-sectional study involved eighty-three (n=83) adults attending a health screening program at Universiti Putra Malaysia (UPM). Demographic data, anthropometric measurements and blood samples for fasting blood glucose (FBG), fasting lipid profile (FSL), glycated haemoglobin (HbA1c) and hsCRP were taken. Respondents were grouped according to FRS and the Joint Interim Statement into 10-year CVD risk categories (low, intermediate and high) and MetS, respectively.
RESULTS: hsCRP was significantly increased in patients with high body mass index (BMI) (p=0.001), at-risk waist circumference (WC) (p=0.001) and MetS (p=0.009). Spearman's correlation coefficient showed a significant positive correlation between hsCRP level and total FRS score (r=0.26, p<0.05) and HDL-C score (r=0.22, p<0.05).
CONCLUSION: The significant difference of hsCRP levels across obesity levels and MetS with its modest correlation with FRS scores supported the adjunctive role of hsCRP in CVD risk prediction, most likely capturing the inflammatory pathological aspect and thus partly accounting for the residual CVD risk.