METHOD: Intriguing evidences discussed the contribution of different intracellular compartments in autophagy membrane formation. Furthermore, autophagy serves to mobilise membranes within cells, thereby promoting cytoplasmic components reorganisation. The intent of this review is to focus on the possibility of autophagy to act as a carrier for GLUT4 through regulating GLUT4 endocytosis, intracellular trafficking in different compartments, and translocation to cell membrane.
RESULTS: The common themes of autophagy and GLUT4 have been highlighted. The review discussed the overlapping of endocytosis mechanism and intracellular compartments, and has shown that autophagy and GLUT4 utilise similar proteins (SNAREs) which are used for exocytosis. On top of that, PI3K and AMPK also control both autophagy and GLUT4.
CONCLUSION: The control of GLUT4 trafficking through autophagy could be a promising field for treating type 2 diabetes.
Methods: 2,2-diphenyl-1-picrylhydrazyl (DPPH) and Ferric reducing antioxidant power assay (FRAP) were applied to evaluate the antioxidant activity of carob. In vitro cytotoxicity of carob was conducted on human hepatocytes (WRL68) and rat pancreatic β-cells (RIN-5F). Acute oral toxicity of carob was conducted on a total of 18 male and 18 female Sprague-Dawley (SD) rats, which were subdivided into three groups (n = 6), namely: high and low dose carob-treated (CS5000 and CS2000, respectively) as well as the normal control (NC) receiving a single oral dose of 5,000 mg kg-1 carob, 2,000 mg kg-1 carob and 5 mL kg-1 distilled water for 14 days, respectively. Alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, total bilirubin, creatinine and urea were assessed. Livers and kidneys were harvested for histopathology. In vitro inhibitory effect against α-amylase and α-glucosidase was evaluated. In vivo glycemic activity was conducted on 24 male SD rats which were previously intraperitoneally injected with 55 mg kg-1 streptozotocin (STZ) followed by 210 mg kg-1nicotinamide to induce type 2 diabetes mellitus. An extra non-injected group (n = 6) was added as a normal control (NC). The injected-rats were divided into four groups (n = 6), namely: diabetic control (D0), 5 mg kg-1glibenclamide-treated diabetic (GD), 500 mg kg-1 carob-treated diabetic (CS500) and 1,000 mg kg-1 carob-treated diabetic (CS1000). All groups received a single oral daily dose of their treatment for 4 weeks. Body weight, fasting blood glucose (FBG), oral glucose tolerance test, biochemistry, insulin and hemostatic model assessment were assessed. Pancreases was harvested for histopathology.
Results: Carob demonstrated a FRAP value of 3191.67 ± 54.34 µmoL Fe++ and IC50 of DPPH of 11.23 ± 0.47 µg mL-1. In vitro, carob was non-toxic on hepatocytes and pancreatic β-cells. In acute oral toxicity, liver and kidney functions and their histological sections showed no abnormalities. Carob exerted an in vitro inhibitory effect against α-amylase and α-glucosidase with IC50 of 92.99 ± 0.22 and 97.13 ± 4.11 µg mL-1, respectively. In diabetic induced rats, FBG of CS1000 was significantly less than diabetic control. Histological pancreatic sections of CS1000 showed less destruction of β-cells than CS500 and diabetic control.
Conclusion: Carob pod did not cause acute systemic toxicity and showed in vitro antioxidant effects. On the other hand, inhibiting α-amylase and α-glucosidase was evident. Interestingly, a high dose of carob exhibits an in vivo antihyperglycemic activity and warrants further in-depth study to identify the potential carob extract composition.
METHODS: A total of 1065 patients aged ≥18 years with T2DM initiating insulin therapy in normal clinical course were enrolled from Hong Kong, Malaysia, Philippines, Taiwan and Thailand. Participants' data was recorded by the treating physicians. Patient-reported outcomes (PROs) were assessed using questionnaires completed by participants.
RESULTS: The mean age of patients was 57.2 years with mean glycosylated hemoglobin (HbA1c) of 10.0%. About 66% of patients had an HbA1c ≥9.0% at insulin initiation despite 74% of them being on two or more oral antidiabetic agents at the time of insulin initiation. Basal insulin was initiated in 72% and premixed insulin in 27% of patients. Changes in insulin therapy was observed in 63% of patients and, by the end of study, 28% achieved HbA1c levels of <7.5%. The proportion of patients completely satisfied with their insulin treatment increased over the study course and the quality of life (QoL) score increased from baseline to the study end.
CONCLUSION: As high HbA1C levels indicate a delayed start of insulin therapy, timely initiation and early intensification of insulin therapy is necessary in the region to achieve adequate glycemic control in time and prevent diabetes complications. Data from PROs suggests that the insulin treatment improves QoL in most patients.
METHODS: A total of 243 participants from MyBFF@home were included in this study. Fasting blood samples at baseline, 6- and 12-month were assessed for fasting plasma glucose (FPG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides. The effect of the intervention on cardiometabolic risk markers were investigated within and between study groups using t-test and general linear model (GLM) repeated measure ANOVA.
RESULTS: Results from repeated measures ANOVA showed intervention effect only in TC where significant reduction was found in the intervention group (- 0.26 mmol/L [95% CI: - 0.47 to - 0.06], p
METHODS: Healthy participants consumed pure forms of a non-nutritive sweetener (NNS) mixed with water that were standardized to doses of 14% (0.425 g) of the acceptable daily intake (ADI) for aspartame and 20% (0.136 g) of the ADI for sucralose every day for two weeks. Blood samples were collected and analysed for glucose, insulin, active glucagon-like peptide-1 (GLP-1), and leptin.
RESULTS: Seventeen participants (10 females and 7 males; age 24 ± 6.8 years; BMI 22.9 ± 2.5 kg/m2) participated in the study. The total area under the curve (AUC) values of glucose, insulin, active GLP-1 and leptin were similar for the aspartame and sucralose treatment groups compared to the baseline values in healthy participants. There was no change in insulin sensitivity after NNS treatment compared to the baseline values.
CONCLUSIONS: These findings suggest that daily repeated consumption of pure sucralose or aspartame for 2 weeks had no effect on glucose metabolism among normoglycaemic adults. However, these results need to be tested in studies with longer durations. Novelty: • Daily consumption of pure aspartame or sucralose for 2 weeks had no effect on glucose metabolism. • Daily consumption of pure aspartame or sucralose for 2 weeks had no effect on insulin sensitivity among healthy adults.