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1.
Diabet Med ; 39(2): e14680, 2022 02.
Article in English | MEDLINE | ID: mdl-34449919

ABSTRACT

AIMS: The study aimed at determining 5-year incidence and prediction nomogram for new-onset type 2 diabetes (T2D) in a middle-aged population in Vietnam. METHODS: A population-based prospective study was designed to collect socio-economic, anthropometric, lifestyle and clinical data. Five-year T2D incidence was estimated and adjusted for age and sex. Hazard ratio (HR) for T2D was investigated using discrete-time proportional hazards model. T2D prediction model entering the most significant risk factors was developed using the multivariable logistic-regression algorithm. The corresponding prediction nomogram was constructed and checked for discrimination, calibration and clinical usefulness. RESULTS: The age- and sex-adjusted incidence was 21.0 cases (95% CI: 12.2-40.0) per 1000 person-years in people with mean BMI of 22.2 (95% CI: 21.9-22.7 kg/m2 ). The HRs (95% CI) for T2D were 1.14 (1.05-1.23) per 10 mmHg systolic blood pressure, 1.05 (1.03-1.08) per 1 cm waist circumference, 1.40 (1.13-1.73) per 1 mmol/L fasting blood glucose, 1.77 (1.15-2.71) per sleeping time (<6 h/day vs 6-7 h/day) and 2.12 (1.25-3.61) per residence (urban vs rural). The prediction nomogram for new-onset T2D had a good discrimination (area under curve: 0.711, 95% CI: 0.666-0.755) and fit calibration (mean absolute error: 0.009). For the predicted probability thresholds between 0.03 and 0.36, the nomogram showed a positive net benefit, without increasing the number of false positives. CONCLUSION: This study highlighted an alarmingly high incidence of T2D in a middle-aged population with a normal range BMI in Vietnam. The individual prediction nomogram with decision curve analysis for new-onset T2D would be valuable for early detection, intervention and treatment of the condition.


Subject(s)
Body Mass Index , Diabetes Mellitus, Type 2/epidemiology , Nomograms , Population Surveillance , Adult , Diabetes Mellitus, Type 2/physiopathology , Female , Follow-Up Studies , Humans , Incidence , Male , Middle Aged , Prospective Studies , ROC Curve , Risk Factors , Time Factors , Vietnam/epidemiology
2.
Biomed Res ; 36(1): 63-70, 2015.
Article in English | MEDLINE | ID: mdl-25749152

ABSTRACT

This study, using C57BL/6J mice with streptozotocin (STZ)-induced diabetes, aimed to determine whether Bifidobacterium species (spp.) both induces the expressions of proteins in the insulin signaling pathway and enhances the expressions of certain adipocytokines. The protein expressions of IκB kinase alpha (IKKα), IκB kinase beta (IKKß), nuclear factor-kappaB inhibitor alpha (IκBα), and the mitogen-activated protein kinase (MAPK) pathway were also investigated. Oral administration of Bifidobacterium spp. reduced blood glucose levels significantly and increased the protein expressions of insulin receptor beta, insulin receptor substrate 1, protein kinase B (Akt/PKB), IKKα, and IκBα. Extracellular-signal-regulated kinase 2 (ERK2) showed increased expression. Bifidobacterium spp. also induced the adiponectin expression and decreased both macrophage chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6) expression. In addition, IKKß, c-Jun NH2-terminal kinase (JNK) and p38 MAP kinase expressions showed no significant changes in both groups. In conclusion, Bifidobacterium spp. may be the promising bacteria for treating diabetes.


Subject(s)
Bifidobacterium/physiology , Blood Glucose/metabolism , Diabetes Mellitus, Experimental/diet therapy , Gene Expression Regulation/drug effects , Insulin/blood , Probiotics/pharmacology , Adiponectin/genetics , Adiponectin/metabolism , Administration, Oral , Animals , Chemokine CCL2/genetics , Chemokine CCL2/metabolism , Diabetes Mellitus, Experimental/blood , Diabetes Mellitus, Experimental/chemically induced , Diabetes Mellitus, Experimental/genetics , I-kappa B Kinase/genetics , I-kappa B Kinase/metabolism , Insulin/genetics , Insulin Receptor Substrate Proteins/genetics , Insulin Receptor Substrate Proteins/metabolism , Interleukin-6/genetics , Interleukin-6/metabolism , Male , Mice , Mice, Inbred C57BL , Mitogen-Activated Protein Kinase 1/genetics , Mitogen-Activated Protein Kinase 1/metabolism , Proto-Oncogene Proteins c-akt/genetics , Proto-Oncogene Proteins c-akt/metabolism , Signal Transduction , Streptozocin , p38 Mitogen-Activated Protein Kinases/genetics , p38 Mitogen-Activated Protein Kinases/metabolism
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