ABSTRACT
Thirty eight patients with type 2 diabetes mellitus (T2DM) signed with the Lingering Garden Subdistrict Community Health Service Center of Suzhou Gusu District from October to December 2015 were enrolled in the study. The patients were classified as low risk group (n=3), moderate risk group (n=11), high risk group (n=21) and extremely high risk group (n=3) according to risk stratification of the JADE program based on estimated glomerular filtration rate (eGFR) and risk factors [obesity, dyslipidemia, hypertension, diabetic retinopathy, urinary protein creatinine ratio, foot disease, glycosylated hemoglobin A1c(HbA1c), fasting plasma glucose(FPG) or non fasting plasma glucose]. The patients were managed by a team consisting of general practitioners, general nurses and specialists; the individualized management was implemented with reduction of controllable risk factors and complications as the goal. After one year of management (March 2016 to February 2017) the indicators of T2DM were evaluated. The results showed that the TC, LDL-C, FPG and HbA1c levels were significantly improved in both moderate and high risk groups (P<0.05); the TC, LDL-C and FPG levels in the extremely high risk group were also significantly improved (P<0.05).
ABSTRACT
Objective To explore the effect of ghrelin on insulin release of mouse pancreatic islet ?-cell line(NIT-1 cells) and its probable mechanism.Methods NIT-1 cells were incubated in high-glucose DMEM with ghrelin.Then,the media was sampled for the assay of insulin by RIA.The(mRNA) expressions of glucose transporter 2(GluT2),pancreatic-duodenal homeobox-1(PDX-1),inwardly rectifying potassium channel with two transmembrane regions(Kir6.2) and sulphonylurea receptor 1(SUR-1) in the cells were detected by using RT-PCR.The cell proliferation was determined by MTT assay.Results(1) 10~(-9)mol/L to 10~(-7)mol/L of ghrelin inhibited dose-dependently the high-glucose challenged insulin release of the NIT-1 cells.(2) The mRNA expression of Kir6.2,but not GluT2,PDX-1and SUR-1,was down-regulated by 10~(-7)mol/L of ghrelin.(3) Ghrelin had no effect on proliferation of the cells.Conclusions Ghrelin inhibits high-glucose induced insulin secretion of the islet ?-cells.This effect may be secondary to the down-regulation for the expression of Kir6.2,(a component) of ATP-sensitive potassium channel.