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Objective:To analyze the clinical features of latent autoimmune diabetes (LADA) in adults among newly diagnosed type 2 diabetes mellitus (T2DM), and to explore whether LADA diagnostic models can be established based on this.Methods:From May 2016 to January 2017, 302 patients with newly diagnosed T2DM in the outpatient and inpatient department of metabolism and endocrinology of Yueyang Central Hospital were analyzed. All of them were tested for glutamic acid decarboxylase antibody (GADA). According to the consensus of the Chinese Medical Association Diabetes Association (CDS) LADA diagnosis and treatment, they were divided into LADA group (18 cases) and T2DM group (284 cases). The general clinical data and clinical biochemical indexes of the two groups were analyzed; Multiple linear regression method was used to evaluate the feasibility of establishing LADA diagnostic model.Results:⑴ Compared with patients in the T2DM group, the patients in the LADA group had a younger age of onset, and " three more and one less" symptoms were more common ( P<0.05); the weight, body mass index (BMI), waist circumference, waist-to-hip ratio (WHR), triglycerides (TG), fasting C peptide (FCP), postprandial 2 h C peptide (2 h-CP), modified islet function index HOMA-islet (CP-DM), and modified insulin resistance index HOMA-IR (CP) in the LADA group were all lower, while high-density lipoprotein cholesterol (HDL-C) and HbA1c were higher ( P<0.05). ⑵ the linear regression method was used to analyze the multicollinearity of patients in LADA group and T2DM group. The biochemical indexes with statistically significant difference were selected as independent variables through correlation analysis, and the GADA value was used as dependent variable. The statistical results showed that the independent variables could not fully meet the conditions of multicollinearity regression analysis. Conclusions:⑴ Related clinical features and glucose metabolism indicators have differential diagnosis significance for LADA, but this study cannot be used for multiple linear regression analysis, and it is difficult to establish a diagnostic model for LADA. ⑵ LADA diagnosis is a comprehensive diagnosis, which should be combined with the results of islet autoantibody and clinical features.
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Objective To evaluate the effects of sitagliptin on blood glucose,blood pressure,blood lip and carotid artery intima media thickness (IMT) in metabolic syndrome patients with type 2 diabetes.Methods The clinical data were collected for 64 cases of inpatient and outpatient patients with metabolic syndrome with type 2 diabetes.Those patients included anti-diabetes native patients and patients only used the stable metformin dose.After signed off the informed consent form,those patients were randomized to the sitagliptin treatment group or original treatment group,and the metabolic index and carotid artery intima-media thickness were evaluated after 24 weeks treatment.Results The body mass index (BMI),waist circumference (WC),fasting plasma glucose (FPG),triglycerides (TG),high density lipoprotein cholesterol (HDL-C),systolic blood pressure (SBP),diastolic blood pressure (DBP),glycated hemoglobin a1c (HbA1c),and carotid artery IMT in two groups were comparable at baseline.After 12 weeks treatment,the FPG,TG,DBP,and HbA1c in the sitagliptin group were significantly better than original treatment group and the baseline,while there was no different between two groups in other index.After 24 weeks treatment,the FPG,TG,HDL-C,DBP,HbA1c,and carotid artery IMT in the sitagliptin group were significantly better than original treatment group and the baseline.Conclusions Sitagliptin presents the functions of lowering blood pressure,adjusting blood lipid,and protecting vascular endothelial in addition to lowering blood glucose.
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Objective To investigate whether the non-alcoholic fatty liver disease ( NAFLD) can independently increase the risk of cardiovascular events in type 2 diabetes .Methods The cardiovascular endpoints were observed after 5 years follow up for fat liver group (46 cases, patient with fat liver and with diabetes more than 10 years), non-fatty liver group (50 cases, patients without fatty liver disease and with diabetes more than 10 years), and normal glucose group (46cases, patient with NAFLD and with normal glucose) in the same demographic characteristics.Results ⑴ Patient status before enrollment: The body mass index (BMI), and blood glucose levels in fat liver group and non-fatty liver group were higher than normal glucose group , while the high-density lipopro-tein cholesterol ( HDL-C) was lower than normal glucose group ( P 0.05 ) .⑵After 5 years observation:The BMI , blood glucose , and TG levels in fat-ty liver disease group were significant higher than other two groups , while the HDL-C was lower than other two groups .The glucose control level of fat liver group was higher than normal glucose group ( P 0.05 ) .Conclusions NAFLD can independent-ly increase the risk of cardiovascular events in type 2 diabetes.
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This study investigated the variation of serum monocyte chemoattractant protein-1 (MCP-1) in patients with both diabetes mellitus (DM) and metabolic syndrome (MS). Based on the International Diabetes Federation (IDF) diagnostic criteria, 93 patients enrolled in this study were divided into four groups: normal control (NC), simple DM, simple MS, and DM plus MS (DM-MS) groups. The main measures included height, weight, waist circumference (WC), hip circumference, blood pressure, fasting blood glucose, insulin resistance index (HOMA-IR), serum triglyceride (TG), HDL-ch, LDL-ch, and MCP-1. The results showed that the serum levels of MCP-1 in the DM-MS group were significantly increased as compared with those in the DM and MS groups (P<0.05), and the increase in the MCP-1 level in the DM group was much higher than in the MS group (P<0.05). The DM-MS group had the highest HOMA-IR levels, followed by MS, DM and NC groups (P<0.05). Correlation tests showed that the association of MCP-1 with age, HDL-ch, or LDL-ch was insignificant, whereas that of MCP-1 with body mass index (BMI), waist hip rate (WHR), WC, systolic blood pressure (SBP), diastolic blood pressure (DBP), TG, and HOMA-IR was significantly positive. It was concluded that circulating MCP-1 was substantially increased in patients with both DM and MS as compared with that in the patients with DM or MS alone, and the central obese state may contribute to a more vicious proinflammatory condition and insulin resistance in patients with diabetes.
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The expression of serum and glucocorticoid-induced protein kinase in the renal cortex of diabetic rats was examined, and the function of signal transduction mediated by SGK1 in diabetic nephropathy and its modulatiqn by fluvastatin were also investigated. 24 male Wistar rats were randomly divided into normal control group (n = 8), diabetic nephropathy group (n = 8) and fluvastatin-treated diabetic nephropathy group (15 mg/kg/d, n = 8). The metabolic parameters were measured at the 8th week. The expression of transforming growth factor beta1 (TGF-beta1) and fibronectin (FN) was immunohistochemically examined. The expression of SGK1 was detected by RT-PCR and Western blot, and CTGF mRNA was assessed by RT-PCR. As compared to DN, blood glucose, 24-h urinary protein, Cer and kidney weight index were all decreased and the weight was increased obviously in group F. At the same time, mesangial cells and extracellular matrix proliferation were relieved significantly. The levels of cortex SGK1 mRNA and protein were up-regulated, and both TGF-beta1 and FN were down-regulated by fluvastatin. The mRNA of SGK1 was positively correlated with the CTGF, TGF-beta1 and FN. SGK1 expression is markedly up-regulated in the renal cortex of DN group and plays an important role in the development and progress of diabetic nephropathy by means of signal transduction. Fluvastatin suppressed the increased SGK1mRNA expression in renal cortex and postponed the development of diabetic nephropathy.
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The antinephritic effect of lipo-prostaglandin E1, prostaglandin E1 incorporated in lipid microspheres was investigated using an experimental model of mesangial proliferative glomerulonephritis (MsPGN). Twenty-two female rats were randomly divided into nephritic group (N, n= 6),lipo-prostaglandin E1 treated group (NL, n = 8) and control group (C, n = 6). Lipo-prostaglandin E1 was given intravenously at 40 μg · kg-1 · d-1 from the 6th week to the 8th week. Twenty-four h urinary protein contents and blood creatinine (Cr) were determined and the pathological changes were observed in the experiment. The expression of proliferating cell nuclear antigen (PCNA), extracellular matrix (fibronectin, FN; collagen type Ⅳ, Col Ⅳ) and transforming growth factor β1(TGFβ1) was detected by using immunohistochemistry. The results showed that lipo-prostaglandin E1 significantly inhibited the glomerular histopathological changes as well as the elevation of plasma Cr (P＜0.05). The overexpression of PCNA, FN, Col Ⅳ and TGFβ1 were also obviously inhibited in group NL as compared with the group N (P＜0.01). It was suggested that lipo-prostaglandin E1could improve renal function, inhibit the proliferation of glomerular cells and reduce the deposition of extracellular matrix, which may be related to the down-regulation of the TGFβ1 expression.
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The expression of serum and glucocorticoid-induced protein kinase in the renal cortex of diabetic rats was examined, and the function of signal transduction mediated by SGK1 in diabetic nephropathy and its modulation by fluvastatin were also investigated. 24 male Wistar rats were randomly divided into normal control group (n = 8), diabetic nephropathy group (n= 8) and fluvastatin-treated diabetic nephropathy group(15 mg/kg/d, n=8). The metabolic parameters were measured at the 8th week. The expression of transforming growth factor β1 (TGF-β1 ) and fibronectin (FN) was immunohistochemically examined. The expression of SGK1 was detected by RT-PCR and Western blot, and CTGF mRNA was assessed by RT-PCR. As compared to DN, blood glucose,24-h urinary protein, Cer and kidney weight index were all decreased and the weight was increased obviously in group F. At the same time, mesangial cells and extracellular matrix proliferation were relieved significantly. The levels of cortex SGK1 mRNA and protein were up-regulated, and both TGF-β1 and FN were down-regulated by fluvastatin. The mRNA of SGK1 was positively correlated with the CTGF, TGF-β1 and FN. SGK1 expression is markedly up-regulated in the renal cortex of DN group and plays an important role in the development and progress of diabetic nephropathy by means of signal transduction. Fluvastatin suppressed the increased SGK1mRNA expression in renal cortex and postponed the development of diabetic nephropathy.