Objective To assess the tolerance of preoperative carbohydrate-rich beverage, to determine its effect on postoperative insulin resistance and analyze its potential mechanism. Methods Thirty-two patients undergoing elective colorectal cancer resection were recruited to this randomized controlled study and assigned to two groups at random. Patient in control group was fasted before operation, while patient in study group was given oral water. Homeostasis model assessment (HOMA) indexes, activity of PTK, and mRNA and (or) protein expressions of PKB, PI3K and GluT4 were measured before and (or) immediately after surgery. Furthermore preoperative well-beings of patients were studied. Results Among well-beings, feeling of thirst, hunger and anxiety tended to be better in patients receiving carbohydrate-rich beverages compared with fasted ones (P＜0.05). Whole body insulin sensitivity decreased by 33% in the study group while 38% in the control group (P=0.007 2), and the activity of PTK, expressions of PI3K and PKB in study group were higher than those in control group (P＜0.05， P＜0.01), but no significantly difference was observed about GluT4 in both groups (Pgt;0.05）. Conclusion Preoperative consumption of carbohydrate-containing fluids is safe and effective. Provision of carbohydrate energy source prior to surgery may attenuate immediate postoperative insulin resistance. A carbohydrate-rich drink enhances insulin action at the time of onset of anaesthesia or surgery by activating three kinases named PTK, PI3K, PKB which are key enzymes in pathway of insulin signal transduction. It is likely to explain the effects on postoperative insulin resistance.
ObjectiveTo systematically evaluate the changes in placental protein expressions in gestational diabetes mellitus (GDM) and their correlations with maternal insulin resistance (IR). Methods PubMed, Cochrane Library, Scopus, Web of Science, Embase, China National Knowledge Infrastructure, VIP database, Wanfang Database and CBMdisc were searched for case-control studies published from January 2009 to November 2021, which reported the placental protein expressions in GDM and their correlations with IR. Two researchers independently reviewed the literature, extracted data and evaluated the literature quality. RevMan 5.4 software was used for meta-analysis, and descriptive analysis was performed on data that cannot be combined. ResultsA total of 19 studies were included, comprising 2 012 patients. The results of meta-analysis showed that: the expression level of retinol binding protein 4 (RBP4) [standard mean difference=2.11, 95% confidence interval (CI) (1.64, 2.58), P<0.000 01] and the positive rate of protein tyrosine phosphatase-1B (PTP1B) [relative risk (RR)=1.56, 95%CI (1.29, 1.88), P<0.000 01] were up-regulated, and the positive rate of insulin receptor substrate 1 (IRS-1) [RR=0.69, 95%CI (0.60, 0.78), P<0.000 01] was down-regulated. The protein expression levels of RBP4 (P<0.000 01) and PTP1B (P<0.000 01) were positively correlated with homeostasis model assessment of insulin resistance (HOMA-IR), while the protein expression levels of IRS-1 (P<0.000 01) and APN (P=0.002) were negatively correlated with HOMA-IR, and glucose transporter 4 (GLUT 4) was not correlated with HOMA-IR (P=0.79). Descriptive analysis found that the expression levels or positive rates of adipocytokines (leptin, resistin), oxidative stress markers (xanthione oxidase, malondialdehyde, 8-isoprostaglandin),inflammatory factors (tumor necrosis factor α, Toll-like receptor 4, Galectin-3, Galectin-2, migration inhibitory factor),fetuin-A, forkhead box transcription factor 1, forkhead box transcription factor 3a and estrogen receptor α in GDM placenta were up-regulated and all were positively correlated with HOMA-IR. The expression levels or positive rates of insulin signaling pathway proteins [phosphoinositide 3-kinase (PI3K), protein kinases B (AKT), phospho-protein kinases B (p-AKT), GLUT 4] were down-regulated, PI3K and AKT were negatively correlatedwith HOMA-IR, while p-Akt had no correlation with HOMA-IR. ConclusionsThe dysregulation of placental protein expressions may mediate maternal IR exacerbation, thus promote the occurrence and development of GDM and other pregnancy complications. The causal relationship and regulatory mechanism are still unclear, which need to be further studied.
Objective To investigate the changes of CD4 + CD25 + Foxp3 + regulatory T cells( Treg) in peripheral blood of patients with acute exacerbation of COPD( AECOPD) , and analyze the relationship of CD4 + CD25 + Foxp3 + Treg with insulin resistance. Methods A total of 79 patients with AECOPD were divided into four groups according to disease severity( 11 cases in stage Ⅰ,31 cases in stage Ⅱ,28 cases in stage Ⅲ, an 9 cases in stage Ⅳ) .42 healthy volunteers were recruited as control. Fast blood glucose( FBG) and fast insulin( FINS) were measured for calculating the insulin resistance index. The CD4 + CD25 + Foxp3 + Treg were detected by flow cytometry. The relationship between the proportion and number of CD4 + CD25 + Foxp3 + Treg with insulin resistance was statistically analyzed. Results Compared with the healthy control group, the levels of FBG, FINS, and insulin resistance index in the AECOPD patients were significantly higher ( P lt; 0. 01, P lt; 0. 05) . The proportion and number of CD4 + CD25 + Foxp3 + Treg in peripheral blood decreased significantly( P lt; 0. 01, P lt; 0. 05) . The insulin resistance index increased with the severity of AECOPD while the proportion and number of CD4 + CD25 + Foxp3 + Treg in peripheral blood decreased. The insulin resistance index in the AECOPD patients of stage Ⅲ and Ⅳ were higher than those of stage Ⅰ and Ⅱ. The proportion and number of CD4 + CD25 + Foxp3 + Treg in the AECOPD patients of stage Ⅲ and Ⅳ were significantly lower than those of stage Ⅰ and Ⅱ. Both the proportion and number of CD4 + CD25 + Foxp3 + Treg were negatively correlated with insulin resistance ( r = - 0. 633, - 0. 871, P lt; 0. 01) . Conclusions CD4 + CD25 + Foxp3 + Treg cells might may play important role in modulating insulin resistance in AECOPD. The more serious the disease, the lower the CD4 + CD25 + Foxp3 + Treg and the worse insulin resistance.
ObjectiveTo explore the clinical curative effect of high flux hemodialysis on diabetic nephropathy (DN) and impact on patients' insulin resistance (IR). MethodsA total of 96 patients with DN meeting the inclusion criteria treated between January 2013 and January 2014 were selected. The patients were randomly divided in to the observation group and control group with 48 in each. The control group received low flux hemodialysis, while the observation group underwent high flux hemodialysis. Before the treatment and in the first half of the year after the treatment, the clinical renal function and inflammatory indexes, lipid metabolism, and glucose metabolism related markers were recorded, and IR index (HOMA-IR) were calculated and compared. ResultsBefore and after the treatment, the Kt/V showed no significant change in the two groups (P > 0.05). Serum creatinine levels was lower after the treatment compared with that before the treatment in both of the two groups; in the observation group, C-reactive protein, interleukin-6 and tumor necrosis factorαwere significantly lower than those before the treatment and than those in the control group after the treatment (P < 0.05). HOMA-IR and fasting insulin levels in the observation group after the treatment were significantly lower than those before the treatment and than those in the control group after the treatment (P < 0.05). No significant changes of fasting plasma glucose and glycosylated hemoglobin levels in the two groups before and after the treatment in patients were found (P > 0.05). ConclusionHigh flux hemodialysis therapy is effective on DN, which can effectively remove the body and large molecular type of inflammatory mediators, alleviate the micro inflammatory state, improve the IR status and correct the lipid metabolic abnormalities.
Objective We investigated the effect of supplementation with alanyl-glutamine dipeptide on insulin resistance and outcome in patients with chronic obstructive pulmonary disease (COPD) and respiratory failure. Methods A prospective, randomized, open and controlled trial was conducted. Patients with COPD and respiratory failure were recruited between Jan 2005 to Feb 2006 and randomly assigned to a trial group (n=14) with glutamine dipeptide supplmented parenteral nutrition and a control group (n=16) with isocaloric, isonitrogenic parenteral nutrition. On the third day and fifth day of nutrition treatment, blood glucose was clamped at level of 4.4 to 6.1 mmol/L by intravenously bumped insulin. Blood gas, blood glucose level, insulin dosage were recorded everyday. The outcomes were mortality, length of stay (LOS) in hospital and in ICU, mechanical ventilation times and the costs of ICU and hospital.Results Thirty patients successfully completed the trial. There was no difference in blood gas between two groups, but PaO2 increased gradually. Compared with control group, blood glucose level had trend to decrease in trial group. The average insul in consumption decreased significantly in trial group on the fifth day. There was no statistical difference between two groups in mortality, length of stay in hospital and the costs of hospital. But compared with control group, length of stay in ICU and mechanical ventilation days had trend to decrease in trial group. Conclusion Alanyl-glutamine dipeptide do not improve pulmonary function of patients with COPD and respiratory failure. However, alanyl-glutamine dipeptide attenuated insul in resistance and stabilized blood glucose. This trial does not confirm alanyl-glutamine di peptide can improve outcome in critically ill patients with COPD and respiratory failure between two groups in mortality at the end of 30 days, length of stay in hospital and the costs of hospital. But the length of stay in ICU and the duration of mechanical ventilation does decrease, but not significantly, in the trial group.
Objective To explore the association between 25-hydroxyvitamin D (25OHD) level and risk of the onset of metabolic syndrome (MS) in people in Chengdu. Methods In total, 474 participants were selected randomly by cluster sampling from one urban district and two rural villages in Longquanyi district of Chengdu. The data of sociodemographic information, lifestyle and family history were collected by questionnaires. Binary logistic regression was performed to assess the relationship between baseline 25OHD level and incident of MS, while multiple linear regression was conducted to analyze the relationship between baseline 25OHD level and insulin resistance. Results Four hundred seventy-four people were enrolled in the cohort study, 39 of them developed MS, with the incidences of 20.8 events per 1 000 person years. Among women, low 25OHD status was significantly associated with the risk of developing MS (OR=4.29, 95%CI 1.05 to 29.50, P=0.044) after adjustment for multiple potential confounders. In a multiple linear regression analysis, low 25OHD level of baseline was independently associated with the increased HOMA-IR over a 4-year period among Chengdu individuals (P<0.05) and was independently related to the decreased ISIcomp over a 4-year period in female (P<0.05). Conclusions The current prospective study suggests that low 25OHD level may contribute to increase insulin resistance in Chengdu population. Furthermore, low 25OHD level may increase the risk of MS among women in Chengdu.
ObjectiveTo investigate the relationship between glucose metabolism and endocannabinoid system (ECS) in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS).MethodsA total of 64 OSAHS patients (18 cases of mild OSAHS, 24 cases of moderate OSAHS, 22 cases of severe OSAHS) and 24 controls were included in the study. Body mass index, waist circumference, fasting blood lipids, fasting blood glucose, fasting blood insulin, homeostasis model of assessment for insulin resistance index (HOMA-IR), polysomnography and endogenous cannabinoid receptor 1 (CB1R) protein expression levels in peripheral blood mononuclear cells (PBMC) were measured in participants.ResultsThe incidence of diabetes and impaired fasting glucose (IFG) in the OSAHS group was significantly higher than that in the control group (28.12% vs. 8.33%). With the increase of apnea hypopnea index (AHI), HOMA-IR and the expression levels of CB1R protein increased gradually (HOMA-IR: 2.40±0.90, 2.34±0.59, 2.94±0.99, 3.46±0.77, respectively; CB1R protein: 0.04±0.01, 0.37±0.09, 0.40±0.07, 0.62±0.14, respectively). Correlation analysis showed that HOMA-IR, AHI and the expression of CB1R protein were significantly positively correlated with each other (P<0.05).ConclusionOSAHS patients are prone to insulin resistance, IFG and diabetes mellitus, which are closely related to the activation of ECS induced by OSAHS.
Objective To summarize the relationship of diabetes and its complications with microRNA. Methods Domestic and international researches were collected by searching to summarize the role of microRNA in diabetes and its complications. Results MicroRNA could affect the secretion of insulin and interfer metabolism of gulcose in fat cells， muscle cells， and liver cells， which resulting in insulin resistance. At the same time， the microRNA also played an role in damage of vascular endothelial cells and myocardial cell in diabetes. Conclusion MicroRNA acts an important role in the process of diabetes and its complications.
ObjectiveTo explore the effect of gastric bypass (GBP) on metabolic syndrome (MS) and the related mechanisms. MethodsThe literatures addressed the effect of GBP on glucose metabolism and blood pressure were retrospectively analyzed. ResultsIt showed that GBP achieved durable level of blood glucose, remission of dylipidemia and hypertension, however, which occurred before significant weight loss. The changes of many factors such as food intake, gastrointestinal hormones, adipocytokines, fat distribution might be involved in GBP to improve MS. ConclusionGBP seems to achieve the control of MS as a primary and independent effect, rather than secondary to the treatment of overweight.
Objective To evaluate the effects of saxagliptin on β cell function of type 2 diabetic patients. Methods The Cochrane Library, PubMed, EMbase, CBM, VIP, and CNKI were searched from their establishment to November, 2011, for relevant randomized controlled trials on the effects of saxagliptin on β cell function in type 2 diabetic patients. Language was limited to Chinese and English only. Two reviewers independently screened the literature according to the inclusion and exclusion criteria, extracted the data, and evaluated and cross-checked the methodological quality. Then meta-analysis was conducted using RevMan 5.0 software. Results Five RCTs were included. The results of meta-analysis showed that: HOMA-B was significantly increased in the saxagliptin (or saxagliptin plus routine treatment) 2.5 mg, 5 mg, and 10 mg groups (MD=8.03, 95%CI 4.57 to 11.48, Plt;0.000 01; MD=7.50, 95%CI 4.27 to 10.73, Plt;0.000 01; MD=17.45, 95%CI 13.93 to 20.97, Plt;0.000 01); HOMA-IR was similar between saxagliptin 2.5 or 10 mg group, and control group (MD= –0.05, 95%CI –0.18 to 0.08, P=0.47; MD= –0.18, 95%CI –0.60 to 0.24, P=0.4). Conclusion Current evidence shows that saxagliptin is effective in improving β cell function and insulin resistance. Due to short follow-up and small sample size, this conclusion has to be further proved by more high-quality RCTs.