Fasting Hyperglycemia Increases In-Hospital Mortality Risk in Nondiabetic Female Patients with Acute Myocardial Infarction: A Retrospective Study

Previous studies had shown that elevated admission plasma glucose (APG) could increase mortality rate and serious complications of acute myocardial infarction (AMI), but whether fasting plasma glucose (FPG) had the same role remains controversial. In this retrospective study, 253 cases of AMI patients were divided into diabetic (n=87) and nondiabetic group (n=166). Our results showed that: compared with the nondiabetic patients, diabetic patients had higher APG, FPG, higher plasma triglyceride, higher rates of painless AMI (P<0.01), non-ST-segment elevation myocardial infarction (NSTEMI), and reinfraction (P<0.05). They also had lower high density lipoprotein cholesterol and rate of malignant arrhythmia, but in-hospital mortality rate did not differ significantly (P>0.05). While nondiabetic patients were subgrouped in terms of APG and FPG (cut points were 11.1 mmol/L and 7.0 mmol/L, resp.), the mortality rate had significant difference (P<0.01), whereas glucose level lost significance in diabetic group. Multivariate logistic regression analysis showed that FPG (OR: 2.014; 95% confidence interval: 1.296–3.131; p<0.01) but not APG was independent predictor of in-hospital mortality for nondiabetic patients. These results indicate that FPG can be an independent predictor for mortality in nondiabetic female patients with AMI

Fasting Hyperglycemia Increases In-Hospital Mortality Risk in Nondiabetic Female Patients with Acute Myocardial Infarction: A Retrospective Study

Previous studies had shown that elevated admission plasma glucose (APG) could increase mortality rate and serious complications of acute myocardial infarction (AMI), but whether fasting plasma glucose (FPG) had the same role remains controversial. In this retrospective study, 253 cases of AMI patients were divided into diabetic (n=87) and nondiabetic group (n=166). Our results showed that: compared with the nondiabetic patients, diabetic patients had higher APG, FPG, higher plasma triglyceride, higher rates of painless AMI (P<0.01), non-ST-segment elevation myocardial infarction (NSTEMI), and reinfraction (P<0.05). They also had lower high density lipoprotein cholesterol and rate of malignant arrhythmia, but in-hospital mortality rate did not differ significantly (P>0.05). While nondiabetic patients were subgrouped in terms of APG and FPG (cut points were 11.1 mmol/L and 7.0 mmol/L, resp.), the mortality rate had significant difference (P<0.01), whereas glucose level lost significance in diabetic group. Multivariate logistic regression analysis showed that FPG (OR: 2.014; 95% confidence interval: 1.296–3.131; p<0.01) but not APG was independent predictor of in-hospital mortality for nondiabetic patients. These results indicate that FPG can be an independent predictor for mortality in nondiabetic female patients with AMI

Independent Association between Nonalcoholic Fatty Liver Disease and Cardiovascular Disease: a Systematic Review and Meta-Analysis

Nonalcoholic fatty liver disease (NAFLD) is closely correlated with insulin resistance and several metabolic syndrome features, but whether it could increase the risk of cardiovascular disease remains undefined. To assess the association between NAFLD and the risk of cardiovascular outcomes, we systematically searched the MEDLINE, Embase, and the Cochrane Library database (1947 to October 2012) by using Medical Subject Heading search terms and a standardized protocol. Randomized controlled trials, casecontrol, and prospective studies carried out in human adults, in which the unadjusted and multivariate adjusted odds ratios with corresponding 95% confidence interval (CI) for cardiovascular disease with NAFLD were reported. The search yielded 4 crosssectional studies and 2 prospective cohort studies including 7,042 participants. The pooled effects estimate showed that NAFLD was a predictor of cardiovascular disease (odds ratio 1.88, 95% CI, 1.68 to 2.01; &lt; 0.001). The random effects summary estimate indicated that NAFLD retained a significant association with cardiovascular outcomes independent of conventional risk factors after adjustment for established cardiovascular risk factors (odds ratio 1.50, 95% CI, 1.21 to 1.87; &lt; 0.001). These results indicate that NAFLD is a strong independent predictor of cardiovascular disease and may play a central role in the cardiovascular risk of metabolic syndrome

The HIF-2α/PPARα pathway is essential for liraglutide-alleviated, lipid-induced hepatic steatosis

Liraglutide has been demonstrated to alleviate hepatic steatosis in clinical practice, but the underlying mechanism remains unclear. Our previous study indicated that the HIF-2α/PPARα pathway was involved in hepatic lipid accumulation induced by hypoxia.We aimed to investigate whether liraglutide could alleviate lipid-induced hepatic steatosis via the HIF-2α/PPARα pathway. Whole-body HIF-2α heterozygous knockout (HIF-2α+/-) mice and littermate wild-type (WT) mice were successfully established. Male mice challenged with a high-fat diet were treated with liraglutide (0.6 mg/kg/d) or normal saline by intraperitoneal injection for 4 weeks. We observed that, compared with WT mice, many indicators of HIF-2α+/- mice improved, including GTT, ITT, fasting blood glucose, body weight, liver weight, and lipid profile in serum or liver lipid deposition, and the expression level of PPARα, mitochondrial function genes, and fatty acid oxidation genes were upregulated, while those of HIF-2α and lipogenesis genes were downregulated significantly. After liraglutide treatment in WT mice, we found that significant improvements were observed in the fat mass, GTT, ITT, fasting blood glucose, body weight, liver weight, lipid profile in serum or liver lipid deposition; the β-oxidation genes were upregulated and the lipogenesis genes were downregulated; and the abundance of intestinal Akkermansia muciniphila increased significantly. However, the effects of liraglutide on WT mice were not observed in HIF-2α+/- mice. In addition, in the HepG2 steatotic hepatocyte model, liraglutide alleviated lipid deposits by repressing lipid synthesis and enhancing fatty acid β-oxidation, which were substantially suppressed by the HIF-2α modulators. Therefore, the HIF-2α/PPARα pathway is essential for liraglutide-alleviated lipid-induced hepatic steatosis

Ketosis Onset Type 2 Diabetes Had Better Islet β-Cell Function and More Serious Insulin Resistance

Diabetic ketosis had been identified as a characteristic of type 1 diabetes mellitus (T1DM), but now emerging evidence has identified that they were diagnosed as T2DM after long time follow up. This case control study was aimed at comparing the clinical characteristic, β-cell function, and insulin resistance of ketosis and nonketotic onset T2DM and providing evidence for treatment selection. 140 cases of newly diagnosed T2DM patients were divided into ketosis (62 cases) and nonketotic onset group (78 cases). After correction of hyperglycemia and ketosis with insulin therapy, plasma C-peptide concentrations were measured at 0, 0.5, 1, 2, and 3 hours after 75 g glucose oral administration. Area under the curve (AUC) of C-peptide was calculated. Homoeostasis model assessment was used to estimate basal β-cell function (HOMA-β) and insulin resistance (HOMA-IR). Our results showed that ketosis onset group had higher prevalence of nonalcoholic fatty liver disease (NAFLD) than nonketotic group (P=0.04). Ketosis onset group had increased plasma C-peptide levels at 0 h, 0.5 h, and 3 h and higher AUC0–0.5, AUC0–1, AUC0–3 (P<0.05). Moreover, this group also had higher HOMA-β and HOMA-IR than nonketotic group (P<0.05). From these data, we concluded that ketosis onset T2DM had better islet β-cell function and more serious insulin resistance than nonketotic onset T2DM