Insulin resistance in Chinese patients with type 2 diabetes is associated with C-reactive protein independent of abdominal obesity

<p>Abstract</p> <p>Background</p> <p>There is debate as to whether the association between C-reactive protein (CRP) and insulin resistance is independent of body fatness, particularly central obesity. Therefore, the association among CRP, insulin resistance and obesity was analyzed in Chinese patients with type 2 diabetes.</p> <p>Methods</p> <p>The study included 520 Chinese patients diagnosed with type 2 diabetes with CRP levels not exceeding 10 mg/L. The degree of insulin resistance was determined with the homeostasis model assessment of insulin resistance (HOMA-IR). The CRP levels were categorized into quartiles from the lowest to the highest concentrations (Q1-Q4).</p> <p>Results</p> <p>Body mass index (BMI) and waist circumference (WC) were both higher in Q4, Q3 and Q2 than those in Q1. HOMA-IR was higher in Q2, Q3 and Q4 than that in Q1 (Q1 vs Q4, P < 0.001; Q1 vs Q3, P < 0.001; Q1 vs Q2, P = 0.028). Log CRP was significantly correlated with log HOMA-IR (correlation coefficient: 0.230, P < 0.001) and BMI (correlation coefficient: 0.305, P < 0.001) and WC (correlation coefficient: 0.240, P < 0.001) by Spearman correlation analysis. Multiple linear regression analysis adjusting for age, gender and components of metabolic syndrome, log CRP was also independently associated with log HOMA-IR (β coefficient, 0.168; P < 0.001) and WC (β coefficient, 0.131; P = 0.006).</p> <p>Conclusion</p> <p>These findings showed that insulin resistance was associated with CRP levels independent of abdominal obesity in Chinese patients with type 2 diabetes, suggesting that abdominal obesity could only partly explain the link between subclinical inflammation and insulin resistance.</p

Prevalence of non-alcoholic fatty liver disease and its relation to hypoadiponectinaemia in the middle-aged and elderly Chinese population

Introduction: Hypoadiponectinaemia is an important risk factor for non-alcoholic fatty liver disease (NAFLD). However, little is known about its role in the Chinese population. This study sought to assess the prevalence of NAFLD and its association with hypoadiponectinaemia in middle-aged and elderly Chinese. Material and methods: We conducted a population-based cross-sectional study in an urban Shanghai sample of 2201 participants age 50 years to 83 years (973 men, 1228 women). Hepatic ultrasonographic examination was performed for all participants. Serum adiponectin concentrations were measured by ELISA methods. Results: The prevalence of NAFLD was 19.8% (16.0% in men, 22.8% in women). Serum adiponectin levels were significantly higher in female than in male subjects (p < 0.001). Serum adiponectin levels were significantly lower in NAFLD subjects than those in control subjects (p < 0.001). The prevalence of NAFLD progressively increased with declining adiponectin levels (p(for) (trend) < 0.001). The participants in the lowest adiponectin quartile had a significantly increased risk for acquiring NAFLD (OR = 2.31, 95% CI 1.72-3.15) after adjustment for potential confounders. Conclusions: Population-based screening suggests that NAFLD is highly prevalent in middle-aged and elderly people in Shanghai, particularly among women. Serum adiponectin level is negatively associated with NAFLD independently of potential cofounders, indicating that hypoadiponectinaemia may contribute to the development of NAFLD

Lipocalin-2, glucose metabolism and chronic low-grade systemic inflammation in Chinese people

<p>Abstract</p> <p>Background</p> <p>Lipocalin-2 is a novel adipokine with connection to insulin resistance. In this study, we aimed to investigate the association of serum lipocalin-2 with glucose metabolism and other metabolic phenotype in a large-scale Chinese population.</p> <p>Methods</p> <p>We evaluated serum lipocalin-2 in a cross-sectional sample of 2519 Chinese aged from 50 to 82 year in a Shanghai downtown district by ELISA. Glucose, insulin, lipid profile, inflammatory markers, and adipokines were also measured.</p> <p>Results</p> <p>Serum lipocalin-2 was significantly higher in subjects with isolated impaired fasting glucose, isolated impaired glucose tolerance, combined impaired fasting glucose/impaired glucose tolerance and newly-diagnosed type 2 diabetes than in those with normal glucose regulation. Lipocalin-2 elevation was clearly associated with a higher risk for impaired glucose regulation (OR 1.30 for each 10 ng/ml increase in serum lipocalin-2, 95% CI 1.23-1.62, <it>p </it>= 0.009) after adjustment of age, gender, smoking, alcohol drinking, family history of diabetes, serum CRP, serum adiponectin, serum CXCL5, HOMA-IR, BMI, and waist/hip ratio. The OR for participants with impaired glucose regulation and type 2 diabetes was 1.31 (95% CI 1.21-1.69, <it>p </it>< 0.001).</p> <p>Conclusions</p> <p>Our findings suggest that elevated serum lipocalin-2 is closely and independently associated with impaired glucose regulation and type 2 diabetes.</p

CD133-Positive Cells Might Be Responsible for Efficient Proliferation of Human Meningioma Cells

Owing to lack of appropriate model systems, investigations of meningioma biology have come to a stop. In this study, we developed a comprehensive digestion method and defined a culture system. Using this method and system, primary meningioma cells in conditioned suspension medium and a hypoxic environment could be amplified in spheres and were passaged for more than ten generations. Meningioma sphere cells were positive for meningioma cell markers and negative for markers of neural cell types. Importantly, we found the cells expressed the stem cell marker, CD133, but not nestin. All of the tumor sphere cell populations showed a slower degree of cell proliferation than that of human glioma cells and fetal neural stem cells (NSCs). Further studies showed that the proliferative rate was positively correlated with CD133 expression. The higher the CD133 expression, the faster the cell proliferation. With the increase in cell generations, the cell proliferation rate gradually slowed down, and CD133 expression also decreased. Single CD133+ cells rather than CD133− cells could form spheres. Thus, the results above indicated that those cells expressing CD133 in spheres might be stem-like cells, which may be responsible for efficient amplification of human meningioma cells. Decreased expression of CD133 may lead to the failure of long-term passaging

Insulin Resistance in Vascular Endothelial Cells Promotes Intestinal Tumor Formation

The risk of several cancers, including colorectal cancer, is increased in patients with obesity and type 2 diabetes, conditions characterized by hyperinsulinemia and insulin resistance. Because hyperinsulinemia itself is an independent risk factor for cancer development, we examined tissue-specific insulin action in intestinal tumor formation. In vitro, insulin increased proliferation of primary cultures of intestinal tumor epithelial cells from ApcMin/+ mice by over 2-fold. Surprisingly, targeted deletion of insulin receptors in intestinal epithelial cells in ApcMin/+ mice did not change intestinal tumor number or size distribution on either a low or high-fat diet. We therefore asked whether cells in the tumor stroma might explain the association between tumor formation and insulin resistance. To this end, we generated ApcMin/+ mice with loss of insulin receptors in vascular endothelial cells. Strikingly, these mice had 42% more intestinal tumors than controls, no change in tumor angiogenesis, but increased expression of vascular cell adhesion molecule-1 (VCAM-1) in primary culture of tumor endothelial cells. Insulin decreased VCAM-1 expression and leukocyte adhesion in quiescent tumor endothelial cells with intact insulin receptors and partly prevented increases in VCAM-1 and leukocyte adhesion after treatment with tumor necrosis factor-α. Knockout of insulin receptors in endothelial cells also increased leukocyte adhesion in mesenteric venules and increased the frequency of neutrophils in tumors. We conclude that although insulin is mitogenic for intestinal tumor cells in vitro, its action on tumor cells in vivo is via signals from the tumor microenvironment. Insulin resistance in tumor endothelial cells produces an activated, proinflammatory state that promotes tumorigenesis. Improvement of endothelial dysfunction may reduce colorectal cancer risk in patients with obesity and type 2 diabetes

Singular limits of Klein Gordon Schrödinger equations to Schrödinger Yukawa equations

10.1137/100790586Multiscale Modeling and Simulation851742-176

Elevated Serum Chemokine CXC Ligand 5 Levels Are Associated with Hypercholesterolemia But Not a Worsening of Insulin Resistance in Chinese People.

Objective: Recent study showed high chemokine CXC ligand 5 (CXCL5) is thought to be associated with insulin resistance in humans. However, evidence from large-scale populations about the relationship between serum CXCL5 level and metabolic phenotypes is scarce. Here we sought to evaluate serum CXCL5 distribution and its association with metabolic phenotypes among middle-aged and older Chinese. Research Design and Methods: We evaluated serum CXCL5 in a cross-sectional sample of 3225 Chinese aged from 50 to 88 yr in a Shanghai downtown district by ELISA. Glucose, insulin, lipid profile, inflammatory marker, and adipokine were also measured. Results: The crude mean of serum CXCL5 concentrations were 1493.31 pg/ml for men and 2059.42 pg/ml for women (P 0.05). Conclusions: Elevated circulating CXCL5 concentrations were associated with higher risk of hypercholesterolemia in middle-aged and elderly Chinese independent of obesity, inflammation, adipokines, and other risk factors but not insulin resistance

Genetic variation in the GCKR gene is associated with non-alcoholic fatty liver disease in Chinese people

Recent genome-wide association studies reported that GCKR rs780094 polymorphism is associated with elevated fasting serum triglyceride levels and elevated levels of C-reactive protein (CRP). There are a ample of data on the association between circulating triglyceride, CRP concentrations and risk of non-alcoholic fatty liver (NAFLD). To determine whether the GCKR rs780094 polymorphism contributes to the development of non-alcoholic fatty liver, a case-control study was performed in 903 Chinese subjects. Among study population, 436 patients with B-mode ultrasound-proven NAFLD (318 with steatosis hepatis IA degrees, 90 with steatosis hepatis IIA degrees and 28 with steatosis hepatis IIIA degrees) and 467 controls were genotyped by using TaqMan allelic discrimination assays. We confirmed the association of GCKR rs780094 with NAFLD in Chinese people (OR = 1.607, 95% CI 1.139-2.271, P ([dom]) = 7.2 x 10(-3)). In this study, polymorphism in GCKR rs780094 was not significantly associated with the degree of fatty infiltration of the liver. In addition, the T-allele of GCKR rs780094 was significantly associated with increasing fasting triglyceride (P ([add]) = 3.8 x 10(-4)) and CRP (P ([add]) = 2.9 x 10(-4)) concentrations after adjusting for age, gender, and BMI. The association with NAFLD remained significant after adjustment for triglyceride, while adjustment for CRP abolished the association. Genetic variation in GCKR gene rs780094 polymorphism contributes to the risk of NAFLD in Chinese people. The effect of genotype on NAFLD is probably mediated through chronic low-grade systemic inflammation rather than through dislipidemia