Dao-Ming Chang

Visfatin in overweight/obesity, type 2 diabetes mellitus, insulin resistance, metabolic syndrome and cardiovascular diseases: a meta-analysis and systemic review.

There are controversies regarding the association of visfatin with overweight/obesity, type 2 diabetes mellitus, insulin resistance (IR), metabolic syndrome and cardiovascular disease in published articles. A meta‐analysis was performed to identify the significance of visfatin in these diseases. We searched for relevant articles in Pubmed, Scopus and SCIE. A total of 1035 articles were surveyed and 46 articles were identified, with 14 reports reporting more than one of our investigated diseases. A total of 13 (n = 644), 19 (n = 2405), 20 (n = 2249), 5 (n = 527) and 5 (n = 851) articles/(participants) were included in each meta‐analysis regarding the association of visfatin and overweight/obesity, type 2 diabetes mellitus, insulin resistance, metabolic syndrome and cardiovascular diseases, respectively. Plasma visfatin concentrations were increased in participants diagnosed with overweight/obesity, type 2 diabetes mellitus, metabolic syndrome and cardiovascular diseases, with pooled log odds ratios of 1.164 [95% confidence interval (CI): 0.348 to 1.981, p = 0.005], 1.981 (95% CI: 1.377 to 2.584, p < 0.001), 1.094 (95% CI: 0.678 to 1.511, p < 0.001), and 2.902 (95% CI: 0.924 to 4.879, p < 0.005), respectively. The circulating visfatin level was positively associated with insulin resistance, with a Fishers z of 0.089 (95% CI: 0.013 to 0.165, p = 0.022). No single study was found to affect the overall result of each analysis by sensitivity testing. No publication bias was found by the Egger test. Our study suggests that the use of visfatin may be promising for predicting obesity, diabetes status, insulin resistance, metabolic syndrome and cardiovascular disease. Copyright

Association of peripheral total and differential leukocyte counts with metabolic syndrome and risk of ischemic cardiovascular diseases in patients with type 2 diabetes mellitus.

There is increasing evidence that leukocytes play a central role in obesity, glucose intolerance, type 2 diabetes mellitus (T2DM), and cardiovascular diseases, but the role of differential leukocytes in metabolic syndrome (MetS) and atherosclerosis is largely unknown. The aim of this study was to examine the relationship between the component features of MetS and peripheral leukocyte counts and to explore whether leukocyte counts are associated with clustering of MetS and macrovascular diseases in patients with T2DM.

ENPP1 K121Q polymorphism is not related to type 2 diabetes mellitus, features of metabolic syndrome, and diabetic cardiovascular complications in a Chinese population.

BACKGROUND Ectoenzyme nucleotide pyrophosphate phosphodiesterase 1 (ENPP1) is known to influence insulin sensitivity by inhibiting insulin receptor signaling. A DNA polymorphism in the ENPP1 gene at exon 4 (K121Q) was demonstrated to be associated with insulin resistance, type 2 diabetes mellitus (T2DM), and a risk of early myocardial infarction, albeit with controversy. Our aim was to investigate any association of ENPP1 K121Q alleles with T2DM, features of the metabolic syndrome, and diabetic cardiovascular complications in a Chinese population of Han origin. METHODS The ENPP1 K121Q polymorphism was determined by a restriction fragment-length polymorphism-polymerase chain reaction in 1,862 patients with T2DM and 844 non-diabetic subjects. RESULTS The genotype distributions or Q-allele frequency were not statistically different between the diabetic and non-diabetic groups. The anthropometric parameters, systolic and diastolic blood pressures, lipid profiles, and serum creatinine levels of subjects with different ENPP1 K121Q polymorphisms were not statistically different in the two groups or even in the pooled data. When sub-group analyses of diabetic subjects were stratified according to BMI levels (greater or less than 27), gender, age of diabetes onset (older or younger than 60 years), and the presence or absence of a diabetic family history; this polymorphism was still not associated with T2DM. Nor was the ENPP1 K121Q polymorphism associated with the prevalence of coronary artery disease and ischemic cerebrovascular disease in patients with T2DM. CONCLUSION The ENPP1 K121Q polymorphism is not related to T2DM, features of the metabolic syndrome, or diabetic macrovascular complications in a Chinese population.

Areca nut chewing is associated with metabolic syndrome: role of tumor necrosis factor-alpha, leptin, and white blood cell count in betel nut chewing-related metabolic derangements.

Areca nut ( Areca catechu )/betel quid (BQ) is said to be the fourth most commonly used psychoactive substance in the world and is chewed regularly by at least 10% of the world’s population (1). High prevalences of BQ chewing were observed especially in South and Southeast Asia (1). High prevalences of insulin resistance and metabolic syndrome were also observed in this area (2). Specific areca alkaloids act as competitive inhibitors of γ-aminobutyric acid receptors …

Serum uric acid level as an indicator for CKD regression and progression in patients with type 2 diabetes mellitus—a 4.6-year cohort study

To investigate the association of serum uric acid level with renal function change in patients with type 2 diabetes mellitus (T2DM).

Association of a 27-bp repeat polymorphism in intron 4 of endothelial constitutive nitric oxide synthase gene with serum uric acid levels in chinese subjects with type 2 diabetes

Nitric oxide (NO) was found to modulate uric acid production through its influence on xanthine oxidase activity, and a close circadian relationship of serum uric acid (SUA) and NO was reported. Studies also revealed that serum NO activity could be determined by endothelial constitutive nitric oxide synthase gene (ecNOS) polymorphism. This study was designed to investigate whether SUA could be influenced by a 27-bp repeat polymorphism in intron 4 of ecNOS gene. A total of 398 nondiabetic subjects and 800 patients with type 2 diabetes were studied. The ecNOS gene intron 4 polymorphism was determined by polymerase chain reaction (PCR). The mean SUA level of patients having type 2 diabetes was significantly lower than that of control subjects (6.1 +/- 1.8 mg/dL v 6.6 +/- 1.8 mg/dL, P<.001); and the mean SUA level of diabetic patients with ecNOS ab/aa genotypes was lower than that of patients with bb genotype (5.7 +/- 1.6 mg/dL v 6.2 +/- 1.8 mg/dL, P=.008). When subgrouped by gender, the SUA of female diabetic subjects was found to be significantly associated with ecNOS genotype. Using Pearsons correlation analysis and multiple linear regression analysis, ecNOS genotype was noticed to be an independent factor in contributing to SUA variability in female diabetic patients. Our results suggest that SUA levels may be associated with NO activity and can be genetically predetermined.

A case of acquired generalized lipodystrophy with cerebellar degeneration and type 2 diabetes mellitus.

Acquired generalized lipodystrophy (AGL) is a rare disorder of adipose tissue characterized by loss of fat from large regions of the body, occurring after birth. Its etiology remains unknown. Most AGL patients have had fasting and/or postprandial hyperinsulinemia, diabetes mellitus, hypertriglyceridemia, and fatty liver. We describe the case of a 30-year-old woman with a progressively unsteady gait and a generalized loss of body fat beginning at the age of 7. Cerebellar degeneration was revealed by imaging study, and the patient was eventually bedridden at the age of 15, due to progressive ataxia. She developed diabetes at the age of 25 without the presence of any evidence of ketoacidosis. The glutamic acid decarboxylase antibody was negative, C-peptide level 3.6 ng/ml, HbA1c 13%, triglyceride 412 mg/dl, total cholesterol 196 mg/dl, high-density lipoprotein-cholesterol 28 mg/dl, adiponectin 0.76 microg/ml, and resistin was 22.8 ng/ml at the initial state of diabetes. AGL accompanied by type 2 diabetes and cerebellar degeneration was diagnosed on the basis of the clinical features and metabolic derangements.

Elevated serum cytokeratin-18 concentration in patients with type 2 diabetes mellitus and non-alcoholic fatty liver disease

Background Serum cytokeratin-18 is believed to be a marker of hepatic cell damage. However, few studies have discussed about the serum cytokeratin-18 concentration in type 2 diabetes mellitus patients and investigated its association with non-alcoholic fatty liver disease as well as metabolic biomarkers. Methods Healthy participants and type 2 diabetes mellitus patients were enrolled. Physical and metabolic factors were recorded, and non-alcoholic fatty liver disease was screened by abdominal ultrasound and the fatty liver index. The cytokeratin-18 concentration was detected using two commercially available immunoassay kits (M30 and M65 ELISA kit, Previa AB, Sweden). Results Overall, 22.8% (29/127) and 35.9% (42/117) of the participants were diagnosed with non-alcoholic fatty liver disease in the non-diabetes mellitus group and type 2 diabetes mellitus group, respectively. In the non-diabetes mellitus group and type 2 diabetes mellitus group, our result showed that participants with non-alcoholic fatty liver disease had a higher serum cytokeratin-18 M30 and cytokeratin-18 M65 concentration as compared with participants without non-alcoholic fatty liver disease. Interestingly, as compared with healthy participants without non-alcoholic fatty liver disease, our result also demonstrated that type 2 diabetes mellitus patients without non-alcoholic fatty liver disease had a higher serum cytokeratin-18 M30 (108.4 ± 66.2 vs. 87.1 ± 34.6 U/L; P = 0.038) and cytokeratin-18 M65 concentration (285.4 ± 115.3 vs. 248.5 ± 111.3 U/L; P = 0.031). The independent relationship between type 2 diabetes mellitus and cytokeratin-18 was further strengthened by the significant positive association between fasting plasma glucose and serum cytokeratin-18 concentration via multivariate regression analyses (cytokeratin-18 M30: β = 0.034, P = 0.029; cytokeratin-18 M65: β = 0.044, P = 0.002). Conclusions Independent of non-alcoholic fatty liver disease, our results suggested that the cytokeratin-18 concentration is closely associated with the hyperglycaemic milieu. The association between serum cytokeratin-18 and type 2 diabetes mellitus may be worthy of further investigation.