Correlation between income and non-alcoholic fatty liver disease in a Chinese population.

OBJECTIVE: The aim of the study was to analyze the correlation between income and non-alcoholic fatty liver disease (NAFLD) in a Chinese population. METHOD: subjects were divided into three groups according to liver fat content (LFC). (1) normal: LFC < 9.15%, 197 cases; (2) low LFC: LFC 9.15-20%, 532 cases; and (3) high LFC: LFC > 20%, 201 cases. Participants' clinical and social background were collected, including a routine fasting test to assess the relevant indices. Intergroup differences were compared on 1-way ANOVA, to analyze the relation between income and each index on Pearson correlation, and independent factors for LFC were identified on binary logistic regression. RESULTS: (1) In retired persons, prevalence of NAFLD was greater in females (81.2%) than males (75%), but fell with age: the highest prevalence was between 40 and 49 years of age (87.5%), and the lowest above 70 years (68%). (2) Income correlated positively with triglyceride and serum uric acid levels and LFC (P < 0.05) and negatively with alanine aminotransferase (P = 0.01). (3) As income increased from level I to V, prevalence of NAFLD increased progressively (P < 0.05). In the study, LFC was taken as the dependent variable, and the traditional NAFLD risk factors and income level (I-V) were taken as independent variables. Income emerged as an independent risk factor for NAFLD. Risk in group V was 1.964-fold higher than in group I. CONCLUSION: Prevalence of NAFLD was closely related to socio-economic level. Demographic risk factors include female gender, age 40-49 years, and monthly income > 5,000 RMB. Thus, if income is increased without improving educational level and health awareness, NAFLD prevalence will rise.

Low ketolytic enzyme levels in tumors predict ketogenic diet responses in cancer cell lines in vitro and in vivo.

The ketogenic diet (KD) is a high-fat, very-low-carbohydrate diet that triggers a fasting state by decreasing glucose and increasing ketone bodies, such as ß-hydroxybutyrate (ßHB). In experimental models and clinical trials, the KD has shown anti-tumor effects, possibly by reducing energy supplies to cells, which damage the tumor microenvironment and inhibit tumor growth. Here, we determined expression levels of genes encoding the ketolytic enzymes 3-hydroxybutyrate dehydrogenase 1 (BDH1) and succinyl-CoA: 3-oxoacid CoA transferase 1 (OXCT1) in 33 human cancer cell lines. We then selected two representative lines, HeLa and PANC-1, for in vivo examination of KD sensitivity in tumors with high or low expression, respectively, of these two enzymes. In mice with HeLa xenografts, the KD increased tumor growth and mouse survival decreased, possibly because these tumors actively consumed ketone bodies as an energy source. Conversely, the KD significantly inhibited growth of PANC-1 xenograft tumors. ßHB added to each cell culture significantly increased proliferation of HeLa cells, but not PANCI-1 cells. Downregulation of both BDH1 and OXCT1 rendered HeLa cells sensitive to the KD in vitro and in vivo. Tumors with low ketolytic enzyme expression may be unable to metabolize ketone bodies, thus predicting a better response to KD therapy.

Metabolic syndrome is independently associated with a mildly reduced estimated glomerular filtration rate: a cross-sectional study.

BACKGROUND: Association between metabolic syndrome (MS) and mildly reduced estimated glomerular filtration rates (eGFRs) remains unclear. Therefore, we aimed to evaluate the association between MS and a mildly reduced eGFR in Chinese adults. METHODS: Anthropometric and biochemical examinations were performed in 2992 individuals. The eGFR was calculated from the creatinine level. MS was defined according to the Adult Treatment Panel III criteria as the presence of three or more risk factors. Mildly reduced eGFR was defined as a value between 60 and 90 mL/min/1.73 m2. Multiple linear regression and multiple logistic regression analysis were used to evaluate association between metabolic syndrome and estimate glomerular filtration rate. RESULTS: After adjusting for several potential confounders, the participants with MS showed a 1.29-fold increased odds ratio for a mildly reduced eGFR compared with those without MS. Additionally, the odds ratios (and 95% confidence intervals (CIs)) for mildly reduced eGFR in participants with elevated triglycerides (TG), decreased high-density lipoprotein (HDL), obesity and elevated fasting blood glucose (FPG) after multivariable adjustment were 1.25 (1.05-1.49), 1.23 (1.03-1.48), 1.22 (1.03-1.45) and 0.64 (0.52-0.78), respectively. The odds ratios (95% CIs) for hyperfiltration in participants with elevated FPG and HbA1c levels after multivariable adjustment were 1.53 (1.30-1.81) and 2.86 (2.00-4.09), respectively. CONCLUSIONS: MS is associated with an increased risk of a mildly reduced eGFR in the Chinese population, and several individual components of MS have different impacts on eGFR levels. MS had dual roles on renal damage. TRIAL REGISTRATION: ChiCTR-TRC- 14005029 . Registered 28 July 2014.

Continuous Glucose Monitoring in Newly Diagnosed Type 2 Diabetes Patients Reveals a Potential Risk of Hypoglycemia in Older Men.

Objectives. We performed continuous glucose monitoring (CGM) to define the features of patients with newly diagnosed type 2 diabetes (T2D) before and after Continuous Subcutaneous Insulin Infusion (CSII) therapy. Methods. This was a retrospective analysis. Newly diagnosed T2D patients (106) were admitted from eight centers in China. They were divided into a younger patient group (<60 years) and an older patient group (≥60 years). Each group was further divided into male and female patients. CSII therapy was maintained for 3 weeks after the glycemic target was reached. CGM was performed 2 times before and after completion of insulin treatment. Results. CGM data showed the expected significant improvement of mean amplitude glycemic excursion (MAGE) with CSII therapy. The older patients had lower hourly glucose concentrations from 0200 to 0700 o'clock compared to the younger patients at baseline. Surprisingly, in the older patient group, the male patients had a potential risk of hypoglycemia after CSII therapy, especially during periods from 2300 to 2400 and 0400 to 0600. Conclusions. Our data suggested that older male patients with newly diagnosed T2D may have lower nocturnal glucose concentrations. This may potentially increase the risk of nocturnal hypoglycemia during CSII therapy. This study was registered with Chinese Clinical Trial Registry, number CliCTR-TRC-11001218.

Serum copeptin as a new biomarker in the early diagnosis of decline in renal function of type 2 diabetes mellitus patients.

OBJECTIVE: This study aimed to investigate the correlation between serum copeptin and glomerular filtration rate (GFR) in type 2 diabetes mellitus (T2DM) patients and to investigate the role of serum copeptin in the diagnosis of early DN in T2DM patients. METHODS: 120 T2DM inpatients were recruited and divided into 2 groups according to 24-h urine albumin excretion (UAE): normal UAE group (UAE<30 mg/24 h) and microalbuminuria group (30 mg/24 h≤UAE≤300 mg/24 h). RESULTS: Decline in GFR was found in 6.1% of patients in normal UAE group and 26.4% in microalbuminuria group. However, serum copeptin was comparable between two groups. Serum copeptin was negatively related to GFR (r=-0.586, P<0.001). Multivariate logistic regression analysis showed, after adjustment for age and gender, the OR of copeptin, 24-h UAE was 1.234 (95% CI: 1.003-1.456) (P<0.05) and 1.068 (95% CI: 1.005-1.187) (P<0.05), respectively. Univariate analysis of ROC showed the sensitivity of copeptin and 24-h UAE was 78.9% and 63.2%, respectively and the specificity was 88.9% and 89.7%, respectively in the diagnosis of DN, but the area under ROC of copeptin in combination with 24-h UAE was 0.90 (95% CI: 0.82-0.99) with the sensitivity of 80.9% and specificity of 91.1%. CONCLUSION: Serum copeptin is an independent risk factor of decline in renal function of T2DM patients. Copeptin in combination with 24-h UAE are helpful for the early diagnosis of DN. The causative relationship between serum copeptin and GFR is required to be further studied in long-term follow up.

Evaluation of serum ischemia-modified albumin levels in pregnant women with and without gestational diabetes mellitus.

OBJECTIVE: To investigate serum ischemia-modified albumin (IMA) levels in gestational diabetes mellitus and the effect of treatment with continuous subcutaneous insulin infusion on the biomarker. METHODS: The gestational diabetes mellitus women in the second trimester were evaluated before and after the two kinds of treatments with continuous subcutaneous insulin infusion and medical nutrition therapy for 6 weeks. Maternal serum ischemia-modified albumin and metabolic parameters were measured at baseline and at the 6th week. RESULTS: Serum ischemia-modified albumin levels and metabolic parameters were higher in patients with gestational diabetes mellitus at baseline than in controls. Ischemia-modified albumin levels were correlated with plasma glucose (p < 0.05). Variables of glycemic control and ischemia-modified albumin levels were significantly reduced at the 6th week. The effect of insulin treatment was generally better than diet therapy. Linear regression analysis showed that fasting plasma glucose was an independent determinant for IMA levels (ß = 0.611, p = 0.035).Fetal outcome was similar except for macrosomia and Apgar score at 5 min. CONCLUSION: Serum ischemia-modified albumin levels were higher in gestational diabetes mellitus compared to normal pregnancy. Continuous subcutaneous insulin infusion consistently improved metabolic disorder control. Gestational diabetes mellitus women were associated to a higher risk of oxidative stress and pregnancy complications.

Evaluation of ischemia-modified albumin and C-reactive protein in type 2 diabetics with and without ketosis.

OVERVIEW: To investigate whether serum ischemia-modified albumin or C-reactive protein is reliable for predicting type 2 diabetic patients with ketosis. APPROACH: One hundred and four diabetic patients, 48 with diabetic ketosis, and 33 controls were enrolled in the study. Serum ischemia-modified albumin and C-reactive protein were measured and evaluated for their ability to distinguish diabetic ketosis. RESULTS: Compared to the controls, the ischemia-modified albumin and C-reactive protein levels were higher in patients with diabetic ketosis and type 2 diabetes at the baseline. The levels of ischemia-modified albumin were higher in patients with type 2 diabetes than in the controls. C-reactive protein and ischemia-modified albumin levels were reduced after insulin treatment. The level of ischemia-modified albumin was an independent risk marker for diabetic ketosis (OR = 1.085, P = 0.008, 95% CI: 1.022-1.152). Receiver operating characteristic curves revealed that the areas under the curve were 0.917 for the modified albumin and 0.357 for C-reactive protein. CONCLUSION: This study indicates that ischemia-modified albumin was significantly associated with diabetic ketosis and was more sensitive than C-reactive protein in reflecting diabetic ketosis.

Ischemia-modified albumin in type 2 diabetic patients with and without peripheral arterial disease.

OBJECTIVE: To determine whether there is an association between serum ischemia-modified albumin and the risk factor profile in type 2 diabetic patients with peripheral arterial disease and to identify the risk markers for peripheral arterial disease. METHODS: Participants included 290 patients (35.2% women) with type 2 diabetes. The ankle-brachial pressure index was measured using a standard protocol, and peripheral arterial disease was defined as an ankle-brachial index <0.90 or >1.3. The basal ischemia-modified albumin levels and clinical parameters were measured and analyzed. The risk factors for peripheral arterial disease were examined by multiple logistic analyses. RESULTS: Age, systolic blood pressure, total cholesterol, low-density lipoprotein cholesterol, urine albumin, homocysteine, and ischemia-modified albumin were significantly higher in patients with peripheral arterial disease than in disease-free patients (p<0.05), while ankle-brachial index was lower in the former group (p<0.05). Ischemia-modified albumin was positively associated with HbA1c and homocysteine levels (r = 0.220, p = 0.030; r = 0.446, p = 0.044, respectively), while no correlation was found with ankle-brachial index. Multiple logistic analyses indicated that HbA1c, systolic blood pressure, homocysteine and ischemia-modified albumin were independent risk factors for peripheral arterial disease in the diabetic subjects. CONCLUSION: The baseline ischemia-modified albumin levels were significantly higher and positively associated with HbA1c and homocysteine levels in type 2 diabetic patients with peripheral arterial disease. Ischemia-modified albumin was a risk marker for peripheral arterial disease. Taken together, these results might be helpful for monitoring diabetic peripheral arterial disease.

Ischemia-modified albumin in type 2 diabetic patients with and without peripheral arterial disease

OBJECTIVE: To determine whether there is an association between serum ischemia-modified albumin and the risk factor profile in type 2 diabetic patients with peripheral arterial disease and to identify the risk markers for peripheral arterial disease. METHODS: Participants included 290 patients (35.2 percent women) with type 2 diabetes. The ankle-brachial pressure index was measured using a standard protocol, and peripheral arterial disease was defined as an ankle-brachial index <0.90 or >1.3. The basal ischemia-modified albumin levels and clinical parameters were measured and analyzed. The risk factors for peripheral arterial disease were examined by multiple logistic analyses. RESULTS: Age, systolic blood pressure, total cholesterol, low-density lipoprotein cholesterol, urine albumin, homocysteine, and ischemia-modified albumin were significantly higher in patients with peripheral arterial disease than in disease-free patients (p<0.05), while ankle-brachial index was lower in the former group (p<0.05). Ischemia-modified albumin was positively associated with HbA1c and homocysteine levels (r = 0.220, p = 0.030; r = 0.446, p = 0.044, respectively), while no correlation was found with ankle-brachial index. Multiple logistic analyses indicated that HbA1c, systolic blood pressure, homocysteine and ischemia-modified albumin were independent risk factors for peripheral arterial disease in the diabetic subjects. CONCLUSION: The baseline ischemia-modified albumin levels were significantly higher and positively associated with HbA1c and homocysteine levels in type 2 diabetic patients with peripheral arterial disease. Ischemia-modified albumin was a risk marker for peripheral arterial disease. Taken together, these results might be helpful for monitoring diabetic peripheral arterial disease.

The R450H mutation and D727E polymorphism of the thyrotropin receptor gene in a Chinese child with congenital hypothyroidism.

BACKGROUND: Congenital hypothyroidism (CH) is the most prevalent congenital endocrine disorder. The molecular cause of CH in the majority of newborns is unknown. The aim of this study was to investigate the mutation of thyrotropin receptor (TSHR) gene in Chinese children with congenital hypothyroidism (CH). and the hereditary characteristic. METHODS: Eighteen Chinese children with CH were enrolled for molecular analysis of the TSHR gene and 105 normal controls were evaluated. The exons 1-9, and 10 of TSHR gene were detected by PCR-SSCP (single-stranded conformation polymorphism) and sequenced. RESULTS: A slower and a faster mobility SSCP shift showed in a 12-year old child with hypoplasic gland. Sequencing of TSHR gene revealed a homozygous mutation (CGC --> CAC, Arg450His) and a polymorphism (GAC --> GAG, Asp727Glu). The controls revealed no variants. The 12 relatives of the proband were enrolled and investigated. Six relatives, including his mother and father, were heterozygous for R450H mutation and D727E polymorphism of the TSHR gene. Thyroid hormone levels were normal except for circulating TSH (5.96-6.92 mU/L) level slightly elevated in six heterozygous family members. CONCLUSIONS: Homozygous mutation R450H of the TSHR gene led to CH. Heterozygous mutation R450H was the cause of subclinical hypothyroidism.