The prevalence of probable migraine and sleep quality among women aged 20-49 living in a semi-rural area in western Turkey

Background: We aimed to evaluate the prevalence of probable migraine, to examine the factors associated with probable migraine and to assess the level of sleep quality among women aged 20-45 who were living in the county town named Mahmudiye, in Eskisehir, in Turkey.Methods: The study was carried out in all women aged 20-45 years in Mahmudiye. 69.2% of women (n=570) comprised the study group. Questionnaire consisted of three parts: The first part included several socio-demographic, nutritional and health characteristics. The second part included questions about the headache type and third part included Pittsburgh Sleep Quality Index (PSQI). Migraine type headache was scanned via the International Headache Society (IHS) criteria for migraine. There were eight criteria which were defined by IHS. Individuals who possessed the six of the eight criteria were defined as “probable migraine”.Results: The mean age of the participants was 32.8±7.3 years. Prevalence of probable migraine was 13.3% (n=60) and it was significantly higher in women who have been smoking and who had a physician diagnosed chronic diseases. Of the women, 45.1% had poor sleep quality based on the PSQI. The sleep quality of probable migraineurs was found significantly lower than healthy women.Conclusions: To control the probable migraine symptoms and attacks, we suggest to giving regular treatment to women with chronic diseases and reducing the smoking.

Eating disorders and anxiety among high school students in Western area of Turkey

Background Eating disorders (ED) are the one of the most common chronic illness among adolescents. The aim of the present study was to investigate eating disorders and it's associations between anxiety among high school students in Sivrihisar in Eskisehir, Turkey.Methods: This cross-sectional study was carried out in the high school students of center of Sivrihisar between 01 January 2014 and 28 February 2014. The questionnaire prepared according to literature, consisting of 3 parts (socio-demographic characteristics, eating attitude test (EAT-40) and beck anxiety inventory (BAI)). The students completed questionnaire in the presence of a member of the research team. The data collected were self-reported by the students.Results: Of the study group 64.4% (n=625) were females and 35.6% (n=345) were males. The prevalence of eating disorder was 13.0% (n=126). The mean and standard deviation of students' total score of EAT-40 were 18.80±9.88 (ranged 3 to 95).  The mean and standard deviation of students' total score of BAI were 20.32±12.32 (ranged 0 to 63). The positive weak correlation was found between the total scores of EAT-40 and BAI (r=0.178; p=0.001).Conclusions: ED is an important health problem for adolescents. On the studies upon epidemiology of ED towards high school students, socio-economic factors should be assessed in more detailed and more comprehensive perspective.

Adipose Tissue Extracellular Matrix and Vascular Abnormalities in Obesity and Insulin Resistance

Context: Insulin resistance is associated with inflammation, fibrosis, and hypoxia in adipose tissue. Objective: This study was intended to better characterize the extracellular matrix (ECM) and vascularity of insulin-resistant adipose tissue. Design: Adipose expression of collagens, elastin, and angiogenic factors was assessed using realtime RT-PCR and immunohistochemistry (IHC) in abdominal sc adipose tissue. Adipocyte-macrophage coculture experiments examined the effects of polarized macrophages on adipose ECM gene expression, and the effects of collagens were measured in an angiogenesis assay. Participants and Setting: A total of 74 nondiabetic subjects participated at a University Clinical Research Center. Interventions: Interventions included baseline adipose biopsy and measurement of insulin sensitivity. Main Outcome Measures: Outcome measures included characterization of vascularity and ECM in adipose tissue. Results: CD31 (an endothelial marker) mRNA showed no significant correlation with body mass index or insulin sensitivity. In a subgroup of 17 subjects (nine obese, eight lean), CD31-positive capillary number in obese was decreased by 58%, whereas larger vessels were increased by 70%, accounting for the lack of change in CD31 expression with obesity. Using IHC, obese (compared with lean) subjects had decreased elastin and increased collagen V expression, and adipocytes cocultured with M2 macrophages had reduced elastin and increased collagen V expression. In obese subjects, collagen V was colocalized with large blood vessels, and the addition of collagen V to an angiogenesis assay inhibited endothelial budding. Conclusions: The adipose tissue from obese/insulin- resistant subjects has fewer capillaries and morelarge vessels as compared with lean subjects.The ECM of adipose tissue may play an important role in regulating the expandability as well as angiogenesis of adipose tissue. (J Clin Endocrinol Metab 96: E1990–E1998, 2011

The Lipogenic Enzymes DGAT1, FAS, and LPL in Adipose Tissue: Effects of Obesity, Insulin Resistance, and TZD Treatment

Acyl-coenzyme A:diacylglycerol transferase (DGAT), fatty acid synthetase (FAS), and LPL are three enzymes important in adipose tissue triglyceride accumulation. To study the relationship of DGAT1, FAS, and LPL with insulin, we examined adipose mRNA expression of these genes in subjects with a wide range of insulin sensitivity (SI). DGAT1 and FAS (but not LPL) expression were strongly correlated with SI. In addition, the expression of DGAT1 and FAS (but not LPL) were higher in normal glucose-tolerant subjects compared with subjects with impaired glucose tolerance (IGT) (P \u3c 0.005). To study the effects of insulin sensitizers, subjects with IGT were treated with pioglitazone or metformin for 10 weeks, and lipogenic enzymes were measured in adipose tissue. After pioglitazone treatment, DGAT1 expression was increased by 33 ± 10% (P \u3c 0.05) and FAS expression increased by 63 ± 8% (P \u3c 0.05); however, LPL expression was not altered. DGAT1, FAS, and LPL mRNA expression were not significantly changed after metformin treatment. The treatment of mice with rosiglitazone also resulted in an increase in adipose expression of DGAT1 by 2- to 3-fold, as did the treatment of 3T3 F442A adipocytes in vitro with thiazolidinediones. These data support a more global concept suggesting that adipose lipid storage functions to prevent peripheral lipotoxicity

Increasing Adipocyte Lipoprotein Lipase Improves Glucose Metabolism in High Fat Diet-Induced Obesity

Lipid accumulation in liver and skeletal muscle contributes to co-morbidities associated with diabetes and obesity. We made a transgenic mouse in which the adiponectin (Adipoq) promoter drives expression of lipoprotein lipase (LPL) in adipocytes to potentially increase adipose tissue lipid storage. These mice (Adipoq-LPL) have improved glucose and insulin tolerance as well as increased energy expenditure when challenged with a high fat diet (HFD). To identify the mechanism(s) involved, we determined whether the Adipoq-LPL mice diverted dietary lipid to adipose tissue to reduce peripheral lipotoxicity, but we found no evidence for this. Instead, characterization of the adipose tissue of the male mice after HFD challenge revealed that the mRNA levels of peroxisome proliferator-activated receptor-γ (PPARγ) and a number of PPARγ-regulated genes were higher in the epididymal fat pads of Adipoq-LPL mice than control mice. This included adiponectin, whose mRNA levels were increased, leading to increased adiponectin serum levels in the Adipoq-LPL mice. In many respects, the adipose phenotype of these animals resembles thiazolidinedione treatment except for one important difference, the Adipoq-LPL mice did not gain more fat mass on HFD than control mice and did not have increased expression of genes in adipose such as glycerol kinase, which are induced by high affinity PPAR agonists. Rather, there was selective induction of PPARγ-regulated genes such as adiponectin in the adipose of the Adipoq-LPL mice, suggesting that increasing adipose tissue LPL improves glucose metabolism in diet-induced obesity by improving the adipose tissue phenotype. Adipoq-LPL mice also have increased energy expenditure

Omega-3 Fatty Acids Reduce Adipose Tissue Macrophages in Human Subjects with Insulin Resistance

Fish oils (FOs) have anti-inflammatory effects and lower serum triglycerides. This study examined adipose and muscle inflammatory markers after treatment of humans with FOs and measured the effects of ω-3 fatty acids on adipocytes and macrophages in vitro. Insulin-resistant, nondiabetic subjects were treated with Omega-3-Acid Ethyl Esters (4 g/day) or placebo for 12 weeks. Plasma macrophage chemoattractant protein 1 (MCP-1) levels were reduced by FO, but the levels of other cytokines were unchanged. The adipose (but not muscle) of FO-treated subjects demonstrated a decrease in macrophages, a decrease in MCP-1, and an increase in capillaries, and subjects with the most macrophages demonstrated the greatest response to treatment. Adipose and muscle ω-3 fatty acid content increased after treatment; however, there was no change in insulin sensitivity or adiponectin. In vitro, M1-polarized macrophages expressed high levels of MCP-1. The addition of ω-3 fatty acids reduced MCP-1 expression with no effect on TNF-α. In addition, ω-3 fatty acids suppressed the upregulation of adipocyte MCP-1 that occurred when adipocytes were cocultured with macrophages. Thus, FO reduced adipose macrophages, increased capillaries, and reduced MCP-1 expression in insulin-resistant humans and in macrophages and adipocytes in vitro; however, there was no measureable effect on insulin sensitivity. Diabetes 62:1709–1717, 201

Monotherapy for hepatitis B infection: a review of treatment options

Chronic hepatitis B (CHB) is a global health problem, causing liver failure, cirrhosis and hepatocellular carcinoma. CHB treatment aims to prevent liver-related complication. The treatment of CHB infection includes monotherapy with either interferons (IFNs) or nucleos(t)ide (NUC) analogs. IFNs have moderate antiviral effects, and their use is limited by side effects. With the availability of NUCs, IFN-intolerant and decompensated cirrhotic patients began to be treated. Lamivudine and telbivudine, nucleoside analogs, have low genetic barrier to resistance. Adefovir, a nucleotide analog, has moderate potency and potential nephrotoxicity. Entecavir and tenofovir, with their high potency, high genetic barrier to resistance and favorable safety profile are the standard of care in CHB treatment. Long-term use of NUCs with maintained viral suppression results in a decrease in liver-related complications

Adipose Tissue Extracellular Matrix and Vascular Abnormalities in Obesity and Insulin Resistance

CONTEXT: Insulin resistance is associated with inflammation, fibrosis, and hypoxia in adipose tissue. OBJECTIVE: This study was intended to better characterize the extracellular matrix (ECM) and vascularity of insulin-resistant adipose tissue. DESIGN: Adipose expression of collagens, elastin, and angiogenic factors was assessed using real-time RT-PCR and immunohistochemistry (IHC) in abdominal sc adipose tissue. Adipocyte-macrophage coculture experiments examined the effects of polarized macrophages on adipose ECM gene expression, and the effects of collagens were measured in an angiogenesis assay. PARTICIPANTS AND SETTING: A total of 74 nondiabetic subjects participated at a University Clinical Research Center. INTERVENTIONS: Interventions included baseline adipose biopsy and measurement of insulin sensitivity. MAIN OUTCOME MEASURES: Outcome measures included characterization of vascularity and ECM in adipose tissue. RESULTS: CD31 (an endothelial marker) mRNA showed no significant correlation with body mass index or insulin sensitivity. In a subgroup of 17 subjects (nine obese, eight lean), CD31-positive capillary number in obese was decreased by 58%, whereas larger vessels were increased by 70%, accounting for the lack of change in CD31 expression with obesity. Using IHC, obese (compared with lean) subjects had decreased elastin and increased collagen V expression, and adipocytes cocultured with M2 macrophages had reduced elastin and increased collagen V expression. In obese subjects, collagen V was colocalized with large blood vessels, and the addition of collagen V to an angiogenesis assay inhibited endothelial budding. CONCLUSIONS: The adipose tissue from obese/insulin-resistant subjects has fewer capillaries and more large vessels as compared with lean subjects. The ECM of adipose tissue may play an important role in regulating the expandability as well as angiogenesis of adipose tissue

Adiponectin translation is increased by the PPARγ agonists pioglitazone and ω-3 fatty acids

Adiponectin, made exclusively by adipocytes, is a 30-kDa secretory protein assembled posttranslationally into low-molecular weight, middle-molecular weight, and high-molecular weight homo-oligomers. PPARγ ligand thiozolidinediones, which are widely used in the treatment of type II diabetes, increase adiponectin levels. PPARγ also has several putative ligands that include fatty acid derivatives. Overnight treatment of rat adipocytes with pioglitazone, docosahexaenoic acid (DHA), or eicosapentaenoic acid (EPA) triggered a twofold increase in the synthesis and secretion of HMW adiponectin, and this increase was blocked by the addition of PPARγ inhibitor GW-9662. Inhibition of glycosylation using 2,2′-dipyridyl decreased the synthesis of high-molecular weight adiponectin by pioglitazone, EPA, and DHA, but there was increased secretion of trimeric adiponectin resulting from increased translation. Although pioglitazone, DHA, and EPA increased adiponectin synthesis by more than 60%, there was no increase in total protein synthesis and no corresponding change in adiponectin mRNA expression, indicating the upregulation of translation. We examined the possibility of transacting factors in the cytoplasmic extracts from adipocytes treated with pioglitazone or DHA. In vitro translation of adiponectin mRNA was inhibited by S-100 fraction of control adipocytes and increased by S-100 extracts from adipocytes treated with pioglitazone or DHA. Consistent with this observation, both pioglitazone and DHA treatments increased the association of adiponectin mRNA with the heavier polysome fractions. Together, these data suggest that pioglitazone and the fish oils DHA or EPA are PPARγ agonists in adipocytes with regard to adiponectin expression, and the predominant mode of adiponectin stimulation is via an increase in translation

Integrative mRNA-microRNA analyses reveal novel interactions related to insulin sensitivity in human adipose tissue

Adipose tissue has profound effects on whole-body insulin sensitivity. However, the underlying biological processes are quite complex and likely multifactorial. For instance, the adipose transcriptome is posttranscriptionally modulated by microRNAs, but the relationship between microRNAs and insulin sensitivity in humans remains to be determined. To this end, we utilized an integrative mRNA-microRNA microarray approach to identify putative molecular interactions that regulate the transcriptome in subcutaneous adipose tissue of insulin-sensitive (IS) and insulin-resistant (IR) individuals. Using the NanoString nCounter Human v1 microRNA Expression Assay, we show that 17 microRNAs are differentially expressed in IR vs. IS. Of these, 16 microRNAs (94%) are downregulated in IR vs. IS, including miR-26b, miR-30b, and miR-145. Using Agilent Human Whole Genome arrays, we identified genes that were predicted targets of miR-26b, miR-30b, and miR-145 and were upregulated in IR subjects. This analysis produced ADAM22, MYO5A, LOX, and GM2A as predicted gene targets of these microRNAs. We then validated that miR-145 and miR-30b regulate these mRNAs in differentiated human adipose stem cells. We suggest that use of bioinformatic integration of mRNA and microRNA arrays yields verifiable mRNA-microRNA pairs that are associated with insulin resistance and can be validated in vitro