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Metab Syndr Relat Disord [journal]
- Mice with Altered Brain Lipoprotein Metabolism Display Maladaptive Responses to Environmental Challenges That May Predispose to Weight Gain. [JOURNAL ARTICLE]
- Metab Syndr Relat Disord 2014 Apr 14.
Abstract Background: Three-month-old neuron-specific lipoprotein lipase (LPL)-depleted mice (NEXLP(-/-)) mice are preobese and have normal body weight before developing obesity by 4.5 months. This series of experiments investigated responses to novel environment stimuli and acute sleep deprivation in preobese NEXLPL(-/-)) mice to test the hypothesis that neuron-specific LPL deletion alters normal adaptive metabolic responses to environmental challenges. Methods: Three-month-old, age- and weight-matched, male NEXLPL(-/-)) (n=10) and wild-type (WT) (n=10) mice were housed in individual metabolic chambers with a 12-hr dark cycle. Food and water intake, locomotor activity, and calorimetry data were recorded in 12-min intervals. Novel environmental responses were elicited by first-time introduction to chambers at dark onset, followed by acclimation, baseline recording, and 6-hr of sleep deprivation on subsequent experimental days. Results: NEXLPL(-/-)) mice displayed a 1.5-fold greater increase in activity in response to a novel environment than seen in WT controls (P=0.0308), and a two-fold greater increase in food intake following acute sleep deprivation (P=0.0117). NEXLPL(-/-)) mice averaged a 27% higher metabolic rate than WT mice throughout the experiments (P<0.0001). Body weight, composition, and temperature did not differ between murine groups throughout the experiments. Levels of free fatty acid, insulin, glucose, and triglycerides were similar between groups at the terminus. Conclusions: A deficiency in neuronal LPL signaling disrupts normal responses to novel environmental exposure and acute sleep deprivation, a maladaptive response that may contribute to weight gain in genetically predisposed mice, and perhaps humans.
- Use of HbA1c in the Diagnosis of Diabetes and Prediabetes: Sensitivity Versus Specificity. [JOURNAL ARTICLE]
- Metab Syndr Relat Disord 2014 Apr 9.
- Early Changes in the Components of the Metabolic Syndrome in a Group of Smokers After Tobacco Cessation. [JOURNAL ARTICLE]
- Metab Syndr Relat Disord 2014 Apr 1.
Abstract Aim: We aimed to examine the prevalence of early changes in some components of metabolic syndrome after smoking cessation. Methods: Forty-eight heavy smokers from the Tobacco Cessation Clinic (24 women/24 men), average age of 49.4 years, were included in this study. They smoked a mean of 19.92 cigarettes per day and had smoked 33.23 packages per year during 33.4 years. Participants were included in a treatment group based on cognitive behavior therapy (CBT); 16 participants received varenicline and the other 16 nicotine replacement therapy (NRT). The target quit day was scheduled for week 3 through abrupt cessation. Abstinence was confirmed with exhaled carbon monoxide (CO) levels. Blood pressure, body mass index (BMI), and waist circumference (WC) were evaluated weekly. Glucose, triglycerides, high density lipoproteins (HDL-C), and insulin to determine the homeostasis model assessment (HOMA) index were determined in blood samples at weeks 1, 4, and 10. As a control group 96 healthy nonsmokers were matched by age and sex. Results: The mean BMI in smokers was 26.94 kg/m(2) and in nonsmokers 26.23 kg/m(2). Smokers showed hypertension, hypertriglyceridemia, and lower levels of HDL-C than nonsmokers. Percentages of cessation in week 3 were 81% for NRT and 93% for CBT and varenicline. The mean weight increase at the end of the treatment was 1.09 kg in the CBT group, 1.06 kg in the NRT group, and 1.17 kg in the varenicline group. The prevalence of metabolic syndrome was 31.25% in week 1 and 29.16% at the end. There were reductions in the number of subjects with hypertension, glucose alterations, hypertriglyceridemia, and low HDL levels. Conclusions: Benefits of quitting smoking exceeded by far the risks associated with the amount of weight gained.
- The Relation Between Carotid Intima Media Thickness and Serum Osteoprotegerin Levels in Nonalcoholic Fatty Liver Disease. [JOURNAL ARTICLE]
- Metab Syndr Relat Disord 2014 Apr 1.
Abstract Aim: This study was designed to evaluate carotid intima media thickness (CIMT) and serum osteoprotegerin (OPG) levels in nonalcoholic fatty liver disease (NAFLD) in comparison to healthy controls and to investigate factors predicting the CIMT increase. Materials and Methods: A total of 60 outpatients [median (min-max) age 44.5 (24.0-65.0) years, 63.3% were females] diagnosed with NAFLD via ultrasonography performed during their admission to our hospital for any reason and 30 control subjects [median (min-max) age 39.5 (24.0-57.0) years, 73.3% were females] with normal liver echogenicity in ultrasonography were included in this study. Data on demographic characteristics, anthropometric measurements, biochemical and hematological tests, CIMT measurement, serum levels for OPG, and predictive factors for the CIMT increase were collected. Results: Median (min-max) CIMT [0.60 (0.40-1.10) vs. 0.50 (0.30-0.60), P<0.001) and OPG (pg/mL) [65.0 (18.1-272.8) vs. 32.0 (10.1-82.3), P<0.001] levels were significantly higher in NAFLD patients compared to controls, while there was a significant positive correlation between CIMT and serum OPG (r=0.42, P<0.001). Mean CIMT value was determined to increase significantly by 0.001 cm (P=0.001) for each 1 pg/mL of increase in OPG levels, by 0.103 cm (P<0.001) in case of concomitant NAFLD (P<0.001), and by 0.006 cm (P<0.001) for each 1 pg/mL of increase in urea levels. Conclusion: Our findings indicate higher levels of serum OPG and CIMT in patients with NAFLD compared to controls along with a positive correlation between serum OPG and CIMT levels. High levels of serum OPG, presence of NAFLD, and high levels of serum urea seem to be the independent risk factors predictive for the CIMT increase.
- Regular Exercise Coupled to Diet Regimen Accelerates Reduction of Hepatic Steatosis and Associated Pathological Conditions in Nonalcoholic Fatty Liver Disease. [JOURNAL ARTICLE]
- Metab Syndr Relat Disord 2014 Apr 1.
Abstract Background: A diet regimen focusing on weight loss is still the most efficient treatment for nonalcoholic fatty liver disease (NAFLD). Recently, specific benefits of exercise against NAFLD independent of weight loss have been reported. Hence, combining exercise with diet-induced weight loss can be expected to have an additive benefit for NAFLD management. We evaluated the effectiveness of diet in conjunction with exercise (DE) compared with that of diet alone (D) on hepatic steatosis and its underlying pathophysiology. Methods: Data obtained from 72 obese, middle-aged men with NAFLD who completed a 3-month program of DE or D in 2011 and 2012 were analyzed. Subjects went through a comprehensive parameters analysis for the pathophysiology of NAFLD. Results: Subjects in the DE group, compared with those in the D group, elicited additive effects on the degree of hepatic steatosis (-82.6% vs. -60.0%) and body weight (-13.3% vs. -8.9%) accompanied by an improvement in serum marker levels: inflammation, ferritin (-16.1% vs. -2.1%); oxidative stress, lipid peroxidation (-31.8% vs. +4.8%); adipokine imbalance, adiponectin, and leptin (+27.4% vs. +2.6% and -74.4% vs. -30.2%). Consequently, subjects in the DE group achieved further attenuation of insulin resistance [homeostatsis model assessment of insulin resistance (HOMA-IR) (-63.6% vs. -40.0%)]. These observed additive benefits in the DE group were closely associated with the increased volume of physical activity. Conclusions: The addition of exercise to a diet regimen potentiates the benefits in NAFLD management through further improvement of hepatic steatosis, inflammatory and oxidative stress levels, and adipokine imbalance, thereby attenuating insulin resistance independent of detectable weight loss.
- Prevalence and Correlates of Erectile Dysfunction in Type 2 Diabetes Mellitus: A Cross-Sectional Single-Center Study Among Turkish Patients. [JOURNAL ARTICLE]
- Metab Syndr Relat Disord 2014 Mar 25.
Abstract Objective: The aim of this study was to evaluate prevalence of erectile dysfunction (ED) in patients with type 2 diabetes mellitus (T2DM) in relation to vascular and neurogenic correlates. Methods: A total of 116 males including T2DM patients [n=68; mean age, 56.7 (5.8) years] and age-matched healthy controls [n=48; mean age, 57.0 (6.6) years] were included in this cross-sectional single-center study. Data on anthropometrics, blood biochemistry, concomitant hypertension, hyperlipidemia, and coronary artery disease (CAD) were recorded in each subject along with measurement of carotid artery intima media thickness (CIMT) and evaluation of erectile dysfunction (ED) via International Index of Erectile Function (IIEF-5) Questionnaire. A univariate analysis was performed to determine the relationship of cardiovascular risk factors and diabetes-related complications to ED. Results: Patient and control groups were similar in terms of percentage patients with hyperlipidemia (51.5% and 39.6%, respectively) and CAD (33.8% and 22.9%, respectively), whereas concomitant hypertension was more common (P=0.05) and CIMT values were significantly higher (P=0.020) in patients with T2DM compared with controls. Polyneuropathy was noted in 46.2% of patients, nephropathy in 30.8%, and retinopathy in 33.8%. ED scores were significantly lower in patients than controls [14.3 (7.3) vs. 18.2 (6.3), P=0.004] with a significantly higher percentage of patients than controls in the category of severe dysfunction (29.4 vs. 10.4%, P=0.014). Univariate analysis revealed that diabetic polyneuropathy was the only factor to be associated with higher likelihood (93.3% in the presence and 60.0% in the absence of neuropathy) and severity (43.3% in the presence and 14.3% in the absence of neuropathy) of ED (P=0.004). Conclusion: Findings from the present cross-sectional single-center study revealed the prevalence of ED to be considerably higher in patients with T2DM than age-matched healthy controls, with identification of diabetic polyneuropathy as the only risk factor associated with higher likelihood and more severe forms of ED.
- Hydrogen Sulfide Upregulates Glutamate-Cysteine Ligase Catalytic Subunit, Glutamate-Cysteine Ligase Modifier Subunit, and Glutathione and Inhibits Interleukin-1β Secretion in Monocytes Exposed to High Glucose Levels. [JOURNAL ARTICLE]
- Metab Syndr Relat Disord 2014 Mar 25.
Abstract Glutathione (GSH) deficiency and interleukin-1β (IL-1β) upregulation are linked to the progression of vascular inflammation and atherosclerosis. The consumption of sulfide-rich vegetables is known to lower the risk of atherosclerosis. This study examined the hypothesis that hydrogen sulfide (H2S) upregulates the glutamate-cysteine ligase catalytic subunit (GCLC) and GSH and inhibits IL-1β in a monocyte cell model. U937 monocytes were supplemented with H2S (0-12.5 μM) for 2 hr and then exposed to a control or high glucose (HG, 25 mM) for 22 hr. Levels of GCLC and glutamate-cysteine ligase modifier subunit (GCLM) expression were determined by western blotting and GSH using high-performance liquid chromatography (HPLC), and IL-1β using enzyme-linked immunoassay (ELISA). H2S significantly (P<0.05) upregulated expression of GCLC and GCLM, and formation of GSH, and inhibited IL-1β secretion in controls and HG-treated monocytes. This is the first demonstration of H2S upregulation of GCLC and GSH and inhibition of IL-1β levels, which may be what mediates the beneficial effects of H2S-rich compounds in mitigating the pathogenesis of metabolic syndrome and atherosclerosis.
- Relation of Acanthosis Nigricans to Metabolic Syndrome in Overweight and Obese Women. [JOURNAL ARTICLE]
- Metab Syndr Relat Disord 2014 Mar 20.
Abstract Objective: Insulin resistance appears to be the most likely underlying mechanism in metabolic syndrome. Acanthosis nigricans (AN) is an easily identifiable skin lesion and associated with insulin resistance. We aimed to determine the prevalence of metabolic syndrome and AN in overweight and obese women and the association between AN and anthropometric and metabolic parameters. Materials and Methods: This study included 250 women [mean age 24±7.05 years; body mass index (BMI) 30.7±9.24 kg/m(2)] who were admitted to our internal medicine and endocrine outpatient clinics because of simple obesity. All the patients were evaluated for AN. We used the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria for the diagnosis of metabolic syndrome. Results: A total of 46.4% of the subjects were diagnosed with metabolic syndrome. Patients with metabolic syndrome were older (26.2±7.7 vs. 23.5±6.2 years, P=0.003) and had more increased BMI (34.1±9.8 and 27.8±7.5 kg/m(2), P=0.0001) and higher homeostasis model assessment of insulin resistance (HOMA-IR) values (3.4±2.1% vs. 2.2±1.5%, p=0.0001) compared to patients without metabolic syndrome. In all, 40% of the all patients had AN. The rate of metabolic syndrome was greater in AN-positive patients (60%) compared to AN-negative patients (37.6%) (P=0.0001). We observed a significant correlation between AN and metabolic syndrome, especially waist circumference, high triglycerides, and low high-density lipoprotein cholesterol levels, and a significant positive correlation was also found between the AN and BMI, fasting insulin,and HOMA-IR. Conclusion: Our study suggests that AN is a simple and useful finding of physical examination, like waist circumference, for identifying patients who are susceptible to the metabolic syndrome.
- Relationships Between TCF7L2 Genetic Polymorphisms and Polycystic Ovary Syndrome Risk: A Meta-Analysis. [JOURNAL ARTICLE]
- Metab Syndr Relat Disord 2014 Mar 10.
Abstract Objective: This meta-analysis was performed to evaluate the relationships between genetic polymorphisms in the TCF7L2 gene and polycystic ovary syndrome (PCOS) risk. Methods: The PubMed, Centralised Information Service for Complementary Medicine (CISCOM), Cumulative Index to Nursing and Allied Health Literature (CINAHL), Web of Science, Google Scholar, EBSCO, Cochrane Library, and Common Biorepository Model (CBM) databases were searched for relevant articles published before November 1st, 2013, without language restrictions. Meta-analysis was conducted using the STATA 12.0 software. The relationships were evaluated by calculating the pooled odds ratios (ORs) and their 95% confidence intervals (CIs). Seven case-control studies with a total 2458 PCOS patients and 5109 healthy subjects' met our inclusion criteria for qualitative data analysis. Two common polymorphisms (rs7903146 C→T and rs12255372 G→T) in the TCF7L2 gene were assessed. Results: The results of our meta-analysis suggested that TCF7L2 genetic polymorphisms might be strongly correlated with an increased risk of PCOS (allele model, OR=1.33, 95% CI=1.15-1.54, P<0.001; dominant model, OR=1.40, 95% CI=1.12-1.75, P=0.003), especially for the rs7903146 C→T polymorphism. A subgroup analysis was done to investigate the effect of ethnicity on an individual's risk of PCOS. Our results revealed positive significant correlations between TCF7L2 genetic polymorphisms and an increased risk of PCOS among Caucasians (allele model, OR=1.26, 95% CI=1.08-1.47, P=0.004; dominant model, OR=1.33, 95% CI=1.00-1.76, P=0.046) and Asians (allele model, OR=2.02, 95% CI=1.42-2.89, P<0.001; dominant model, OR=2.02, 95% CI=1.40-2.92, P<0.001), but not among Africans (all P<0.05). Conclusions: Our findings provide convincing evidence that TCF7L2 genetic polymorphisms may contribute to susceptibility to PCOS, especially for the rs7903146 C→T polymorphism among Caucasians and Asians.