http://www.hindawi.comThe latest articles from Hindawi Publishing Corporation© 2012, Hindawi Publishing Corporation. All rights reserved.http://www.hindawi.com/journals/ije/2012/879134/We examined gender and ethnic differences in the association between sleep disordered breathing (SDB) and diabetes among 6,522 participants aged ≥20 years from the National Health and Nutrition Examination Survey 2005–08. SDB severity was defined based on an additive summary score including sleep duration, snoring, snorting, and daytime sleepiness. We found that the summary SDB score was significantly associated with diabetes after adjusting for potential confounders in the whole population. Compared to those without any sleep disturbance, the multivariable odds ratio (OR) (95% confidence interval (CI)) of diabetes among those with ≥3 sleep disturbances was 2.04 (1.46–2.87). In sex-specific analyses, this association was significant only in women (OR (95% CI) = 3.68 (2.01–6.72)) but not in men (1.10 (0.59–2.04)), P-interaction =0.01. However, there were no ethnic differences in this association, P-interaction =0.7. In a nationally representative sample of US adults, SDB was independently associated with diabetes only in women, but not in men.Charumathi Sabanayagam, Srinivas Teppala, and Anoop ShankarCopyright © 2012 Charumathi Sabanayagam et al. All rights reserved.http://www.hindawi.com/journals/ije/2012/456279/Objective. We performed a systematic review of the literature to evaluate the effects of alpha lipoic acid for symptomatic peripheral neuropathy in patients with diabetes mellitus. Research design and methods. The databases MEDLINE and EMBASE were searched using the key words “lipoic acid’’, “thioctic acid’’, “diabet*’’, and the MeSH-terms “thioctic acid’’ and “diabetes mellitus’’. Randomised controlled trials using the TSS score as the outcome measure were selected and assessed for their methodological quality. Study selection and quality assessment were performed independently by three observers. Results. Overall, the pooled standardized mean difference estimated from all trials revealed a reduction in TSS scores of −2.26 (CI: −3.12 to −1.41; P=0.00001) in favour of alpha lipoic acid administration. Subgroup analyses of oral administration (−1.78 CI: −2.45 to −1.10; P=0.00001) and intravenous administration (−2.81 CI: −4.16 to −1.46; P=0.0001) confirmed the robustness of the overall result. Conclusions. When given intravenously at a dosage of 600 mg/day over a period of 3 weeks, alpha lipoic acid leads to a significant and clinically relevant reduction in neuropathic pain (grade of recommendation A). It is unclear if the significant improvements seen after 3–5 weeks of oral administration at a dosage of >600 mg/day are clinically relevant.Gerritje S. Mijnhout, Boudewijn J. Kollen, Alaa Alkhalaf, Nanno Kleefstra, and Henk J. G. BiloCopyright © 2012 Gerritje S. Mijnhout et al. All rights reserved.http://www.hindawi.com/journals/ije/2012/649149/Background. Infertility is both a clinical and a public problem, affecting the life of the couple, the healthcare services, and social environment. Standard semen analysis is the surrogate measure of male fertility in clinical practice. Objective. To provide information about the relationship between semen parameters and spontaneous conception. Methods. We evaluated retrospectively 453 pregnancies that occurred among 2935 infertile couples evaluated at an infertility clinic of a tertiary-care university hospital, between 2004 and 2009. Results. Normal semen analysis was present only in 158 patients; 295 subfertile patients showed alterations in at least one seminal parameter. A reduction in all seminal parameters was observed in 41 patients. Etiological causes of male infertility were identified in 314 patients. Conclusion. Our data highlights the possibility of a spontaneous conception with semen parameters below WHO reference values. Therefore, we support the importance of defining reference values on a population of fertile men. Finally, we analyzed the related ethical issues.D. Milardi, G. Grande, D. Sacchini, A. L. Astorri, G. Pompa, A. Giampietro, L. De Marinis, A. Pontecorvi, A. G. Spagnolo, and R. MaranaCopyright © 2012 D. Milardi et al. All rights reserved.http://www.hindawi.com/journals/ije/2012/717185/It has been twenty years since the first paper reporting the association between thyroid antibodies (TAIs) and spontaneous miscarriage was published. Following this observation, several studies have clearly demonstrated an increased prevalence of TAI in patients with recurrent miscarriage (RM). However, the exact mechanism underlying this association remains a matter of debate. The aim of the present study was to evaluate the thyroid function, throughout a specific test, in patient with RM and TAI focusing on the hypothesis that TAI should be an indirect sign of a mild thyroid dysfunction. 46 patients with RM and TAI were included in the study. All patients underwent short TRH stimulation test showing an abnormal response in the vast majority of cases (65%). Normal FT4 and FT3 mean values were found whereas TSH values were in the upper normal range (2.64±1.3 mUI/L). Our data support the hypothesis that in patients with RM the presence of TAI is an indirect sign of a subtle thyroid dysfunction detectable by a specific test. This test give the possibility to identify women with RM in which specific therapeutic approaches could effectively improve the possibility for a successful pregnancy.Natalia Lazzarin, Costanzo Moretti, Giovanna De Felice, Elena Vaquero, and Dario ManfellottoCopyright © 2012 Natalia Lazzarin et al. All rights reserved.http://www.hindawi.com/journals/ije/2012/637825/Altered thyroid function during early stages of development is known to affect adversely testicular growth, physiology, and antioxidant defence status at adulthood. The objective of the present study is to investigate the modulation of antioxidant defence status in neonatal persistent hypothyroid rats before their sexual maturation and also to identify the specific testicular cell populations vulnerable to degeneration during neonatal hypothyroidism in immature rats. Hypothyroidism was induced in neonates by feeding the lactating mother with 0.05% 6-n-propyl-2-thiouracil (PTU) through the drinking water. From the day of parturition till weaning (25 day postpartum), the pups received PTU through mother's milk (or) drinking water and then directly from drinking water containing PTU for the remaining period of experimentation. On the 31st day postpartum, the animals were sacrificed for the study. An altered antioxidant defence system marked by elevated SOD, CAT, and GR activities, with decreased GPx and GST activities were observed along with increased protein carbonylation, disturbed redox status in hypothyroid immature rat testis. This compromised testicular antioxidant status might have contributed to poor growth and development by affecting the spermatogenesis and steroidogenesis in rats before puberty as indicated by reduced germ cell number, complete absence of round spermatids, decreased seminiferous tubule diameter, and decreased testosterone level.Dipak K. Sahoo and Anita RoyCopyright © 2012 Dipak K. Sahoo and Anita Roy. All rights reserved.http://www.hindawi.com/journals/ije/2011/746482/A PKA consensus phosphorylation site S1928 at the α11.2 subunit of the rabbit cardiac L-type channel, CaV1.2, is involved in the regulation of CaV1.2 kinetics and affects catecholamine secretion. This mutation does not alter basal CaV1.2 current properties or regulation of CaV1.2 current by PKA and the beta-adrenergic receptor, but abolishes CaV1.2 phosphorylation by PKA. Here, we test the contribution of the corresponding PKA phosphorylation site of the human α11.2 subunit S1898, to the regulation of catecholamine secretion in bovine chromaffin cells. Chromaffin cells were infected with a Semliki-Forest viral vector containing either the human wt or a mutated S1898A α11.2 subunit. Both subunits harbor a T1036Y mutation conferring nifedipine insensitivity. Secretion evoked by depolarization in the presence of nifedipine was monitored by amperometry. Depolarization-triggered secretion in cells infected with either the wt α11.2 or α11.2/S1898A mutated subunit was elevated to a similar extent by forskolin. Forskolin, known to directly activate adenylyl-cyclase, increased the rate of secretion in a manner that is largely independent of the presence of S1898. Our results are consistent with the involvement of additional PKA regulatory site(s) at the C-tail of α11.2, the pore forming subunit of CaV1.2.Niv Bachnoff, Moshe Cohen-Kutner, and Daphne AtlasCopyright © 2011 Niv Bachnoff et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/107904/To determine the relationship between serum concentrations of uric acid and insulin secretion with hyperglycaemic clamp technique among adults with type 2 diabetes mellitus (DM2) without hyperuricemia, we carried out a cross-sectional study on 45 patients of both gender. We observed correlation between uric acid with male gender r=0.710 (P=0.001). Also correlation between uric acid and total insulin secretion was positive r=0.295 (P=0.049). As well as a positive correlation adjusted for body mass index was demonstrated for the first, second, and total phases of insulin secretion, respectively, r=0.438 (P=0.022), r=0.433 (P=0.022), and r=0.439 (P=0.024). Serum concentration of uric acid showed a positive relationship with the total phase of insulin secretion; even in states prior to hyperuricemia, uric acid can play an important role in the function of the beta cell in patients with DM2.J. A. Robles-Cervantes, M. G. Ramos-Zavala, M. González-Ortiz, E. Martínez-Abundis, C. Valencia-Sandoval, A. Torres-Chávez, C. Espinel-Bermúdez, N. J. Santiago-Hernández, and S. O. Hernández-GonzálezCopyright © 2011 J. A. Robles-Cervantes et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/707928/Recent reports point out the importance of the complex GK-GKRP in controlling glucose and lipid homeostasis. Several GK mutations affect GKRP binding, resulting in permanent activation of the enzyme. We hypothesize that hepatic overexpression of a mutated form of GK, GKA456V, described in a patient with persistent hyperinsulinemic hypoglycemia of infancy (PHHI) and could provide a model to study the consequences of GK-GKRP deregulation in vivo. GKA456V was overexpressed in the liver of streptozotocin diabetic mice. Metabolite profiling in serum and liver extracts, together with changes in key components of glucose and lipid homeostasis, were analyzed and compared to GK wild-type transfected livers. Cell compartmentalization of the mutant but not the wild-type GK was clearly affected in vivo, demonstrating impaired GKRP regulation. GKA456V overexpression markedly reduced blood glucose in the absence of dyslipidemia, in contrast to wild-type GK-overexpressing mice. Evidence in glucose utilization did not correlate with increased glycogen nor lactate levels in the liver. PEPCK mRNA was not affected, whereas the mRNA for the catalytic subunit of glucose-6-phosphatase was upregulated ~4 folds in the liver of GKA456V-treated animals, suggesting that glucose cycling was stimulated. Our results provide new insights into the complex GK regulatory network and validate liver-specific GK activation as a strategy for diabetes therapy.Anna Vidal-Alabró, Alícia G. Gómez-Valadés, Andrés Méndez-Lucas, Jordi Llorens, Ramon Bartrons, Jordi Bermúdez, and Jose C. PeralesCopyright © 2011 Anna Vidal-Alabró et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/903918/The zinc finger E-box binding protein 1 (ZEB1) transcription factor belongs to a two-member family of zinc-finger homeodomain proteins involved in physiological and pathological events mostly relating to cell migration and epithelial to mesenchymal transitions (EMTs). ZEB1 (also known as δEF1, zfhx1a, TCF8, and Zfhep) plays a key role in regulating such diverse processes as T-cell development, skeletal patterning, reproduction, and cancer cell metastasis. However, the factors that regulate its expression and consequently the signaling pathways in which ZEB1 participates are poorly defined. Because it is induced by estrogen and progesterone and is high in prostate cancer, we investigated whether tcf8, which encodes ZEB1, is regulated by androgen. Data herein demonstrate that tcf8 is induced by dihydrotestosterone (DHT) in the human PC-3/AR prostate cancer cell line and that this induction is mediated by two androgen response elements (AREs). These results demonstrate that ZEB1 is an intermediary in androgen signaling pathways.Bynthia M. Anose and Michel M. SandersCopyright © 2011 Bynthia M. Anose and Michel M. Sanders. All rights reserved.http://www.hindawi.com/journals/ije/2011/809069/Background/Aims. Vitamin D3 is liposoluble, so dietary fat could increase its oral absorption. Our aim was to compare serum 25-hydroxyvitamin D [25(OH)D] after the oral intake of cholecalciferol with a high- or low-fat meal. Methods. In a single-blind, parallel clinical trial, 32 healthy physicians were divided into two groups. In the same day, they ingested 50,000 IU (1.25 mg) of vitamin D3 with food: group 1 (G1): lipids: 25.6 g and group 2 (G2) lipids: 1.7 g. Serum 25(OH)D (0, 7, and 14 days), and parathyroid hormone (PTH), and calcium (0 and 14 days) were measured. Results. Baseline mean serum 25(OH)D levels were 42.7±19.0 nmol/L in G1 and 36.4±19.0 nmol/L in G2 (P=0.38). After cholecalciferol, mean serum 25(OH)D was higher in G1 (P<0.001): 7 days: G1 = 46.2 (38.4–53.9) nmol/L and G2 = 33.7 (25.4–40.1) nmol/L; 14 days: G1 = 53.7 (45.2–62.1) nmol/L and G2 = 33.7 (25.2–42.2) nmol/L. Serum PTH and 25(OH)D were negatively correlated before and after the intake of vitamin D3, respectively, r=-0.42 (P=0.02) and r=-0.52 (P=0.003). Conclusions. A high-fat meal increased the absorption of vitamin D3, as measured by serum 25(OH)D.Fabiana Viegas Raimundo, Gustavo Adolpho Moreira Faulhaber, Paula Kalinka Menegatti, Leonardo da Silva Marques, and Tania Weber FurlanettoCopyright © 2011 Fabiana Viegas Raimundo et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/350546/Oxytocin, a hormone involved in numerous physiologic processes, plays a central role in the mechanisms of parturition and lactation. It acts through its receptor, which belongs to the G-protein-coupled receptor superfamily, while Gq/phospholipase C (PLC)/inositol 1,4,5-triphosphate (InsP3) is the main pathway via which it exerts its action in the myometrium. Changes in receptor levels, receptor desensitization, and locally produced oxytocin are factors that influence the effect of oxytocin on uterine contractility in labor. Activation of oxytocin receptor causes myometrial contractions by increasing intracellular Ca+2 and production of prostaglandins. Since oxytocin induces contractions, the inhibition of its action has been a target in the management of preterm labor. Atosiban is today the only oxytocin receptor antagonist that is available as a tocolytic. However, the quest for oxytocin receptor antagonists with a better pharmacological profile has led to the synthesis of peptide and nonpeptide molecules such as barusiban, retosiban, L-368,899, and SSR-126768A. Many of these oxytocin receptor antagonists are used only as pharmacological tools, while others have tocolytic action. In this paper, we summarize the action of oxytocin and its receptor and we present an overview of the clinical and experimental data of oxytocin antagonists and their tocolytic action.Nikolaos Vrachnis, Fotodotis M. Malamas, Stavros Sifakis, Efthymios Deligeoroglou, and Zoe IliodromitiCopyright © 2011 Nikolaos Vrachnis et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/269853/Intrauterine growth retardation (IUGR), the most important cause of perinatal mortality and morbidity, is defined as a foetal growth less than normal for the population, often used as synonym of small for gestational age (SGA). Studies demonstrated the relationships between metabolic syndrome (MS) and birthweight. This study suggested that, in children, adolescents, and adults born SGA, insulin resistance could lead to other metabolic disorders: type 2 diabetes (DM2), dyslipidemia, and nonalcoholic fatty liver disease (NAFLD). NAFLD may evolve to nonalcoholic steatohepatitis (NASH), and it is related to the development of MS. Lifestyle intervention, physical activity, and weight reduction represent the mainstay of NAFLD therapy. In particular, a catch-up growth reduction could decrease the risk to develop MS and NAFLD. In this paper, we outline clinical and experimental evidences of the association between IUGR, metabolic syndrome, insulin resistance, and NAFLD and discuss on a possible management to avoid the risk of MS in adulthood.Anna Alisi, Nadia Panera, Carlo Agostoni, and Valerio NobiliCopyright © 2011 Anna Alisi et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/715370/Patients with Graves' hyperthyroidism (GH) treated with a combination of thyrostatic drugs and T4, that is, block and replacement therapy (BRT), often report body weight (BW) gain. We aimed to determine changes in BW and energy metabolism upon cessation of BRT in these patients, and to identify possible endocrine determinants. We analysed 22 patients with GH (i) during BRT, and (ii) 12 weeks after BRT cessation. Patients were euthyroid at both visits. There were no differences in BW or resting energy expenditure (REE) between visits. At visit 1, after 13.5 (9.5–48.0) months of BRT, serum free (F)T4 correlated positively with REE (r=0.433, P=0.044) and negatively with body fat % (r=-0.450, P=0.035). Plasma FT3 and FT3/FT4 ratio showed an increase 12 w after cessation of BRT (20%, P<0.0001 and 16%, P=0.007, resp.). Moreover, the relative change in FT3/FT4 ratio showed a significant, positive correlation with the relative change in REE between the 2 visits (r=0.465, P=0.029). In conclusion, serum FT4 determines REE in euthyroid patients with GH treated with BRT. Twelve weeks after BRT cessation, BW and energy homeostasis are unaltered. However, as serum FT3/FT4 ratio increases after cessation of BRT, which is a positive determinant of changes in REE, a longer term BW decrease is likely to occur.Lars P. Klieverik, Andries Kalsbeek, Mariëtte T. Ackermans, Hans P. Sauerwein, Wilmar M. Wiersinga, and Eric FliersCopyright © 2011 Lars P. Klieverik et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/916380/Varicocele in infertile males is associated with Leydig cell dysfunction and hypogonadism. The effect of varicocelectomy on serum testosterone level is not yet established. We analysed 200 heterosexual infertile men diagnosed to have clinical varicocele they were divided into two groups: group 1 (100 men) had microsurgical varicocelectomy, and group 2 (100 patients) underwent assisted reproduction procedures. All participants had semen analysis, serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, and total testosterone (TT), measured both at recruitment time and 6 months later. In group 1, the mean TT level increased significantly after varicocelectomy (1.644±0.029 to 2.461±0.0198 ng/dL, P<0.0001) and testicular size correlated with the mean change in TT (P=0.001). No similar change was found in group 2. Out of the 100 patients in group 1, 78 had postoperative normalization of TT unlike only 16 men in group 2.Vasan Sathya Srini and Srinivas Belur VeerachariCopyright © 2011 Vasan Sathya Srini and Srinivas Belur Veerachari. All rights reserved.http://www.hindawi.com/journals/ije/2011/707126/Plasma FGF-23 concentrations and its relationship with calcium-phosphate homeostasis were evaluated in 48 perimenopausal obese women and in 29 nonobese controls. Serum parathyroid hormone, 25-hydroxyvitamin D3, CTX1, osteocalcin, total calcium, phosphorus, creatinine, and plasma intact FGF-23 concentrations were assessed. DXA of lumbar spine and femoral neck was performed to determine bone mineral density (BMD). Plasma iFGF-23 concentration was significantly higher in obese patients (by 42%) and correlated with age and BMD of proximal femur (R=-0.346; R=0.285, resp.) but not with markers of bone turnover. However, serum phosphorus level in obese subjects was significantly lower. iFGF-23 concentration correlated significantly with body mass index (R=0.292) and fat content (R=0.259) in all study subjects. Moreover, a significant correlation between iFGF-23 and iPTH (R=0.254) was found. No correlation between serum phosphorus or eGFR and plasma iFGF-23 and between eGFR and serum phosphorus was found. Elevated serum iFGF-23 concentration may partially explain lower phosphorus levels in the obese and seems not to reflect bone turnover.M. Holecki, J. Chudek, A. Więcek, M. Titz-Bober, and J. DuławaCopyright © 2011 M. Holecki et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/458750/Background. Extensive evidence, arising from models of endothelial nitric oxide synthase gene (NOS3)-knockout mice supports the role of endothelial malfunction in the pathogenesis of the metabolic syndrome (MS). Aims. The aim of this study was to evaluate the role of −786T/C polymorphism in the etiology of MS and assess previously reported interaction with cigarette smoking. Methods. Based on International Diabetes Federation 2005 criteria, we recruited randomly 152 subjects with MS and 75 subjects without MS. Results. Allelic and genotype frequencies did not differ significantly between both groups. Total cholesterol level (CHOLT) and intima-media thickness of carotid arteries were significantly higher in −786CC homozygotes, in comparison with −786TC and −786TT patients. Regarding current smoking status, −786C allele was associated with higher CHOLT than −786T allele. Conclusion. Our study indicates the putative role of −786T/C polymorphism in the development of hypercholesterolemia, in patients with MS, which might be enhanced by cigarette smoking.Blazej Misiak, Marta Krolik, Anna Kukowka, Anna Lewera, Przemyslaw Leszczynski, Joanna Stankiewicz-Olczyk, and Ryszard SlezakCopyright © 2011 Blazej Misiak et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/908367/T3 (3,5,3′-triiodothyronine) has drawn relatively little attention in relation to cardiovascular (CVS) diseases. The present study was designed to evaluate the cardioprotective action of T3 in isoproterenol-(ISO-) induced cardiac toxicity. Female Wistar rats were exposed with ISO (100 mg/kg, body weight, subcutaneously) for 2 days at the interval of 24 h followed by T3 (3 μg/kg, body weight, orally) treatment for 3 days. Positive control rats received only ISO (100 mg/kg, body weight, subcutaneously) for 2 days at the interval of 24 hrs. Control group animals received normal saline as a vehicle. As expected, ISO-induced significant changes were observed in low-density lipoprotein, total cholesterol, ALT, CK-MB to TCK ratio, and prolongation of QT interval in electrocardiogram, which is toward normalization after T3 treatment. Lower heart weight, upregulation of cardiac myosin heavy chain alpha (MHC-α), and reduced inflammatory cell infiltration, myonecrosis, vacuolar changes, and a trend toward normal cardiac muscle fiber architecture in microscopic examination of cardiac tissue further support the cardioprotective effect of T3.Vinay Mishra, Priya Ghumatkar, Maulik V. Patel, Shilpesh Devada, Ramchandra Ranvir, Prabodha Swain, Rajesh Sundar, Rajesh Bahekar, and Mukul R. JainCopyright © 2011 Vinay Mishra et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/401258/Mice deficient in the zinc-sensor GPR39, which has been demonstrated to protect cells against endoplasmatic stress and cell death in vitro, display moderate glucose intolerance and impaired glucose-induced insulin secretion. Here, we use the Tet-On system under the control of the proinsulin promoter to selectively overexpress GPR39 in the β cells in a double transgenic mouse strain and challenge them with multiple low doses of streptozotocin, which in the wild-type littermates leads to a gradual increase in nonfasting glucose levels and glucose intolerance observed during both food intake and OGTT. Although the overexpression of the constitutively active GPR39 receptor in animals not treated with streptozotocin appeared by itself to impair the glucose tolerance slightly and to decrease the β-cell mass, it nevertheless totally protected against the gradual hyperglycemia in the steptozotocin-treated animals. It is concluded that GPR39 functions in a β-cell protective manner and it is suggested that it is involved in some of the beneficial, β-cell protective effects observed for Zn++ and that GPR39 may be a target for antidiabetic drug intervention.Kristoffer L. Egerod, Chunyu Jin, Pia Steen Petersen, Nils Wierup, Frank Sundler, Birgitte Holst, and Thue W. SchwartzCopyright © 2011 Kristoffer L. Egerod et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/716214/Background. There are limited data on sleep duration and diabetes from developing countries. We therefore examined the relationship between reported hours of sleep, diabetes prevalence and glucose control in Jamaican adults. Methods. Data on reported hours of sleep and diabetes (based on glucose measurement and medication use) from a national survey of 15–74-year-old Jamaicans were analyzed. Results. The 2,432 participants (31% M, Age 42±16 years, BMI 27.6±6.6 kg/m2, diabetes prevalence 12%) reported sleeping 8.2±1.8 hours. In men, sleeping less than 6 hours (OR (95% CI) = 2.65 (1.09–6.48)) or more than 10 hours (OR (95% CI) = 4.36 (1.56–12.19)) was associated with diabetes when adjusted for age, BMI, and family history of diabetes. In women sleeping less than 6 hours was associated with a reduced likelihood of diabetes after adjusting for the same confounders ((OR (95% CI) = 0.43 (0.23–0.78)). There was no significant association between sleep and glucose control. Conclusion. Insufficient and excessive sleep was associated with increased diabetes prevalence in Jamaican men but not women.Chisa G. Cumberbatch, Novie O. Younger, Trevor S. Ferguson, Shelly R. McFarlane, Damian K. Francis, Rainford J. Wilks, and Marshall K. Tulloch-ReidCopyright © 2011 Chisa G. Cumberbatch et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/724816/We evaluated the association of the sex hormone pattern and the serum level of the main adipokines to metabolic syndrome (MS) and its components in 199 pharmacologically untreated subjects. Men and women included in the age-class subgroups were matched for body mass index, waist circumference, blood pressure, heart rate, fasting plasma glucose, and plasma lipids. Men without MS had significantly lower leptin/adiponectin ratio than men with MS. Women without MS had lower leptin and leptin/adiponectin ratio than women with MS but had significantly higher adiponectin, estrone, and dehydroepiandrosterone levels. In men, the leptin/adiponectin ratio is the main factor associated to MS diagnosis (OR: 3.36, 95% CI 1.40–8.08), while in women adiponectin alone appears to be a protective factor (OR: 0.87, 95% CI 0.79–0.95). In conclusion, in a sample of pharmacologically untreated subjects, leptin/adiponectin ratio seems to be the factor more strongly associated to MS and its components.Arrigo F. G. Cicero, Paolo Magni, Massimo Moré, Massimiliano Ruscica, Elena Dozio, Liliana Steffani, Claudio Borghi, and Felice StrolloCopyright © 2011 Arrigo F. G. Cicero et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/604715/Serum uric acid has been shown to be associated with cardiovascular disease, hypertension, and chronic kidney disease in previous studies. However, few studies have examined the association between serum uric acid and diabetes mellitus and their findings are not consistent. Therefore, we examined the association between serum uric acid levels and diabetes mellitus in participants from the third National Health and Nutrition Examination Survey (n=18,825, 52.5% women). Serum uric acid levels were categorized into quartiles. Diabetes mellitus was defined as fasting glucose ≥126 mg/dL, nonfasting glucose ≥200 mg/dL, or use of oral hypoglycemic medication or insulin (n=395). In multivariable logistic regression models, we found that higher serum uric acid levels were inversely associated with diabetes mellitus after adjusting for age, sex, race/ethnicity, education, smoking, alcohol intake, body mass index, hypertension, and serum cholesterol. Compared to quartile 1 of serum uric acid, the odds ratio (95% confidence interval) of diabetes mellitus was 0.48 (0.35–0.66; P trend <0.0001). The results were consistent in subgroup analysis by gender and hypertension status. Higher serum uric acid levels were inversely associated with diabetes mellitus in a representative sample of US adults.Pavani Bandaru and Anoop ShankarCopyright © 2011 Pavani Bandaru and Anoop Shankar. All rights reserved.http://www.hindawi.com/journals/ije/2011/747835/In this study, we investigate the effect of argan oil consumption on serum lipids, apolipoproteins (AI and B), CRP, and LDL susceptibility to oxidation in type 2 diabetic patients which are known to have a high level of cardiovascular risk due to lipid abnormalities and lipid peroxidation. For that, 86 type 2 diabetic patients with dyslipidemia were randomized to one group consuming 25 mL/day of argan oil during 3 weeks and control group consuming 20 g/day of butter in breakfast. After argan oil intervention, serum triglycerides decreased by 11.84%, (P=0.001), total chol by 9.13%, (P=0.01), and LDL-chol by 11.81%, (P=0.02). However, HDL-chol and Apo AI increased (10.51%, P=0.01 and 9.40%,  P=0.045, resp.). Susceptibility of LDL to lipid peroxidation was significantly reduced by increasing of 20.95%, (P=0.038) in lag phase after argan oil consumption. In conclusion, we show for the first time that consumption of argan oil may have an antiatherogenic effect by improving lipids, and the susceptibility of LDL to oxidation in type 2 diabetes patients with dyslipidemia, and can therefore be recommended in the nutritional management of type 2 diabetes.M. M. Ould Mohamedou, K. Zouirech, M. El Messal, M. S. El Kebbaj, A. Chraibi, and A. AdlouniCopyright © 2011 M. M. Ould Mohamedou et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/530274/Present therapies to minify hyperglycaemia and insulin resistance mainly target ATP-sensitive K+ channels (KATP) of pancreatic cells and PPAR-γ to enhance the insulin secretion and potential for GLUT expression, respectively. These current approaches are frequently associated with the various side effects such as hypoglycaemia and cardiovascular adverse events. CDK5 is a serine/threonine protein kinase, which forms active complexes with p35 or p39 found principally in neurons and in pancreatic β cells. Pieces of evidence from recent studies recommend the vital role of CDK5 in physiological functions in nonneuronal cells such as glucose-stimulated insulin secretion in pancreatic cells. Inhibition of CDK5 averts the decrease of insulin gene expression through the inhibition of nuclear translocation of PDX-1 which is a transcription factor for the insulin gene. The present pieces of evidence designate that CDK5 might be a potential drug target for the regulation of glucose-stimulated insulin secretion in the treatment of diabetes mellitus.Danish Ahmed and Manju SharmaCopyright © 2011 Danish Ahmed and Manju Sharma. All rights reserved.http://www.hindawi.com/journals/ije/2011/541021/Background. Metabolic risk factors like insulin resistance and dyslipidemia are frequently observed in severly obese children. We investigated the hypothesis that moderate weight reduction by a low-threshold intervention is already able to reduce insulin resistance and cardiovascular risk factors in severely obese children. Methods. A group of 58 severely obese children and adolescents between 8 and 17 years participating in a six-month-long outpatient program was studied before and after treatment. The program included behavioral treatment, dietary education and specific physical training. Metabolic parameters were measured in the fasting state, insulin resistance was evaluated in an oral glucose tolerance test. Results. Mean standard deviation score of the body mass index (SDS-BMI) in the study group dropped significantly from +2.5 ± 0.5 to 2.3 ± 0.6 (P<0.0001) after participation in the program. A significant decrease was observed in HOMA (6.3 ± 4.2 versus 4.9 ± 2.4, P<0.03, and in peak insulin levels (232.7 ± 132.4 versus 179.2 ± 73.3 μU/mL, P<0.006). Significant reductions were also observed in mean levels of hemoglobin A1c, total cholesterol and LDL cholesterol. Conclusions. These data demonstrate that already moderate weight reduction is able to decrease insulin resistance and dyslipidemia in severely obese children and adolescents.J. Grulich-Henn, S. Lichtenstein, F. Hörster, G. F. Hoffmann, P. P. Nawroth, and A. HamannCopyright © 2011 J. Grulich-Henn et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/742719/Patients with diabetes mellitus have an increased prevalence of vascular disease. Pathologic thrombosis associated with atherosclerotic plaque rupture is a major cause of morbidity and mortality. Platelets are intimately involved in the initiation and propagation of thrombosis. Evidence suggests that platelets from patients with type 2 diabetes have increased reactivity and baseline activation compared to healthy controls. We review the pathophysiology of platelet hyperreactivity in DM patients and its implications in clinical practice, with particular focus on acute coronary syndromes, percutaneous coronary intervention, and novel antiplatelet agents.Nicholaos Kakouros, Jeffrey J. Rade, Antonios Kourliouros, and Jon R. ResarCopyright © 2011 Nicholaos Kakouros et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/493840/Adults with GH deficiency are known to exhibit reduced sweating. Whether sweating capacity is impacted in obese subjects with impaired GH secretion have not previously been investigated. The main objective was to investigate sweat secretion rate and the GH-IGF-I axis in obese subjects before and after weight loss. Sixteen severely obese women (BMI, 40.6 ± 1.1 kg/m2) were investigated before and after a diet-induced weight loss. Sixteen age-matched nonobese women served as controls. The obese subjects presented the characteristic decreased GH release, hyperinsulinaemia, increased FFA levels, and impaired insulin sensitivity, which all were normalised after diet-induced weight loss of 30 ± 5 kg. Sweat secretion rates were similar comparing obese and nonobese subjects (78 ± 10 versus 82 ± 9 mg/30 minutes) and sweat secretion did not change after a diet-induced weight loss in obese subjects. We conclude that although obese subjects have markedly reduced GH release and impaired IGF-I levels, sweat secretion rate is found to be normal.Michael Højby Rasmussen, Anders Juul, Katharina M. Main, and Jannik HilstedCopyright © 2011 Michael Højby Rasmussen et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/509549/Pseudohypoparathyroidism type Ia (PHP Ia) is defined as a series of disorders characterized by multihormone resistance in end-organs and Albright hereditary osteodystrophy (AHO) phenotype. PHP Ia is caused by heterozygous inactivating mutations in GNAS, which encodes the stimulatory G-protein alpha subunit (Gsa). A patient with typical clinical manifestations of pseudohypoparathyroidism (PHP) (round face, short stature, centripetal obesity, brachydactyly, and multi-hormone resistance: parathyroid hormone (PTH), thyroid-stimulating hormone (TSH), and gonadotropins) presented at our center. The sequence of the GNAS gene from the patient and her families revealed a novel missense mutation (Y318H) in the proband and her mother. An in vitro Gsa functional study showed that Gsa function was significantly impaired. These results stress the importance of GNAS gene investigation.Zhi-Min Miao, Can Wang, Bin-Bin Wang, Dong-Mei Meng, Dong-Mei Su, Zhi Cheng, Qiao-Lian Wen, Lin Han, Qing Yu, Xu Ma, and Chang-Gui LiCopyright © 2011 Zhi-Min Miao et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/789358/Background. We examined the association between insufficient rest/sleep and cardiovascular disease or diabetes mellitus separately among non-Hispanic whites, non-Hispanic blacks, Hispanic Americans, and other races in a contemporary sample of US adults. Methods. Multiethnic, nationally representative, cross-sectional survey (2008 BRFSS) participants who were >20 years of age (n=369, 217; 50% women). Self-reported insufficient rest/sleep in the previous month was categorized into: zero, 1–13, 14–29, and all 30 days. Outcomes were: (1) any CVD, (2) coronary artery disease (CHD), (3) stroke, and (4) diabetes mellitus. Results. Insufficient rest/sleep was found to be positively associated with (1) any CVD, (2) CHD, and (3) stroke among all race-ethnicities. In contrast, insufficient rest/sleep was positively associated with diabetes mellitus in all race-ethnicities except non-Hispanic blacks. The odds ratio of diabetes association with insufficient rest/sleep for all 30 days was 1.37 (1.26–1.48) among non-Hispanic whites, 1.11 (0.90–1.36) among non-Hispanic blacks, 1.88 (1.46–2.42) among Hispanic Americans, and 1.48 (1.10–2.00) among other race/ethnicities. Conclusion. In a multiethnic sample of US adults, perceived insufficient rest/sleep was associated with CVD, among all race-ethnicities. However, the association between insufficient rest/sleep and diabetes mellitus was present among all race-ethnicities except non-Hispanic blacks.Abhishek Vishnu, Anoop Shankar, and Sita KalidindiCopyright © 2011 Abhishek Vishnu et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/469783/Rats(r) with secondary hyperparathyroidism were studied to define the relationship between vitamin D metabolites and rPTH levels measured by 3 different rat ELISAs. Controls and renal failure (RF) rats were on a normal diet, while 2 groups on a low-calcium (-Ca) or a vitamin D-deficient (-D) diet. RF was induced surgically. Mild RF rats had normal calcium and 25(OH)D but reduced 1,25(OH)2D levels (P<.001) with a 2.5-fold increased in rPTH (P<.001). Severe RF rats and those on a -Ca or -D diet had reduced calcium (P<.01) and 25(OH)D levels (P<.05), with rPTH increased by 2 (-Ca diet; P<.05), 4 (-D diet; P<.001), and 20-folds (RF; P<.001) while 1,25(OH)2D was high (-Ca diet: P<.001) or low (-D diet, RF: P<.001). 25(OH)D and 1,25(OH)2D were positively and negatively related on the -Ca and -D diets, respectively. rPTH molecular forms behaved as expected in RF and on -Ca diet, but not on -D diet with more C-rPTH fragments when less were expected. This may be related to the short-time course of this study compared to prior studies.Pierre D'Amour, Louise Rousseau, Stephen Hornyak, Zan Yang, and Tom CantorCopyright © 2011 Pierre D'Amour et al. All rights reserved.http://www.hindawi.com/journals/ije/2011/362981/Introduction. It was reported that 25-hydroxyvitamin D level was independently associated with anemia in chronic kidney diseases, but the relation between vitamin D and anemia in diabetes mellitus is not still certain. We analyzed the relation between plasma 25-hydroxyvitamin D level and hemoglobin concentration. Materials and Methods. A cross-sectional study in male patients with type 2 diabetes was performed. Correlation coefficients and standardized partial regression coefficient for the hemoglobin concentration were evaluated. Results. Hemoglobin concentration was positively correlated with body mass index, HbA1c, estimated glomerular filtration rate, cholinesterase, and 25-hydroxyvitamin D level and negatively correlated with age, duration of diabetes mellitus, serum creatinine, and urinary albumin creatinine ratio. Multiple regression analysis revealed the independent relation of 25-hydroxyvitamin D to hemoglobin concentration. Conclusions. Plasma circulating form of vitamin D is significantly associated with hemoglobin concentration in diabetes mellitus independent of the clinical markers for kidney function or nutrition.Shu Meguro, Masuomi Tomita, Takeshi Katsuki, Kiyoe Kato, Henpiru Oh, Akira Ainai, Ryo Ito, Shu Takeda, Toshihide Kawai, Yoshihito Atsumi, Hiroshi Itoh, and Hideki HasegawaCopyright © 2011 Shu Meguro et al. All rights reserved.