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'Food addiction' shares a similar neurobiological and behavioral framework with substance addiction. However whether, and to what degree, 'food addiction' contributes to obesity in the general population is unknown. to assess 1) the prevalence of 'food addiction' in the Newfoundland population; 2) if clinical symptom counts of 'food addiction' were significantly correlated with the body composition measurements; 3) if food addicts were significantly more obese than controls, and 4) if macronutrient intakes are associated with 'food addiction'. A total of 652 adults (415 women, 237 men) recruited from the general population participated in this study. Obesity was evaluated by Body Mass Index (BMI) and Body Fat percentage measured by dual-energy X-ray absorptiometry. 'Food addiction' was assessed using the Yale Food Addiction Scale and macronutrient intake was determined from the Willet Food Frequency Questionnaire. The prevalence of 'food addiction' was 5.4% (6.7% in females and 3.0% in males) and increased with obesity status. The clinical symptom counts of 'food addiction' were positively correlated with all body composition measurements across the entire sample (p<0.001). Obesity measurements were significantly higher in food addicts than controls; Food addicts were 11.7 (kg) heavier, 4.6 BMI units higher, and had 8.2% more body fat and 8.5% more trunk fat. Furthermore, food addicts consumed more calories from fat and protein compared with controls. Our results demonstrated that 'food addiction' contributes to severity of obesity and body composition measurements from normal weight to obese individuals in the general population with higher rate in women as compared to men.

PYY is an appetite suppressing hormone. Low circulating PYY has been linked to greater BMI. However data is controversial and this association has not been verified in large human populations. The purpose of this study was to investigate if fasting serum total PYY is associated with obesity status and/or adiposity at the population level. A total of 2094 subjects (Male-523, Female-1571) participated in this investigation. Total PYY was measured in fasting serum by enzyme-linked immunosorbent assay. Obesity status (NW-normal-weight, OW-overweight and OB-obese) was determined by the Bray Criteria according to body fat percentage measured by dual-energy x-ray absorptiometry and the WHO criteria according to BMI. One-way ANOVA and multiple regression was used to assess the adiposity-specific association between PYY and the following; weight, BMI, waist-circumference, hip-circumference, waist-hip ratio, percent body fat (%BF), trunk fat (%TF), android fat (%AF) and gynoid fat (%GF). PYY was not significantly different among NW, OW and OB groups defined by neither %BF nor BMI for both men and women. However among women, fasting PYY was positively associated with adiposity measures. Women with the highest (Top 33%) waist-circumference, %BF and %TF had significantly higher PYY (10.5%, 8.3% and 9.2% respectively) than women with the lowest (Bottom 33%). Age, smoking, medication use and menopause were all positively associated with PYY levels in women but not in men. To our knowledge this is the largest population based study, with the most comprehensive analysis and measures of confounding factors, to explore the relationship of circulating PYY with obesity. Contrary to initial findings in the literature we discovered that PYY was positively associated with body fat measures (waist-circumference, %BF and %TF) in women. Although the effect size of the positive association of PYY with obesity in women is small, and potentially negligible, it may in fact represent a protective response against significant weight gain.

Ghrelin, an orexigenic gut hormone secreted primarily from the stomach, is involved in energy homeostasis. However, little data is available regarding its response to energy surplus and the development of human obesity. The present study investigated the response of circulating acylated ghrelin to a 7-day positive energy challenge. A total of 68 healthy young men were overfed 70% more calories than required, for 1-week. Subjects were classified based on percent body fat (measured by dual-energy X-ray absorptiometry) as normal weight, overweight, and obese. Serum acylated ghrelin concentration was measured before and after the positive energy challenge. Additionally, the relationship between acylated ghrelin and obesity-related phenotypes including weight, body mass index, percent body fat, cholesterol, HDL-c, LDL-c, glucose, insulin and homeostasis model assessment of insulin resistance and β-cell function at baseline and change due to overfeeding, were assessed. Contrary to our expectations, serum acylated ghrelin was significantly increased in response to overfeeding and the increase was independent of obesity status. There was no significant difference in fasting acylated ghrelin between normal weight, overweight, and obese men at baseline. Acylated ghrelin was negatively correlated with weight and BMI for normal weight and with BMI in overweight men. Also ghrelin was correlated with change in weight and BMI in overweight (negative relationship) and obese (positive relationship) groups. Our results showed that circulating acylated ghrelin was increased after a 7-day positive energy challenge regardless of adiposity status. However, acylated ghrelin was correlated with change in weight and BMI in opposing directions, in overweight and obese subjects respectively, thus dependent on obesity status.

Adiponectin is an adipose tissue derived hormone which strengthens insulin sensitivity. However, there is little data available regarding the influence of a positive energy challenge (PEC) on circulating adiponectin and the role of obesity status on this response. The purpose of this study was to investigate how circulating adiponectin will respond to a short-term PEC and whether or not this response will differ among normal-weight(NW), overweight(OW) and obese(OB). We examined adiponectin among 64 young men (19-29 yr) before and after a 7-day overfeeding (70% above normal energy requirements). The relationship between adiponectin and obesity related phenotypes including; weight, percent body fat (%BF), percent trunk fat (%TF), percent android fat (%AF), body mass index (BMI), total cholesterol, HDLc, LDLc, glucose, insulin, homeostatic model assessment insulin resistance (HOMA-IR) and β-cell function (HOMA-β) were analyzed before and after overfeeding. Analysis of variance (ANOVA) and partial correlations were used to compute the effect of overfeeding on adiponectin and its association with adiposity measurements, respectively. Circulating Adiponectin levels significantly increased after the 7-day overfeeding in all three adiposity groups. Moreover, adiponectin at baseline was not significantly different among NW, OW and OB subjects defined by either %BF or BMI. Baseline adiponectin was negatively correlated with weight and BMI for the entire cohort and %TF, glucose, insulin and HOMA-IR in OB. However, after controlling for insulin resistance the correlation of adiponectin with weight, BMI and %TF were nullified. Our study provides evidence that the protective response of adiponectin is preserved during a PEC regardless of adiposity. Baseline adiponectin level is not directly associated with obesity status and weight gain in response to short-term overfeeding. However, the significant increase of adiponectin in response to overfeeding indicates the physiological potential for adiponectin to attenuate insulin resistance during the development of obesity.

Ghrelin is a 28-amino acid orexigenic peptide synthesized mainly in the stomach. Acute administration of ghrelin has been found to decrease insulin secretion. However, little data is available regarding whether ghrelin contributes to the long-term regulation of insulin resistance at the population level. The aim of this study is to investigate the association between circulating ghrelin and insulin resistance in a large population based study. A total of 2082 CODING study (Complex Diseases in the Newfoundland population: Environment and Genetics) subjects were assessed. Subjects were of at least third generation Newfoundland descent, between the ages of 20 and 79 years, and had no serious metabolic, cardiovascular, or endocrine diseases. Ghrelin was measured with an Enzyme Immunoassay method. Insulin and fasting glucose were measured by Immulite 2500 autoanalyzer and Lx20 clinical chemistry analyzer, respectively. Homeostatic Model Assessment of β cell function (HOMA-β) and Insulin Resistance (HOMA-IR) and Quantitative Insulin-sensitivity Check Index (QUICKI) were used for measurement of insulin resistance. Partial correlation analyses showed a significant negative correlation between circulating ghrelin and insulin level and insulin resistance in the entire cohort and also in men and women separately. The aforementioned correlation was independent of age, percentage of trunk fat and HDL-cholesterol. According to menopausal status, only pre-menopausal women revealed negative correlations. Our results suggest that except for postmenopausal women, high circulating ghrelin level is associated with lower insulin resistance in the general population.

Determination of vitamin D status in different age-groups in a community and in different climates of a country is necessary and has important implications for general health. The study was conducted to determine the prevalence of vitamin D deficiency among the adult population of Isfahan, a centrallylocated city in Iran. In this cross-sectional study, 1,111 healthy people-243 men and 868 women-aged 41.4 (mean 14 and range 20-80) years, who attended a single-consultation outpatient clinic, were selected. Serum 25-hydroxy vitamin D (25-OHD), parathyroid hormone (PTH), calcium and phosphorus concentrations were measured. Mild, moderate and severe vitamin D deficiencies were defined as 25-OHD values of 20-30 ng/mL, 10-20 ng/mL, and <10 ng/mL respectively. The median (range) concentrations of 25-OHD were 21 (4.0-105.0) ng/mL in males and 18 (1.5-117) ng/mL in females (p=0.05). The prevalence of mild, moderate and severe vitamin D deficiencies among the adult population was 19.6%, 23.9%, and 26.9% respectively. Vitamin D deficiency was more prevalent among women (p=0.001) and younger age-group (p=0.001). Medians of 25-OHD in spring-summer and autumn-winter were 21 ng/mL and 18 ng/mL respectively (p=0.005). The prevalence of severe vitamin D deficiency was higher in autumn-winter than in spring-summer (odds ratio=1.6, 95% confidence interval 1.2-2.2, p=0.001). The prevalence of vitamin D deficiency was high in a sunny city-Isfahan- especially among women and younger population. The high prevalence of vitamin D deficiency in this city emphasizes the necessity of vitamin D supplementation as more exposure to sun is limited due to the type of clothing required by current law.

Background: Considering that serum gamma-glutamyl transferase (GGT) activity could reflect several different processes relevant to diabetes pathogenesis and the increasing rate of type 2 diabetes worldwide, the aim of this study was to assess the association between serum GGT concentrations and glucose intolerance, in the first-degree relatives (FDR) of type 2 diabetic patients. Methods: In this descriptive study, 30-80 years old, non diabetic FDRs of type 2 diabetic patients were studied. Serum GGT was measured by enzymatic photometry method in all studied population. The relationship between GGT and glucose intolerance status (normal, prediabetic and diabetics) was evaluated. Results: During this study 551 non-diabetic FDRs of type 2 diabetic patients were studied. Mean of GGT was 25.3 ± 12.1 IU/L. According to glucose tolerance test, 153 were normal and 217 and 181 were diabetic and prediabetic respectively. Mean of GGT in normal, prediabetic and diabetic patients was 23.5 ± 15.9 IU/L, 29.1 ± 28.1 IU/L and 30.9 ± 24.8 IU/L respectively (p = 0.000). The proportion of prediabetic and diabetic patients was higher in higher quartile of GGT and there was a significant correlation between GGT and BMI, HbA1c, FPG, cholesterol, LDL-C, and triglyceride (p < 0.05). There was a significant relation between GGT and area under the curve (AUC) of oral glucose tolerance test (p = 0.00). Conclusions: Measurement of GGT in FDRs of type 2 diabetic patients may be useful in assessing the risk of diabetes; those with chronically high levels of GGT should be considered as high risk group for diabetes.

Stem cells are undifferentiated cells with the ability of proliferation, regeneration, conversion to differentiated cells and producing various tissues. Stem cells are divided into two categories of embryonic and adult. In another categorization stem cells are divided to Totipotent, Multipotent and Unipotent cells.So far usage of stem cells in treatment of various blood diseases has been studied (such as lymphoblastic leukemia, myeloid leukemia, thalassemia, multiple myeloma and cycle cell anemia). In this paper the goal is evaluation of cell therapy in treatment of Parkinson's disease, Amyotrophic lateral sclerosis, Alzheimer, Stroke, Spinal Cord Injury, Multiple Sclerosis, Radiation Induced Intestinal Injury, Inflammatory Bowel Disease, Liver Disease, Duchenne Muscular Dystrophy, Diabetes, Heart Disease, Bone Disease, Renal Disease, Chronic Wounds, Graft-Versus-Host Disease, Sepsis and Respiratory diseases. It should be mentioned that some disease that are the target of cell therapy are discussed in this article.

Gonadotropin-releasing hormone agonists (GnRHa) are used as an alternative to human chorionic gonadotropin (hCG) to trigger ovulation and decrease the risk of ovarian hyperstimulation syndrome. GnRHa is less potent at inducing ovarian vascular endothelial growth factor (VEGF), but may also affect endometrial angiogenesis and early placental development. In this study, we explore the effect of superovulation on endometrial angiogenesis during critical periods of gestation in a mouse model. We assigned female mice to three groups: natural mating or mating following injection with equine chorionic gonadotropin and trigger with GnRHa or hCG trigger. Females were killed prior to implantation (E3.5), post-implantation (E7.5), and at midgestation (E10.5), and maternal serum, uterus, and ovaries were collected. During peri-implantation, endometrial Vegfr1 and Vegfr2 mRNA were significantly increased in the GnRHa trigger group (P < 0.02) relative to the hCG group. Vegfr1 is highly expressed in the endometrial lining and secretory glands immediately prior to implantation. At E7.5, the ectoplacental cone expression of Vegfa and its receptor, Vegfr2, was significantly higher in the hCG trigger group compared to the GnRHa group (P < 0.05). Soluble VEGFR1 and free VEGFA were much higher in the serum of mice exposed to the hCG trigger compared to GnRHa group. At midgestation, there was significantly more local Vegfa expression in the placenta of mice triggered with hCG. GnRHa and hCG triggers differentially disrupt the endometrial expression of key angiogenic factors during critical periods of mouse gestation. These results may have significant implications for placental development and neonatal outcomes following human in vitro fertilization. Summary Sentence The gonadotropin-releasing hormone agonists and human chorionic gonadotropin agents used to trigger ovulation before in vitro fertilization differentially modulate levels of key angiogenic factors during critical periods of implantation, trophoblast invasion, and placental development in a mouse model.

Uterine tissue-level inflammation triggers human parturition by increasing myometrial cell contractility. Progesterone, via the progesterone receptor (PR) isoforms, PR-A and PR-B, blocks labor by inhibiting the response of myometrial cells to pro-labor/pro-inflammatory stimuli. Human parturition is induced by progesterone/PR withdrawal via changes in PR activity. The research described herein explored the factors regulating progesterone/PR anti-inflammatory activity in human myometrial cells. Two core hypotheses were tested: 1) progesterone/PR anti-inflammatory activity in myometrial cells is affected by site-specific serine phosphorylation (pSer), and 2) cross-talk between progesterone/PR signaling and 3-cyclic adenosine monophosphate (cAMP) signaling affects progesterone/PR anti-inflammatory actions in myometrial cells. The hypotheses were tested using a telomerase immortalized human myometrial cell line model, hTERT-HMA/B, and biopsies of myometrium obtained from women at the time of c-section delivery. Levels of pSer-PRs were determined by immunoblotting and response to interleukin (IL)-1 (IL-1) was used to assess anti-inflammatory activity. The data show that: 1) abundance of pSer344/345-PRA in myometrial cells increased in association with the onset of labor; 2) generation of pSer344/345-PRA in myometrial cells was progesterone dependent and increased by IL- through the stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK); 3) pSer344/345-PRA decreased progesterone/PR anti-inflammatory activity; 4) progesterone/PR and cAMP signaling synergistically inhibited response to IL-1 5) cAMP inhibited the generation of pSer344/345-PRA by inducing expression of dual specificity protein phosphatase 1 (DUSP1) that inhibits SAPK/JNK activation; and 6) P4/PR increased cAMP-induced DUSP1 expression in myometrial cells. Taken together the data suggest that for most of human pregnancy, progesterone/PR and cAMP act synergistically to promote anti-inflammatory effects in myometrial cells to induce uterine quiescence. This interaction may be exploited therapeutically as a strategy to prevent preterm birth.