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Polycystic ovary syndrome (PCOS) is characterized by adiposity and disruptions in the energy metabolic processes of adipose tissue. NRG-4, a protein, is secreted by adipose tissue and plays a role in the regulation of energy metabolism. The purpose of the present study to investigation the relationship between serum level of NRG4 with PCOS patients. In cross-sectional study, there were a total of 120 female participants, who were split up into the following three categories: On the basis of the Rotterdam criteria, there were a total of 90 patients diagnosed with PCOS, including 30 controls, 45 women with normal weight, and 45 women with obesity. The levels of serum NRG4, FBG, insulin, hormone profiles, and insulin resistance (HOMA-IR) were determined. In PCOS groups, the serum levels NRG4 higher than healthy groups. Therefore, the obese PCOS group had higher serum NRG4 levels than the normal-weight PCOS group (P≤0.05). There was a relationship between serum NRG-4 level and other biochemical parameters in the study. NRG-4 was also significantly positively correlated with insulin and HOMA-IR levels in PCOS (obese and normal-weight). Changes in NRG-4 serum levels may serve as a biomarker for polycystic ovary syndrome detection. [ABSTRACT FROM AUTHOR]

The syndrome of polycyctic ovary (PCOS), is a significant disorder of gynocology affects frome three to ten percent of female in the age of reproduction. PCOS is associated with ovulation problems and menstrual irregularities, as well as abdominal obesity. Kisspeptins are peptides that control the hypothalamic-pituitary-gonadal (HPG) axis and are generated by the KISS1 gene. Discuss the association between the action of this peptide on Polycystic ovarian syndrome charecterstics and defferent weight individual. The research involved one handerend and five individuals, with seventy female with PCOS being divided into 17 obese, 18 overweight, and 34 normal weight groups based on their BMI. The remaining 36 women are from the control group, who appear to be in good health. Individual that have poly cystic overy syndrome which chosen from different part such as Karbala Department of infertility Teaching Hospital and individuals that attended to private clinics. The hormonal profile and serum humane Kisspeptin1 were measured using the ELISA method. In comparison to the control group, Kisspeptin1 revealed a highly different results in patient with syndrom for obese (397.4 ± 138.3), overweight (420.2 ± 150.7), and normal weight patients (371.9 ± 87.3). Luteinizing hormone level in PCOS women were substantially greater (P.value = 0.05) than in the control group. Kisspeptin1 levels do not differ significantly (p.value > 0.05) across the three age groups. The results showed that when compared to the control group, highly difference result in Kisspeptin1 concentration patients with syndroms who were obese, overweight, or normal weight. Our findings imply that PCOS groups had greater serum kisspeptin1 concentrations than control groups, as well as significant variations in levels among study groups with varied BMIs. Kisspeptin's significance in PCOS will need to be investigated further in both experimental and clinical investigations. [ABSTRACT FROM AUTHOR]

Exercise with an "exercise machine" that induces optimal total energy expenditure is the right and effective choice for obesity management. Given that obesity is still a public health problem, which will increase morbidity and mortality. Therefore, this study aims to analyze the total energy expenditure of moderate intensity exercise with an ergocycle exercise machine and a treadmill exercise machine in obesity. This study involved 20 adolescent girls with a body mass index (BMI) of 27.10-33.10 kg/m2, healthy and meeting the established requirements. Subjects were randomly divided into two groups: EEG (n=10, ergocycle exercise group), TEG (n=10, treadmill exercise group). Exercise is done by riding an ergocycle and running on a treadmill, for 30 minutes with an intensity of 60-70% HRmax. Total energy expenditure was analyzed using a polar hear rate monitor H10. Independent Samples T-Test with SPSS version 17 was used to analyze the difference in total energy expenditure between pedaling an ergocycle and running on a treadmill. There was a significant difference in the level of total energy expenditure between pedaling an ergocycle and running on a treadmill (P<0.001). Running on a treadmill induces a higher level of total energy expenditure than pedaling an ergocycle. Therefore, a treadmill is recommended as an exercise machine for weight and obesity management. [ABSTRACT FROM AUTHOR]

Obesity is a public health problem in the world. WHO estimates that 2.8 million people die from obesity and overweight. The prevalence of obesity in adults aged >18 years in Indonesia, especially in Yogyakarta has increased from 2007-2018. Genetic is one of the factors contributing to obesity and has been known to be related to obesity in families. The aim of this research was to analyze the inheritance pattern of obesity in families of young women in Yogyakarta. This study was an observational research with a cross sectional design and purposive sampling was also used as the sampling method. The participantss in this research were 36 obese young women aged 15-24 years with BMI ≥25 in Yogyakarta. BMI data of the young women families were also collected. BMI data from three generations of the participantss' families were obtained to analyze the inheritance pattern of obesity. This research was carried out from August 2020 - January 2021. Pedigree diagrams are used to analyze the obesity inheritance pattern based on BMI data from each families. Analysis was undertaken using hypothesis or assumptions for several modes of inheritance usually found for human traits. The results showed that the inheritance pattern of obesity in this research was 50% autosomal dominant and 44.44 % autosomal recessive. In conclusion, obesity in the families of young women in Yogyakarta follow an autosomal dominance and recessive inheritance pattern. [ABSTRACT FROM AUTHOR]

COPD is a chronic inflammatory lung disease which is associated with variety of co-morbidities, as the obesity and cardiovascular diseases (CVDs) are the most frequent. The aim of the current study was to explore the correlations of the age and BMI with the anthropometric indices associated with abdominal obesity in individuals with COPD and to explore the possible difference between the genders. Material and methods: This cross-sectional analysis included 851 citizens from the region of Yambol, Bulgaria. They were interviewed and blood pressure was measured during events organized at the World Diabetes Day, November 14, 2016-2018. One hundred and three of the individuals reported previous diagnosis of COPD. The further statistical analyses were performed only in this group of individuals applying SPSS 16.0 for Windows (SPSS Inc.). Results: Thirty three (32%) of the individuals with COPD were men with a mean age of 58.12 ±13.76 years, while the rest of 70 (68%) persons were women with a mean age of 66.70±10.73 years (p=0.001). The body mass index (BMI) correlated positively with the anthropometric indices associated with central obesity: the waist circumferences (WC, r=0.601, p<0.0001), the hip circumferences (HC, r=0.619, p<0.0001) and waist-to-hip ratio (WHR, r=0.214, p=0.033). The age correlated positively only with the WHR ratio in men (r=0.390, p=0.025), but not in women. When comparing the BMI between genders we did not observed difference (p=0.802). However when classified into groups according to the BMI, women were more frequently with normal weight (30.4%) and obese (33.3%) compared to men (25.8% and 16.1%, respectively), while men were more often with overweight than women (58.1% vs. 36.2%, p=0.091). Men had higher WC (99.23±11.40 cm, p=0.080) and especially WHR (0.922±0.067, p<0.0001) than women (94.17±14.50 cm and 0.855±0.084, respectively). According to the WHR the abdominal obesity was more frequently observed in men with COPD (78.8%) than in COPD women (58.6%. p=0.045). The measured high blood pressure was significantly associated with central obesity both in women (p=0.038) and in men (p=0.035). Conclusions: The results of our study confirm the positive correlation of the BMI with other anthropometric indices associated with abdominal obesity. Based on the results we could conclude that central obesity is more common in men than in women and determines a risk for higher blood pressure in patients with COPD. [ABSTRACT FROM AUTHOR]

Social media (SM) has rapidly evolved over the years to become a dominant platform used globally by millions of users for a variety of applications. In contrast, health problems, in particular, obesity have worsened over recent years. The literature review undertaken in this study has revealed that obesity remains one of the significant health issues globally. Also, despite the widespread use of SM among the population in developing countries, such as Sudan, the use of technology interventions to mitigate adverse health habits remains in its infancy. Likewise, there are limited theoretical models which lead towards the intention to use SM such as Facebook to address these sorts of problems. Therefore, this study proposes a model for the intention to use Facebook as the most popular platform in Sudan to mitigate the problem of obesity with particular emphasis on investigating the important factors that lead to the intention to use Facebook for dieting among middle-aged Sudanese women. In this study, a framework model was developed by hybridising the Theory of Planned Behaviour (TPB) and the Health Beliefs Model (HBM) which included factors that could predict preventive health behaviours from the HBM, namely; perceived susceptibility, perceived seriousness, and perceived threat. This also included the factors related to the TPB such as attitude, perceived behavioural control and subjective norms. This research study is a progress paper that contributes to the body of knowledge in this domain, in particular, obesity. While the framework model has not been tested, it is proposed that future research is undertaken to empirically investigate the proposed model by using smart PLS3 for further analysis. [ABSTRACT FROM AUTHOR]

Obesity has become a worldwide concern, particularly for its relationships to public health and body image issues. A large part of this public health discourse deals with different perceptual discourses surrounding the word 'obesity'. African Americans in particular have been targeted by health interventions since they are found to weigh more than Caucasians. But African American women have resisted this label instead arguing that dominant measures of health are white norms and oppressive to other ethnicities. Through the use of in-depth interviews, the purpose of this study is to understand how African American women define measures of health and body image. In addition, the study investigated the challenges that African American women face when trying to access or maintain a healthy lifestyle. Preliminary findings suggest that African American women are ambivalent in their acceptance of dominant markers of health but they critiqued the health status of the thin ideal. Further, African American women articulated a suspicion of formal medical structures. Finally, they identified socioeconomic status, schooling and motherhood as important barriers to health, while they think conversations on mental health, sexuality and body image need more focus. [ABSTRACT FROM AUTHOR]

The prevalence of maternal obesity has more than doubled in the past two decades with approximately 1 in 5 UK pregnant women now obese [1]. Maternal obesity and excessive gestational weight gain (GWG) constitute some of the most common obstetric risk factors and have direct implications for pregnancy outcome [2]. However, recent evidence suggests that maternal obesity may also have deleterious consequences for the cardiovascular health of the next generation. Mother-child cohort studies have established that both pre-pregnancy BMI and GWG are independently associated with cardio-metabolic risk factors in young adult offspring, including systolic and diastolic blood pressure [3, 4]. Animal models in sheep and nonhuman primates provide further evidence for the influence of maternal obesity on offspring cardiovascular function, whilst our recent studies in rodents have shown that fetal exposure to the metabolic milieu of maternal obesity may permanently change the regulatory pathways in the hypothalamus that contribute to cardiovascular homeostasis. Leptin plays an important role in the central control of appetite, and is also involved in activation of efferent sympathetic pathways to both thermogenic and non-thermogenic tissues, such as the kidney, and is therefore implicated in obesity-related hypertension. Leptin is also thought to have a neurotrophic role in the development of the hypothalamus and we have recently reported that altered neonatal leptin profiles secondary to maternal obesity were associated with evidence of permanently altered hypothalamic structure and function. Hyperphagia and increased adiposity in the adult offspring of obese rodents is associated with region specific hypothalamic leptin resistance in the appetite regulatory pathways of the arcuate nucleus[5]. We have recently reported compelling evidence from our rodent model that maternal obesity confers persistent sympathoexcitatory hyper-responsiveness and hypertension acquired in the early stages of development. Juvenile offspring develop hypertension as early as 30 days of age and, importantly, prior to the onset of obesity. Hypertension in the offspring of obese rats results from persistent sympathoexcitatory hyper-responsiveness[6] with enhanced cardiovascular stress reactivity, an increase in low/high frequency ratio of heart rate variability (HRV), and increased pressor response to exogenous leptin, all evidence of increased sympathetic tone. Disturbed sympathetic control of blood pressure has not previously been reported as a consequence of maternal obesity. The baroreflex response was also abnormal in OffOb rats (90days) and may also represent a primary programmed defect secondary to maternal obesity. To investigate the role of neonatal hyperleptinaemia in offspring cardiovascular dysfunction, we have treated naive rats with exogenous leptin on postnatal days 9-14. At 1 month of age leptin-treated rats displayed increased mean arterial pressure (MAP) compared to saline treated controls which continued into adulthood. These data provide proof of principle that hyperleptinaemia during a critical window of hypothalamic development may directly lead to adulthood hypertension. These data add to increasing evidence for developmental plasticity in the central efferent pathways of the autonomic nervous system, and further implicates a central role for an acquired selective leptin resistance and 'hardwiring' of the developing hypothalamus for a hyperphagic and hypertensive offspring phenotype in offspring of obese rodents. Insight from these animal models raises the possibility that early life exposure to leptin in humans leads to early onset essential hypertension. On-going mother-child cohort and intervention studies in obese pregnant women provide a unique opportunity to address associations between maternal obesity and offspring cardiovascular function. [ABSTRACT FROM AUTHOR]

The obesity epidemic has resulted in more women entering pregnancy overweight or obese. Offspring of obese women have increased risk of obesity and impaired glucose tolerance in childhood and adult life. It has therefore been proposed that there is an 'intergenerational cycle' of obesity and insulin resistance. Studies have shown that changes in the abundance of insulin signalling molecules in skeletal muscle and adipose tissue precede the development of insulin resistance and type 2 diabetes (1,2). It is not clear, however, whether exposure to maternal obesity results in insulin resistance in her offspring as a consequence of the impact of increased adiposity on insulin sensitive tissues (3,4) or as a consequence of the programming of specific changes in the abundance of insulin signalling molecules in these tissues (2,5). It has previously been shown in sheep that exposure to maternal obesity around the time of conception alone led to increased adiposity in female lambs at 4 months of age and that dietary restriction in the obese ewe during the periconceptional (PC) period abolished this effect (6). While dieting before pregnancy may have metabolic benefits for the offspring, there are also potential metabolic and endocrine costs for the offspring (7). The pathways and critical periods during which the metabolic consequences of maternal obesity or dietary restriction are transduced from mother to the offspring are, however, not known. Moreover, there is a paucity of knowledge on the possible epigenetic mechanisms that are recruited in the oocyte/early embryo, which could contribute to such changes. We used an embryo transfer model in sheep to investigate the effects of maternal obesity and of dietary restriction during the PC period on insulin signalling in liver and skeletal muscle of the offspring. Furthermore, we also investigated the role of miRNAs in regulating hepatic insulin signalling in these offspring. Donorewes were allocated to 1 of 4 groups & were fed the following diets in the PC period: 100% metabolisable energy requirements (MER) for ≥ 20wks (CC); 100% MER for ≥ 16wks & then 70% MER for 4 wks (CR); ~180% MER for ≥ 20wks (HH);~180% MER for ≥ 16wks & then 70% MER for 4wks(HR). This continued for 1 wk post-conception before single embryos were transferred into recipient ewes of normal weight. At 16wks after birth, liver and skeletal muscle samples were collected to determine insulin signalling gene expression (by qRT-PCR) and protein abundance (by Western Blotting) and expression of key miRNAs (by qRT-PCR) in the offspring. The effects of PC nutrition and sex on protein abundance and miRNA expression were determined using a two-way ANOVA. A Duncan's post hoc test was used to determine significant differences between groups. We found decreased insulin receptor (IR) (P<0.05), Akt2 (female lambs) (P<0.05), phospho-Akt (P<0.01) and phospho-FoxO1 (P<0.01) abundance and in contrast, an increased Cave-olin-1 (P<0.05) abundance in the liver of HH lambs. There was a parallel increase in miR-29b (P<0.05), miR-103 (P<0.01) and miR-107 (P<0.05) expression in these lambs. Maternal dietary restriction abolished some of the effects of maternal obesity. The abundance of Akt2, however, remained low (female lambs) and Caveolin-1 and miR-103 remained increased in HR lambs. Furthermore, there was decreased hepatic PDK1 gene expression (P<0.01) and phospho-PDK1 and aPKCζ protein abundance (P<0.05) in CR and HR lambs. In contrast to the liver, maternal obesity resulted only in decreased GLUT4 abundance in muscle of female lambs. There was, however, increased IR abundance and decreased aPKCζ, phospho-AS160 and GLUT4 abundance in both CR and HR lambs. We have found that exposure of the oocyte/early embryo to maternal obesity leads to differential changes in gene expression and protein abundance of key insulin signalling molecules in liver and muscle in postnatal life. Our results also suggest that miRNAs may be potential epigenetic regulators that are sensitive to programming by the maternal metabolic/nutritional environment and may play a key role in transducing the metabolic consequences of maternal obesity from the mother to her offspring. Importantly, we also found that in most instances, dietary restriction was unable to ablate the effects of maternal obesity in both liver and skeletal muscle of lambs. Instead, exposure to dietary restriction itself irrespective of whether the ewes were previously on a normal or high plane of nutrition led to changes in a different suite of molecules within both liver and skeletal muscle of the offspring. These results suggest that maternal metabolic response to weight loss around conception, irrespective of her pre-pregnancy body weight has long lasting metabolic consequences for the offspring, which may contribute to the emergence of insulin resistance in later life. [ABSTRACT FROM AUTHOR]

Background: Diets high in sugar and fat (HSHF) are commonly eaten by women of reproductive age and contribute to the increasing prevalence of obesity during pregnancy. In animals, obesogenic diets fed during pregnancy alter the metabolic phenotype of the adult offspring (1) but little is known about the mechanisms involved prenatally. Preliminary work has shown that feeding a HSHF diet throughout mouse pregnancy increased maternal adiposity, glucose and insulin levels, but reduced insulin like growth factor (IGF-I) and fetal growth (2). This project examined the effect of a HSHF diet on the fat content and expression of proteins involved in insulin/IGF-I signalling and lipid metabolism in the maternal liver, muscle and white adipose tissue (WAT) in late pregnancy. Methods: C57BL6 mice were fed a control diet (energy from fat 11%, sugar 3%) or a HSHF diet (energy; fat 30%, sugar 36%) from day (D)1 of pregnancy (term D20). On D16 and D19, dams were killed and maternal liver, biceps femoralis and retroperitoneal WAT and were dissected and snap frozen for Western blotting. The content of hepatic and muscle fat was measured by the modified Folch method (3). Dietary differences were assessed using ttest and considered significant when, P<0.05. Results: Relative to the control diet, HSHF feeding increased hepatic abundance of specific proteins involved in insulin/IGF signalling in the dam on D16 and D19 (Fig1, P<0.05). In contrast HSHF feeding reduced expression of several proteins involved in this signalling pathway in skeletal muscle (Fig2, P<0.05) and WAT (IGF1R, PI3K p110α/β and p85α, total Akt and pAkt, P<0.03), at both ages. Hepatic lipid metabolic markers were unaffected by HSHF feeding on D16, but PPARα was reduced and LPL, PPARγ, and FAS were increased by D19 (Fig1, P<0.04). In maternal skeletal muscle, a HSHF diet increased expression of FAS on D16, and decreased FATP on both D16 and D19 (Fig2, P<0.05). HSHF diet reduced FATP, PPARα and FAS on D16 and PPARα and FAS on D19 in maternal WAT (P<0.04). The content of fat in maternal liver and muscle was increased by a HSHF diet at D19 (P<0.001) but not day 16. Conclusion: The current study shows that HSHF feeding during mouse pregnancy induces tissue-specific changes in the expression of proteins involved in insulin/IGF signalling and lipid metabolism, consistent with the hyperinsulinaemia and indicative of muscle insulin resistance. These dietary-induced changes in maternal metabolic profile may influence the partitioning of nutrients to fetal growth and thereby explain the intrauterine programming of adult metabolic phenotype. [ABSTRACT FROM AUTHOR]

Nearly two-thirds of American women enter pregnancy overweight or obese and the prevalence of maternal overweight and obesity is increasing rapidly in many other countries, including the UK. The obese mother is at higher risk for many pregnancy complications and fetal overgrowth is common in these pregnancies. Fetal overgrowth increases the risk for perinatal complications and predisposes the child for obesity, diabetes and hypertension later in life. The mechanisms underlying increased fetal growth in overweight and obese women are poorly understood. Since fetal growth largely depends on the transfer of nutrients across the placenta, we hypothesize that altered placental function in obese women may lead to fetal overgrowth and its' associated long term health consequences. We are exploring the role of altered maternal metabolism associated with obesity in regulating placental nutrient transport. The placenta, uniquely juxtapositioned between the maternal and fetal blood supplies, must integrate both maternal supply and fetal demand signals. In cases of maternal obesity the signals impinging on the placenta are diverse and include high levels of macronutrients (glucose, amino acids, fatty acids), hyperinsulinemia, elevated adipokines (leptin, TNF-alpha, IL1-beta) and low levels of adiponectin. We evaluated alterations in placental nutrient transport capacity and multiple placental signaling pathways including 1) Toll Like Receptor 4 (TLR4), 2) insulin/IGF-I 3) mammalian target of rapamycin and 4) PPARs in term placentas from women of varying pre-pregnant body mass index (BMI). We found mTOR and inflammasome pathway activation, decreased PPARgamma activation and increased expression of amino acid and fatty acid transporters in placentas of high BMI women. Additionally, we developed a model of obesity without diabetes in mice based on feeding a highly palatable high-fat and high-sugar diet. The maternal metabolic phenotype resembles that of obese women with increased leptin and decreased adiponectin. Our model results in increased fetal growth and the placentas of obese mice were found to have an activation of insulin/IGF-I and mTOR signaling and a greater nutrient transport capacity. We used cultured primary human trophoblast cells to directly study regulation of placental nutrient transporters and demonstrated that saturated and monounsaturated fatty acids stimulate trophoblast System A amino acid uptake in a TLR4 dependent manner while omega3 long chain polyunsaturated fatty acids inhibit amino acid uptake by System A. Insulin, leptin and pro-inflammatory cytokines also increased trophoblast amino acid uptake. These data suggest that in obese mothers with high leptin, insulin resistance, and chronic proinflammatory activation, the placenta is stimulated by the maternal metabolic environment to deliver excess nutrients to the fetus. Adiponectin is insulin sensitizing in some tissues however elevated adiponectin, a feature of lean women, inhibits placental insulin signaling at the level of IRS-1 in cultured trophoblast cells. This would tend to decrease amino acid uptake in normal healthy pregnancies. In contrast, low adiponectin, which is associated with obesity, would promote insulin stimulated amino acid transfer across the placenta. Our experiments in cultured trophoblast cells indicate that adiponectin treatment leads to PPARalpha and p38 MAPK activation and increased ceramide biosynthesis, resulting in decreased insulin sensitivity. Additionally, we performed chronic infusion of full-length adipoenctin in normal mice and found an inhibition of placental insulin/IGF-I and mTOR signaling along with decreased fetal growth (-20%). These studies have identified mechanistic links between the perturbed maternal metabolism in pregnancies complicated by obesity and changes in placental signaling and nutrient transport capacity that likely lead to increased nutrient delivery to the fetus. We have discovered that adiponectin constitutes an endocrine link between maternal adipose tissue and placental function, supporting our hypothesis that the maternal metabolic environment is of key importance in regulating placental function. The role of the placenta in integrating signals from both the mother and fetus involves a complex interaction of extrinsic signals such as hormones, cytokines, maternal nutrient and energy levels with intrinsic placental signaling pathways for nutrient sensing, inflammation, and growth. Understanding the complex placental signaling pathways that lead to alterations in fetal growth will allow for the development of strategies to prevent short- and long-term health consequences of pathological fetal growth. [ABSTRACT FROM AUTHOR]

Fatism remains one of the last acceptable prejudices in the United States. For women, weight is a defining, if not the defining, characteristic. Due to the importance and value that society and media have placed on physical appearance, and in particular weight, a woman's weight communicates who she is as a person. Unfortunately, what her weight communicates includes a whole host of negative stereotypes that reflect the anti-fat bias that is deeply embedded in American culture. This bias, according to some, is based on the belief that weight is an entirely controllable factor. This study explores whether there exist any conditions under which female fatness is considered socially acceptable. Findings generated from thematic analysis suggest that while there exists a handful of "acceptable" causes of female fatness, generalized dislike of obese women might be an even bigger issue that the overweight female population must face. ..PAT.-Unpublished Manuscript [ABSTRACT FROM AUTHOR]