bluuebunny/crossref_metadata_2025_split huggingface dataset:
MON-LB310 Relationship Between Obesity-Induced Metabolic Abnormalities and Nutrient Intake: Sex Differences in Japanese University Students
Authors: Yamamoto Mayumi , Mehta Mausam , Nishio Akihiro , Horita Ryo , Izurieta Ricardo 
Published: May 2020

Abstract
Background: Preventive measures and interventions for obesity in young adults are urgently needed. However, evidence-based guidelines for interventional programs in this generation have not been established worldwide because of limited access to data on this group. To establish effective methods of obesity prevention in young adults, we analyzed the relationship between nutrient intake and obesity-related metabolic factors in each body mass index (BMI) group among Japanese university students. Methods: A cross-sectional analysis was performed using annual health checkup data, which is conducted mandatory for all students according to the School Health and Safety Act in Japan, from Gifu University’s incoming class of 2017. Nutrient intake information was obtained from the brief-type self-administered diet history questionnaire (BDHQ), which has been adjusted and validated for the Japanese population. Inclusion criteria were aged 18-30 years and completed the all examination items including BDHQ. From a total of 1277 students’ data, 1202 satisfied and were included in the analyses (participation rate: 94.1%). Nutrition and metabolic data were compared among BMI groups (lean, &lt;18.5 kg/m2; normal, 18.5-24.9 kg/m2; obese, ≥25.0 kg/m2, according to criteria of the Japan Society for the Study of Obesity [2002]) using one-way analysis of variance with post-hoc Tukey honestly significant difference analysis in SPSS software version24 (IBM Corporation, Armonk, New York). Results: The percentage of obesity was 8.1% in men and 1.4% in women, showing a significant difference. Among men, BMI groups were significantly (p&lt;0.05) different in the intake of 11 nutrients which were protein, fat, saturated fat, cholesterol, omega 3 and 6 fatty acids and micronutrients K, Mg, P, Fe, and Zn, significantly high in nine metabolic parameters, which were blood glucose, hemoglobin A1c, uric acid (UA), aspartate aminotransferase (AST), alanine aminotransferase (ALT), systolic and diastolic blood pressure (BP), low-density lipoprotein (LDL) cholesterol, triglycerides (TG) and significant low in high-density lipoprotein (HDL) cholesterol among obese group. Among women, BMI groups were not significantly different in nutrient intake, significantly high in five metabolic parameters, which were UA, ALT, systolic BP, LDL, and TG, and significant low in HDL among obese group. Conclusion: This study suggested that the effect of obesity on metabolic abnormalities in Japanese university students may be more remarkable in men than in women. This sex difference might be partially explained by the significant increase in protein and fat intake in obese men. For women, other factors may contribute to obesity and metabolic abnormalities. Education for appropriate volumes of nutrient intake could be effective in male university students.
SAT-LB37 Frailty in Patients With Mild Autonomous Cortisol Secretion Is Higher Than Patients With Nonfunctioning Adrenal Tumors
Authors: singh sumitabh , Atkinson Elizabeth , Achenbach Sara , Bancos Irina 
Published: May 2020

Abstract
Background: Mild autonomous cortisol secretion (MACS) affects up to 50% of patients with adrenal adenomas. Frailty is a syndrome characterized by diminished strength and endurance and serves as a marker of declining health and dependency. We hypothesized that patients with MACS are more frail when compared to patients with nonfunctioning adrenal tumors (NFAT).
Methods: This is a retrospective study of adult patients with adrenal adenoma evaluated at a tertiary center from 2004 to 2018. MACS and NFAT were defined as cortisol after 1 mg overnight dexamethasone suppression (DST) between 1.8-5 mcg/dl and &lt;1.8 mcg/dl, respectively. Frailty index (FI, range 0-1) was calculated using a 47 variables -deficit model (20 comorbidities, 14 activities of daily living, and 13 symptoms). Patients were excluded if treated with exogenous glucocorticoids, if diagnosed with overt adrenal hormone excess, another adrenal disorder, or if missing variables of interest.
Results: MACS was diagnosed in 168 patients (67% women) at a median age 65 (30-91) years and NFAT in 275 patients (61% women) at a median age of 59 (21-84) years. Patients with MACS demonstrated higher prevalence of hypertension (73% vs 62%), cardiac arrhythmias (50% vs 40%), and chronic kidney disease (25% vs 17%), but lower prevalence of asthma (5% vs 14%), when compared to patients with NFAT, p&lt;0.05 for all. Patients with MACS reported more symptoms of weakness (21% vs 11%), falls (7% vs 2%), and sleep difficulty (26% vs 15%) as compared to patients with NFAT, p&lt;0.05 for all. Age, sex and BMI-adjusted FI was higher in patients with MACS vs patients with NFAT (0.17 vs 0.15, p=0.009). Using cut-off FI of 0.2, 42% of patients with MACS were frail, versus 30% of patients with NFAT (p=0.01).
Conclusion: Higher frailty in patients with MACS supports a more aggressive management, such as adrenalectomy over conservative follow up. Future prospective studies are needed to characterize frailty in greater detail in patients with MACS, as well as to examine frailty reversal by adrenalectomy.
SUN-LB131 Association of Receptor for Advanced Glycation End Product (RAGE) Gene Polymorphisms & Serum Levels of Soluble RAGE (sRAGE) With Metabolic Syndrome (MS) in Mexican Population
Authors: Gonzalez-Guerrero Diana Elizabeth , Rojas-Rubio Armando , Lazo-de-la-Vega-Monroy Maria-Luisa , Gomez-Ojeda Armando , Luevano-Contreras Claudia , Macias-Cervantes Maciste , Fajardo-Araujo Martha Eugenia , Garay-Sevilla Ma Eugenia 
Published: May 2020

Abstract
Background. RAGE, a multi-ligand type 1 transmembrane glycoprotein belonging to the immunoglobulin superfamily, transduces biological signals associated with chronic cellular stress related with inflammatory responses, tissue damage, chronic and degenerative diseases (1). sRAGE is a variant of RAGE derived from cell surface cleavage mechanisms that could potentially act as endogenous inhibitors of RAGE activity (2). RAGE gene is highly polymorphic, with polymorphisms that could be responsible for disease development, like -374T/A (rs1800624) and -429T/C (rs1800625) polymorphisms. These are located in the promoter region and have marked effect on transcriptional activity. However, there have been conflicting findings between the potential association of RAGE polymorphisms and the development of diseases. In this work, we evaluated -374T/A (rs1800624) and -429T/C (rs1800625) polymorphisms and measured serum sRAGE levels in Mexican population with MS.
Methods. A group of healthy men without any component of the MS (n=80), and a group of men with the MS (n=80) according to the harmonized criteria for the MS were included in this study. Blood genomic DNA was isolated and genotyped by RT-PCR for the -374T/A and -429T/C polymorphisms of RAGE gene. sRAGE in serum was measured with an ELISA kit. Results. The studied population complied with the Hardy-Weinberg equilibrium (p=0.58 for -374T/A, and p=0.79 for -429T/C). Differences were observed in all the components of the MS between the two groups (MS vs. healthy subjects, p&lt;0.000). However, there were no differences in the population according to their genotype for the -374T/A (p=0.57) and -429T/C (p=0.59) polymorphisms. There was no difference in glucose (p=0.22), triglycerides (p=0.99), and cHDL (p=0.88) levels, or waist circumference (p=0.84) according to the genotype for the -374T/A polymorphism. The same was observed for the -429T/C polymorphism (glucose p=0.57, triglycerides p=0.69, cHDL p=0.77, waist circumference p=0.99). No association of MS with the -374T/A nor 429T/C polymorphism was found. There were no differences between groups in circulating sRAGE levels (p=0.132). Conclusion. According to our results, the -374T/A and -429T/C polymorphisms of RAGE gene are not associated with the MS in Mexican population, and have no influence on serum sRAGE levels. Some other factors could be playing a role for the high prevalence of the MS, such as eating habits. Gender should be taken into consideration, for our study was performed in men exclusively. References. (1) Serveaux-Dancer M et al., Dis Markers. 2019 Feb 4;2019:2067353. (2) Schmidt AM. Vascul Pharmacol. 2015 Sep;72:1-8.
SUN-LB40 Chronic Cortisol Works Through the Transcription Factor KLF9 to Deregulate Immune Response and Metabolism
Authors: Gans Ian M , Hartig Ellen I , Tilden Andrea R , Graber Joel H , Coffman James 
Published: May 2020

Abstract
Chronically elevated levels of glucocorticoids (GC) are associated with a number of disease states and negative side effects, including metabolic syndrome. Epidemiological studies show that elevated GC during a brief but vulnerable developmental window can have life-long and potentially multi-generational impacts on health. To elucidate underlying pathogenic mechanisms, our lab has used chronic treatment with a physiological dosage of cortisol (CORT) in developing zebrafish, Danio rerio, a model organism that has emerged as a useful tool for investigating GC signaling. In this paradigm, we have found evidence that high CORT during development alters a set point for the HPA axis and leads to continuous induction of aberrant GC production and transport, accompanied by altered immune gene regulation and decreased ability to maintain blood glucose homeostasis. To identify molecular and genetic pathways perturbed by chronic CORT treatment, we used CRISPR to generate mutant lines lacking the glucocorticoid receptor (GR) or the transcription factor Klf9, which we have found to be an important target/regulator of GC signaling. We performed RNA sequencing in these mutant lines and compared the transcriptomes of wild type (WT) and mutant animals treated with either chronic CORT or vehicle control (VEH). A broad overview of the data shows similarities between CORT treated wild-type fish and VEH treated GR mutants suggestive of GC resistance in the CORT treated WT animals. In Klf9 mutants, a number of genes involved in immune processes that were upregulated by chronic CORT in WT animals were not similarly upregulated, suggesting that Klf9 is an important feed-forward mediator of immune gene regulation by GC. Additionally, CORT increased expression of a number of metabolic genes in Klf9 mutants that were not similarly upregulated in WT, suggesting that Klf9 plays a regulatory role in the response of cellular metabolism to GC. To further investigate Klf9’s role in governing cellular metabolism, metabolic rate assays were performed on live animals. The results show that Klf9 mutants have lower total respiration, and that chronic CORT increases non-mitochondrial respiration in both WT and Klf9 mutants. Mitochondrial respiratory capacity was unaffected across conditions. This, coupled with gene expression data, suggests that measured metabolic differences are due to shifts in substrate usage and differential reliance on non-mitochondrial metabolic pathways such as glycolsis and peroxisomal beta-oxidation. Additional studies are required, but the regulation of glycolysis by Klf9 could contribute to this gene’s known tumor-suppresive role, and regulation of peroxisomal metabolism—key in immune cells—could partially explain the role of Klf9 in mediating these cells’ responsiveness to CORT.
SAT-015 Incidence and Predictors of Hypertension in a Cohort of Australian Women with and Without Polycystic Ovary Syndrome
Authors: Kakoly Nadira Sultana , Earnest Arul , Loxton Deborah , Teede Helena Jane , Joham Anju Elizabeth 
Published: May 2020

Abstract
Background: There is a lack of longitudinal studies exploring the relationships between polycystic ovary syndrome (PCOS) and hypertension, in population-based settings.
Objectives: To identify predictors of hypertension in women with and without PCOS and the relationship to body mass of index (BMI).
Methods: We undertook a community-based cohort analysis of the Australian Longitudinal Study (ALSWH) data conducted on 9,688 young adult women, aged 21–42 years from 2000–2015. We conducted survival analysis using the Cox Proportional Hazards Model to identify predictors and person-time analysis to calculate incidence rates of hypertension.
Results: Overall, 9,508 women were followed for 145,159 PY (person-years) and 1,556 (16.37%) women developed hypertension during the follow-up. The incidence of hypertension was significantly higher (p = 0.001) among women with PCOS (17/1000 PY) compared to women without (11/1000 PY). There were significant differences in time to hypertension development between women +/- PCOS. Hypertension was observed among women with PCOS from early adulthood and across BMI categories. The difference in the actual number of incident hypertension cases (incidence rate difference (IRD)) between women with and without PCOS, was fourfold higher (15.8 vs. 4.3 respectively) among women who were obese at baseline, compared to age-matched lean women. PCOS was independently associated with hypertension with a 36% greater risk, adjusting for BMI and other confounders.
Conclusion: Our results suggest women with PCOS as more likely to develop hypertension from early adulthood, independent of BMI and with risk exacerbated by obesity.
SAT-LB124 Phosphatidylcholine Transfer Protein Interacts With PPARδ to Modulate Activity
Authors: Druzak Samuel Adam , Mays Suzanne , Ortlund Eric 
Published: May 2020

Abstract
Obesity is one of the largest public health crises in the USA. Obesity can be lethal due to the development of cardiovascular complications such as, hypertension, heart attack, and stroke. Recently, peroxisome proliferator-activated receptor δ (PPARδ), the least-characterized member of the PPAR family of nuclear receptors (NRs), has shown great promise in treating obesity and associated cardiovascular complications. Recent reports have shown that PPARδ activation is tuned, in part, through an interaction with fatty acid binding protein 5 (FABP5) in a polyunsaturated Fatty acids (PUFAs) dependent manner. This enhancement is thought to occur due to ligand transfer, however, FABP5 only binds a subset of reported PPARδ ligands. To find other candidate lipid transport proteins (LTPs), we performed a protein complementation assay (PCA) between LTPs and NRs. We uncovered a novel interaction between PPARδ and phosphatidylcholine transfer protein (PC-TP), sensitive to cellular nutrient levels. Preliminary data show that this interaction opposes canonical PPARδ signaling, leading to a decrease in PPARδ transactivation in cells and isolated mice livers. This led me to hypothesize that PC-TP senses nutrient status through membrane composition. Specific PC molecular species drive PC-TP translocation to inhibit PPARδ transactivation of genes. Utilizing our novel PCA assay I have shown that the interaction is modulated in part by cellular levels of methionine and choline, as cells cultured in media depleted of methionine and choline (MCD) show a decreased in the interaction. Using the same assay, I have shown a requirement of full length PPARδ for the interaction with PC-TP. This analysis will be complimented by mutagenesis and chemical perturbations aimed to alter PC-TP and PPARδ function. Additionally, I have assayed the in vivo relevance of PC-TP interaction with PPARδ using livers harvested from PCTP-/- and littermate control mice fed a variety of diets. Preliminary RNA-seq characterization, show interesting alterations in gene expression that suggest more complex regulation between PC-TP and PPARδ in vivo. MCD, which was shown to reduce the inhibitory interaction between PC-TP and PPARδ in vitro, seems to lead to an increased effect on PPARδ transactivation when PC-TP is depleted. Analysis comparing the effect of diet within each genotype shows a loss of differential PPARδ regulation for both CHEA and KEGG analysis when comparing WT to PCTP -/- mice supporting a role for PC-TP in differential PPARδ regulation caused by MCD diet. These studies will further the understanding of how lipid homeostasis is sensed and maintained through PPARδ by interactions with two separate LTPs.
SAT-LB4 Novel Hormonal and Metabolic Markers of Recovery From Overtraining Syndrome Unveiled by the Longitudinal ARM of the Eros Study - the Eros-Longitudinal Study
Authors: Cadegiani Flavio , da Silva Pedro Luiz H , Abrao Tatiana P C , Kater Claudio E 
Published: May 2020

Abstract
Background: Overtraining Syndrome (OTS) is an unexplained underperformance syndrome triggered by excessive training, insufficient caloric intake, inadequate sleep, and excessive cognitive and social demands. Investigations of markers of the challenging recovery from OTS have not been reported to date. The objective of the present study is to describe novel markers, and biochemical and clinical behaviors during the restoration process of OTS.Design: A 12-week interventional protocol in 12 athletes affected by OTS was conducted, including increased food intake, transitory interruption of the trainings, improvement of sleep quality, and management of stress.Methods: We assessed 50 parameters, including hormonal responses to an insulin tolerance test (ITT), basal hormonal and non-hormonal biochemical markers, body metabolism and composition. Results: In response to an ITT, early cortisol (p = 0.026), early GH (p = 0.004), and late GH (p = 0.037) improved significantly. Basal estradiol (p = 0.0002) and nocturnal urinary catecholamines, (p = 0.043) reduced, while testosterone (p = 0.014), testosterone:estradiol (T:E) ratio (p = 0.0005), freeT3 (p = 0.043), IGF-1 (p = 0.003), and cortisol awakening response (CAR) (p = 0.001) increased significantly. All basal parameters and early responses to ITT normalized, when compared to healthy athletes. Basal metabolic rate, fat oxidation, body fat, muscle mass, and hydration status had partial but non-significant improvements. Conclusion: After 12 weeks, athletes affected by actual OTS demonstrated substantial improvements, remarkably IGF-1, freeT3, CAR, testosterone, estradiol testosterone:estradiol ratio, CK and catecholamines, and early cortisol, early prolactin, and overall GH responses to stimulations.
MON-266 The Association Between Prolactinomas and Weight Gain
Authors: Tariq Zunera , Sabie Farah Al , Donegan Diane 
Published: May 2020

Abstract
Introduction: The prevalence of obesity is increasing worldwide and treatment remains challenging. Certain endocrine disorders may contribute to weight gain. These are important to recognize as treatment may have beneficial impact on weight. Studies have reported an increased prevalence of obesity in patients with prolactinomas. While several studies have examined the association between weight gain and prolactinomas, the results are conflicting. Therefore, the aim of this study was to determine if BMI is higher among those with a prolactinoma compared to those without.
Methods: We identified all patients ≥18 years of age referred to endocrinology between 2008–2018 with a newly diagnosed prolactinoma (defined as a prolactin levels ≥40 ng/ml on 2 separate occasions and a pituitary adenoma evident on MRI without secondary causes for hyperprolactinemia). We extracted the following variables from the medical record: patient demographics, presenting symptoms, prolactin level and tumor size at diagnosis. Comparative data was obtained from the National Health and Nutrition Examination Survey (NHANES) 2015–2016, from which we included only those ≥18 years of age who had BMI data.
Results: In total 34 patients with a newly diagnosed prolactinoma (female: 27 /34, 79%, mean age at diagnosis: 35.4 ± 10.7 years) met inclusion criteria. The majority of patients (23/34, 68 %) had microadenomas defined as &lt;1cm. The median prolactin level at diagnosis was 103.3 (IQR 51.3- 249.25). Although the most common presenting symptoms were those consistent with hypogonadism (27/34, 79%) and galactorrhea (16/34, 47%), 1/3 patients also described weight gain. In comparison, 5662 individuals from NHANES (48 ± 18 years, female: 2955/5662, 52%) reported their BMIs. BMI was significantly increased among those with a prolactinoma compared to survey population [median BMI 30.9 kg/m2 (IQR, 24.9- 39) vs 28.3 kg/m2 (24.3- 33), P= 0.02]. This difference persisted even when adjusted for age and sex (P= 0.0002). In addition the prevalence of class II obesity (BMI ≥35 kg/m2) was higher in those with a prolactinoma compared to survey population (38% vs 18%, P=0.005). Among prolactinoma patients, there was a correlation between BMI and log-transformed prolactin levels (R2= 0.24, P=0.003).
Conclusion: Weight gain is a presenting symptom for many patients with a newly diagnosed prolactinoma. When compared to a large cohort of adults in the US, those with a prolactinoma have higher BMI and an increased prevalence of class II obesity. Based on the correlation between BMI and log-transformed prolactin levels, we hypothesize that this weight difference may be related to hyperprolactinemia. These findings suggest that, in the appropriate context, hyperprolactinemia should be considered when a patient presents with weight gain.
MON-639 Melanocortin 4 Receptor Contributes to Glucose Homeostasis by Regulating Kidney Glucose Reabsorption via the Glucose Transporter GLUT2
Authors: de Souza Cordeiro Leticia M , Devisetty Nagavardhini , Chhabra Kavaljit H 
Published: May 2020

Abstract
Melanocortin 4 receptor (MC4R) is essential for normal body weight and food intake. Deficiency of MC4R causes obesity in humans and mice. While the function of MC4R is well established in appetite regulation, its direct role in glucose homeostasis is unclear. Humans and mice with MC4R deficiency exhibit hyperinsulinemia and insulin resistance; however, they remain protected from fasting hyperglycemia/diabetes. To determine the role of MC4R in glucose homeostasis, we performed oral glucose and intra-peritoneal insulin tolerance tests (OGTT / ITT) in male and female Mc4r knockout (KO) and wild type (WT) mice. Remarkably, Mc4r KO mice exhibited improved glucose tolerance compared to WT mice (Area under the curve for OGTT, male: 29,125±2,028 vs. 38,493±1,161 mg/dL.min; female: 36,322±1,100 vs. 49,539±1,911 mg/dL.min, p&lt;0.0001). The improvement in glucose tolerance was despite insulin resistance in Mc4r KO mice (Plasma insulin, male: 9.9±1.7 vs. 0.7±0.1 ng/mL, female: 6.2±2.0 vs. 1.1±0.3 ng/mL, p&lt;0.05; Area under the curve for ITT, male: 13,174±1,073 vs. 8,132±255 mg/dL.min; female: 13,927±1,253 vs. 7,506±267 mg/dL.min, p&lt;0.01). Based on our previous findings from POMC deficient mice, we hypothesized that the improved glucose tolerance in the Mc4r KO mice is due to their elevated glycosuria (excretion of glucose in urine). To test this hypothesis, we challenged Mc4r KO and WT mice with oral glucose (250 mg) and collected their 24h urine to evaluate glycosuria. Indeed, the KO mice demonstrated elevated glycosuria compared to their WT littermates (Urine glucose, male: 284±48 vs. 0.4±0.03 mg/24h, female: 63.4±14 vs. 1±0.6 mg/24h, p&lt;0.002). To assess molecular mechanisms underlying elevated glycosuria in Mc4r KO mice, we measured the gene expression and levels of the kidney glucose transporters GLUT1, GLUT2, SGLT1 and SGLT2. Glut2 mRNA was reduced by ̴ 40% and the protein level was decreased by ̴ 20% in Mc4r KO mice compared to their WT littermates. The other glucose transporters remained unchanged. Altogether, our study demonstrates that MC4R contributes to glucose homeostasis by regulating kidney glucose reabsorption via GLUT2. These findings may explain why MC4R deficient mice or humans remain protected from diabetes despite their longstanding obesity and insulin resistance.