bluuebunny/crossref_metadata_2025_split huggingface dataset:
SAT-LB132 3-Generation Study of Metabolic Disruption by Pregnancy Serum PFASs: Associations With Abdominal and Whole-Body Obesity in Granddaughters in a 60-Year Follow-Up of the Child Health and Development Studies Cohort
Authors: Cohn Barbara A , Krigbaum Nickilou , Cirillo Piera 
Published: May 2020

Abstract
Introduction. We previously found a 3.6-fold increased risk of breast cancer in daughters associated with high maternal (F0) early postpartum serum EtFOSAA combined with high F0 cholesterol (https://doi.org/10.1016/j.reprotox.2019.06.012). Here we test the hypothesis that F0 early postpartum EtFOSAA, in combination with F0 serum cholesterol predicts abdominal obesity (waist circumference &gt; 88cm) and/or whole-body overweight or obesity (body mass index &gt; 25 kg/m2) in daughters (F1) at age 30 and granddaughters (F2) at age 20. Methods. We measured F1 and F2 weight, height, waist circumference and blood pressure when F1 were an average age of 50 years and adult F2 were an average age of 20 years (N=213 triads). F1 also reported their weight at age 30, near the mean age of their pregnancies with their daughters (F2) to allow control for obesity during F2 gestation. EtFOSAA, PFOS, and cholesterol were assayed in archived early postpartum F0 serum samples collected within 3 days of delivery. Results. F0 cholesterol significantly (p&lt;0.05) modified the association of F0 EtFOSAA with self-reported obesity at age 30 in F1 and measured abdominal and whole-body obesity, and blood pressure at age 20 in F2. Association patterns were similar for all outcomes: F0 EtFOSAA was associated with high metabolic risk when F0 serum cholesterol was low (Quartile 1): e.g. 20-year-old F2 had an estimated 2.3 fold increase in the joint risk of abdominal and whole-body obesity over the inter-quartile range of F0 ETFOSAA, 95% Confidence Interval= 1.1, 4.8. F0 EtFOSAA associations with F2 metabolic risk were independent of F0 race, early pregnancy overweight (BMI &gt;25 kg/m2), and serum PFOS. F1 obesity at age 30 did not mediate F0 EtFOSAA associations with F2 outcomes, but additionally predicted high metabolic F2 risk. Conclusions. Findings support the hypothesis that in utero exposure to EtFOSAA impacts metabolic risk factors in female F2 exposed as germline and also independently via promotion of overweight in F1 (their mothers) during F2 gestation.
SUN-497 Life-Saving Management of Thyrotoxicosis with a Single Session of Plasmapheresis
Authors: Rakhra Varundeep , Patel Parth , Cabandugama Peminda K 
Published: May 2020

Abstract
Thyroid hormones are essential in controlling numerous metabolic and regulatory processes in the human body. Thyroid storm is a medical emergency and is the most extreme manifestation of the overproduction of thyroid hormones. It is critical to recognize thyroid storm at its earliest state and conventional practice recommends initiating treatment immediately with steroids, thionamides, and beta-blockers.Here we present a case of a patient with Graves’ disease in which thionamides could not be continued due to acute thionamide-induced hepatotoxicity. With the patient’s worsening thyrotoxic state, declining mental status and clinical deterioration; the decision was made to initiate plasmapheresis as a life-saving therapy to remove the thyroid stimulating antibodies responsible for the patient’s deteriorating status.After one session of plasmapheresis, the patients’ clinical condition began to significantly improve to baseline, along with normalization of his thyroid function and the patient was discharged home with plans for emergent thyroidectomy.This case demonstrates the importance of considering plasmapheresis as a life saving measure in the treatment algorithm of patients with extreme thyrotoxicosis and thyroid storm in which traditional therapies such as thionamides, steroids, and beta-blockers cannot be used or are ineffective. Reference:Ono, Y., Ono, S., Yasunaga, H., Matsui, H., Fushimi, K., & Tanaka, Y. (2016, February 18). Factors Associated With Mortality of Thyroid Storm: Analysis Using a National Inpatient Database in Japan. Retrieved April 6, 2019, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4998648/
SAT-LB86 Improvement In Metabolic Indices Including Thyroid HormonesVia Enhanced Absorption Of Nutrients By Teduglutide In Short Bowel Syndrome
Authors: Oba Ken C , Kabadi Udaya M 
Published: May 2020

Abstract
Background: Short bowel syndrome is characterized by maldigestion and malabsrption resulting in deficiencies of multiple nutrients including vitamins and minerals. Most subjects required parental elimination for survival. GLP 2 RA Teduglutide was recently approved for treatment of short-bowel syndrome especially for those requiring parenteral support. Objective: To demonstrate the utility of GLP2 Receptor Agonist Teduglutide in improvising multiple metabolic indices In presence of short bowel syndrome. Case presentation: 66-year-old Caucasian female presented with a history of short bowel syndrome and associated vitamin deficiencies, hypothyroidism requiring large dose of levothyroxine, diarrhea, and liver cirrhosis. Upon starting teduglutide the subject saw improvement in her symptoms. Moreover, daily dose of levothyroxine required reductions from 300 mcg to 150 mcg to maintain desirable serum concentrations of free T4, free T3 and TSH. Finally, serum levels of several vitamins attained greater than therapeutic concentrations requiring dosage reductions. Also notable was the improvement in her liver function tests, remission from ascites and regeneration of liver nodules. Conclusion: Herein, we report an adult subject with short bowel syndrome with concurrent hypothyroidism and multiple vitamin deficiencies who following administration of GLP2 RA therapy demonstrated a marked improvement in her metabolic parameters with some requiring reduction in daily dose along with improvement in manifestations of liver cirrhosis.
MON-LB122 Psychiatric Medication Induced Diabetes Mellitus
Authors: Khanal Bishal , Tharu Biswaraj , Tharu Sunraj , Khanal Asmita 
Published: May 2020

Abstract
Psychiatric medications are well established cause of diabetes. Our case had similar presentation. 67-year-old African-American male with history of hypertension and dementia was brought to the ER for auditory hallucination and bizarre behavior. His home medications were Hydrochlorothiazide, Nifedipine and Spironolactone. Psychiatry was consulted and he was admitted to psychiatric floor. He was diagnosed for first time with psychosis and depression. He was treated with citalopram 20 mg for depression; donepezil 10 mg for dementia and risperidone 0.5 mg twice a day for psychosis. 2 weeks later he developed difficulty swallowing and weakness, blood glucose level of 1263 mg/dl. All of his psychiatric medications were stopped except for citalopram 10 mg daily and patient was transferred to ICU. In the ICU, pH was 7.28 (normal 7.34-7.45), normal anion gap, bicarbonate 29mmol/L (normal 20-24), plasma osmolality 428 mOsm/kg (normal 280-320), HbA1c 10% (normal 4-5.6). He was intubated and managed as Hyperosmolar Hyperglycemic Non-Ketotic coma (HONK). He was started on insulin drip and later transitioned to Lantus and short-acting insulin. He improved and was then extubated. After 40 days, repeat A1C was 7.4%. The patient moved to another state and follow-up was lost.
Discussion While the patient was on thiazide for a long time, he had a fairly good glucose control; his A1C ranged from normal to prediabetic (A1c 5.7%-6.4%). This makes thiazide unlikely cause of diabetes mellitus for him. The fact that right after 21 days of starting psych medications caused him to land in ICU for HONK, with A1c of 10% and glucose of 1273 mg/dl, strongly suggests that this is a case of psych medications induced T2DM. This is also supported by the fact that discontinuation of those medications lowered the A1c to 7.4% in 40 days. 3 weeks before the hospitalization his A1c was 5.1%. Metformin is demonstrated to be most promising long term medication in cases like this.
Conclusion Psychiatric medications are important cause of drug induced diabetes and should always be thought as a cause of acute new onset diabetes. Stopping the offending drugs ensues good glycemic control.
SUN-LB119 Role of HNF4a Isoforms in the Carbohydrate/Lipid Switch in the Liver and Responsiveness to AMPK
Authors: Radi Sarah , Deol Poonamjot , Deans Jonathan Robert , Fekry Baharan , Eckel-Mahan Kristin , Sladek Frances M 
Published: May 2020

Abstract
Hepatocyte Nuclear Factor 4α (HNF4α), the master regulator of liver-specific gene expression, is regulated by two promoters (P1 and P2) which drive expression of two groups of HNF4α isoforms referred to here as HNF4α1 and HNF4α7. HNF4α is a known regulator of gluconeogenesis and is mutated in maturity onset diabetes of the young one (MODY1). Conventionally, it was thought that HNF4α1, but not HNF4α7, is expressed in the normal adult liver, with HNF4α1 downregulated and HNF4α7 upregulated in liver cancer. Now, we identify a previously undescribed role for HNF4α7 in the normal adult mouse liver - one involved in the diurnal variations of lipid and carbohydrate metabolism. More specifically, HNF4α1 appears to be a major driver of gluconeogenesis while HNF4α7 is a driver of ketogenesis: we hypothesize that alterations in the levels of the HNF4α isoforms during the day function as a molecular switch between the two. Moreover, our preliminary data show that HNF4α7 is required for increased levels of circulating ketone bodies in female mice, suggesting interactions with the estrogen pathway. AMP-Activated Protein Kinase (AMPK), an energy-sensing kinase that also plays a major role in carbohydrate and lipid metabolism, has been shown to phosphorylate HNF4α1 in vitro, but effects in vivo and on HNF4α7 are not known. In order to investigate the impact of AMPK on HNF4α isoforms, we employed HNF4α isoform-specific mice α7HMZ (express only HNF4α7) and α1HMZ mice (express only HNF4α1), as well as heterozygous mice which express both. Intraperitoneal injection of the mice with AMPK activator AICAR leads to a rapid decrease in glucose. Interestingly, half the α7HMZ males and all the females began seizing 30 min post injection, while very few α1HMZ males/females and none of the heterozygous mice seized. Moreover, there were differences in the survival of the different genotypes: a third of α1HMZ mice die within 24hrs, while two thirds of α7HMZ mice die within a week, with all heterozygous mice surviving. We suspect the seizures could be due to an electrolyte imbalance exacerbated by AICAR or extremely low glucose caused by AICAR. The α7HMZ females have significantly lower potassium levels compared to α1HMZ and wildtype mice. Additionally, AMPK is known to regulate Na+/glucose transporters, and HNF4α1 is expressed in the proximal tubules in the kidney (responsible for Na+ uptake). To elucidate the cause of the seizures, AICAR injections were repeated with α1HMZ males followed by a glucose or saline gavage. Interestingly, half of the glucose-gavaged mice died within 24hrs, while all of the saline-gavaged mice survived. Our work underscores the critical role that the HNF4α isoforms play in the metabolic switch, and suggests that the kidney as well as the liver could be involved.
MON-LB130 Glucocorticoid Receptor Signaling and Stress in the Developing Mammalian Germline
Authors: Cincotta Steven Anthony , Laird Diana 
Published: May 2020

Abstract
While the consequences of stress on organs such as the heart and immune system have long been established, it has only recently been shown in mice that stress experienced during pregnancy can cause molecular and behavioral changes in the exposed fetus, and even their offspring. The transmission of such phenotypes across generations implies that fetal germ cells can sense and maintain epigenetic memories of stress experienced in the womb. However, how the fetal germ cells within the developing embryo detect and respond to these stress signals is unknown. In response to stress, the major circulating hormone released is cortisol, which is the ligand for the nuclear hormone receptor known as the glucocorticoid receptor (GR). GR induces highly cell type-specific transcriptional changes in many cell types, although its function in germ cells has yet to be explored. Our preliminary studies have shown, for the first time, the robust expression and dynamic localization of GR in fetal germ cells, suggesting its activity during a crucial window of epigenetic reprogramming in male and female germ cell development. Fetal germ cells naturally undergo genome-wide demethylation of somatic and parental imprints, which leads to the de-repression of transposons that are normally silenced by methylation at their promoters. If not properly re-silenced, these transposons will generate large numbers of DNA double strand breaks during transposition, posing a serious risk to germline integrity. When GR was genetically deleted from all cells of the mouse body, we discovered elevated expression of the retrotransposon, Line1 (L1), specifically in the developing germ cells. Surprisingly, mice with a conditional deletion of GR specifically in germ cells were unable to phenocopy the full body knockout, implying that GR-mediated repression of L1 in fetal germ cells is a non-cell autonomous effect. Rather, conditional deletion of GR from the surrounding somatic cells (e.g. granulosa cells of the ovary) demonstrated increased germ cell L1 expression, strongly suggesting that GR signaling through the somatic niche is indirectly regulating L1 expression in neighboring germ cells. We therefore hypothesize that GR signaling from the somatic cell niche is functioning to indirectly suppress L1 expression within the developing fetal germ cells, which holds broad implications for how stress signals mediated by GR signaling can influence germline integrity and thus the health of future generations.
SUN-LB80 Thyroglossal Duct Cyst Carcinoma in a 12 Year Old Boy. Should Total Thyroidectomy Be Done?
Authors: Sitja Marina Mora , Montane Lucía Sentchordi , Fernández María Sanz , Berrocal Julio Cerdá , Navazo Sara de la Mata , González-Pinto Lucía Carrascón , de León Esther González Ruiz , Rodríguez Arnao Dolores , Sánchez Amparo Rodríguez 
Published: May 2020

Abstract
INTRODUCTION The thyroglossal duct cyst (TGDC) is the most common congenital anomaly of the neck in childhood. However, thyroid carcinoma of the thyroglossal duct cyst is rare. It occurs in less than 1% of cases and the diagnosis is usually made from histopathologic findings after cyst surgery. Papillary carcinoma is the most common histologic subtype. The management of the TGDC carcinoma is not well defined. Sistrunk procedure (resection of the cyst and hyoid bone) followed by total thyroidectomy is the classic treatment, due to frequency of concomitant thyroid cancer (20-60%). However some authors propose a more conservative management performing thyroidectomy only in certain cases (positive margins, abnormal preoperative imaging, extension of TGDC carcinoma beyond the cyst wall). Lymph node resection and radioactive iodine therapy are used on advanced stages. CLINICAL CASE A 12-year-old boy presented with a four-month history of neck swelling. There was no previous exposure to irradiation or positive family history of thyroid cancer. Physical examination revealed a 5 cm mass located in the midline region of the neck, slightly tilted to the left, above the hyoid bone, covered by normal skin. A neck ultrasound was performed showing a normal thyroid gland, and a cystic lesión compatible with a TGDC. A CT scan corroborated this finding, showing a cystic lesión of about 3.1 cm x 2.1 cm x 3.7 cm (anteroposterior, transverse and craniocaudal planes) with a small solid pole in the posterior portion of the cyst, 1x1 cm on the axial plane. Small cervical lymph nodes with no suspicious features were also described. Thyroid function tests were normal. Sistrunk operation was performed for resection of the TGDC. Histologic examination revealed papillary carcinoma in a thyroglossal duct cyst. It measured 17 mm at its maximal diameter and invaded the cyst wall 1 mm with negative margins. Consequent to the diagnosis of TGDC carcinoma, total thyroidectomy was performed on a second surgery whithout side effects. Thyroid tissue showed usual morphological features without signs of malignancy. Currently the patient undergoes levothyroxine replacement treatment.CONCLUSIONS Papillary thyroid carcinoma in thyroglossal duct cysts is rare entity and even rare in children. Given that several studies in adults show a non-negligible percentage of patients with TGDC carcinoma and a normal thyroid ultrasound who had a concomitant thyroid cancer, the most controversial part of its management is whether total thyroidectomy should be done or not. Although some groups advocate thyroidectomy only in specific cases of TGDC carcinoma, its multifocal nature and the low risk of complications of thyroid surgery in pediatric referral centers make us supporters of performing total thyroidectomy to all patients.
SUN-LB61 Differential and Opposite Regulation of Acid Labile Subunit (ALS) Versus Insulin-Like Growth Factor I (IGF-I) by Oral Estrogens in Premenopausal Women
Authors: Schilbach Katharina , Haenelt Michael , Nicolay Shiva Sophia , Schwerdt Laura , Schwaiger Rita , Benedix Sarina , Longo Schweizer Junia Ribeiro de Oliveira , Störmann Sylvère , Schopohl Jochen , Bidlingmaier Martin 
Published: May 2020

Abstract
Background: The impact of estrogens (E2) on the growth hormone (GH)/IGF-I axis is known to depend on route of administration: While oral E2 increases GH and decreases IGF-I, transdermal E2 has only limited or no effect. However, data concerning the impact of E2 on IGF binding protein 3 (IGFBP 3) and ALS are less clear. One study in girls demonstrated higher ALS with oral E2, while the opposite was suggested for postmenopausal women. No data are available for healthy premenopausal women.Methods: We measured IGF-I, IGFBP 3 and ALS in fasted healthy adults (93 males (M), 35 premenopausal women without E2-containing oral contraception (FPRE), 37 premenopausal women with E2-containing oral contraception (FPREOC) and 34 postmenopausal women (FPOST)). IGF-I and IGFBP 3 were measured using the IDS-iSYS chemiluminescence immunoassay, and ALS by an in-house immunofluorometric assay (limit of quantification (LoQ) &lt; 50 mU/ml, range 50 - 4000 mU/mL).Results: Median age (range) was 33 (20 - 76), 28 (20 - 44), 24 (21 - 36) and 56 (49 - 70) years for M, FPRE, FPREOC and FPOST, respectively. As expected, IGF-I was lower in FPREOC compared to FPRE (median IGF-I xULN (IQR) 0.56 (0.45 - 0.73) and 0.72 (0.63 – 0.80), P = 0.0017, Kruskal-Wallis). ALS was significantly higher in FPREOC compared to all other groups (mean ALS in M, FPRE, FPREOC and FPOST: 636, 708, 861 and 648 mU/mL, respectively, ANOVA P &lt; 0.0001, Dunnett’s post-hoc test: M vs FPREOC: P &lt; 0.0001, FPRE vs FPREOC: P = 0.0007, FPOST vs FPREOC: P &lt; 0.0001). IGFBP 3 was not different in females with and without oral E2 (median IGFBP 3 xULN (IQR) FPREOC vs FPRE: 0.62 (0.54 - 0.67) vs 0.60 (0.49 – 0.76), Kruskal-Wallis P = 0.295, Dunn’s post-hoc test: P &gt; 0.9999). This was also true between all other groups (Dunn’s post-hoc test: P ≥ 0.4). In our adult cohort, ALS exhibited negative correlation with age (Pearson r = -0.282, P = 0.0003), similar to IGF-I and IGFBP 3. While IGF-I exhibited a moderate negative correlation to BMI (Pearson r = -0.25, P = 0.0013), IGFBP 3 and ALS were not significantly related to BMI.Conclusion: While IGF-I, IGFBP 3 and ALS all are known to be secreted in response to GH, and IGF-I and ALS are assumed to be produced by the same cells in the liver (hepatocytes), the three GH dependent biomarkers appear to be differently regulated by metabolic factors and oral E2. Only IGF-I has some modest association with BMI. Oral E2 is associated with reduced IGF-I, unchanged IGFBP 3 but increased ALS. While the mechanism behind the differential regulation remains to be uncovered, E2 therapy must be taken into account when interpreting IGF-I and ALS concentrations.
MON-LB6 Association Between Sex Steroid and Metabolic Parameters in Cord Blood With Placental Fatty Acid Transporter in Obese Pregnant Women
Authors: Maliqueo Manuel , Álvarez Daniela , Ortíz Macarena , García Madian , Flores Cristian , Echiburú Bárbara , Crisosto Nicolás 
Published: May 2020

Abstract
Obesity reduces maternal insulin sensitivity and alters sex steroid serum concentrations. However, it is not clear if these changes are reflected in the fetal circulation. On the other hand, similar to other metabolic tissues, modifications in sex steroid concentrations and metabolic parameters could modify the transport and metabolism of fatty acids (FA) in the placenta increasing their availability for the fetus. Therefore, we aimed to study, in pregnant women with normal-weight and obesity, sex steroid serum concentrations in cord blood and their relationship with the gene expression of FA transporters and of molecules related with FA metabolism in the placenta. We included 26 pregnant women with normal-weight and 26 pregnant women with obesity without pregnancy complications. At term of pregnancy, mixed cord blood and placenta samples were collected and stored at -80°C. Serum concentrations of dehydroepiandrosterone (DHEA), DHEA sulfate (DHEAS), androstenedione, testosterone, estrone, estradiol, estriol, insulin and TNF-α were measured by RIA or ELISA. Glycemia and lipid profile were also analyzed. In placental samples, the gene expression of MFSD2A, CD36, FABP4, SLC27A4, PPARG, LPL and DGAT were determined by quantitative PCR. No differences were observed in sex steroid concentrations and metabolic parameters between groups. On the other hand, the gene expression of MFSD2A, CD36 and FABP4 were higher in placentas from women with obesity compared to women with normal-weight (P = 0.050, P = 0.037 and P = 0.038, respectively). When distributed according to fetal sex, cholesterol levels were higher in cord blood of women with obesity and female fetuses (P = 0.005), whereas glycemia was lower in women with obesity and male fetuses (P = 0.045). In turn, the gene expression of CD36 and FABP4 were higher (P = 0.024 and P = 0.034, respectively), whereas MFSD2A tended to be higher (P = 0.092) only in placentas from women with obesity and male fetuses. Moreover, in women with obesity and male fetuses, glycemia was positively correlated with MFSD2A (r = 0.650; P = 0.022), and in women with obesity and female fetuses FABP4 was inversely correlated with triglyceride levels (r = -0.580; P = 0.048). In conclusion, these data suggest that modifications in placental steroidogenesis do not affect sex steroid serum concentrations in the fetal circulation. On the other hand, metabolic parameters in cord blood of pregnant women with obesity are associated with an abnormal expression of FA transporters in placental tissue.