bluuebunny/crossref_metadata_2025_split huggingface dataset:
PSUN286 A Rare Case of Non-Islet Cell Tumor Hypoglycemia in Young Female With Metastatic Neuroendocrine Tumor
Authors: Zweibach Eugenia , Izkhakov Neriy , Zweibach Eugenia , Vernetti Nicholas , Nakhle Samer 
Published: November 2022

Abstract

Background
Non-islet cell tumor hypoglycemia (NICTH) is a rare paraneoplastic syndrome caused by a benign or cancerous tumor that over-secretes various hormones that lead to hypoglycemia. Multiple etiologies were described in literature, the most common of them is abnormal secretion of insulin-like growth factor-2 (IGF-2) known as Doege-Potter syndrome (first described in 1929). Other etiologies include oversecretion of proinsulin, IGF-1, and somatostatin. Estimated incidence of NICTH is one per one million person-years. Tumors of mesenchymal origin are most often described in association with NICTH. Laboratory diagnosis of fasting hypoglycemia associated with serum insulin levels below 3 μU/ml confirm the diagnosis of NICTH. In the case of Doege-Potter syndrome, lab findings show low levels of insulin, c-peptide, IGF-1 and a high IGF-2: IGF-1 ratio, which indicate non-insulin-mediated hypoglycemia due to IGF-2 oversecretion. Neuroendocrine tumors presented with NICTH are rare and only described in several case reports.

Clinical Case
We report a case of a 34 year old female with metastatic neuroendocrine high grade tumor (WHO grade 3, non small cell, diagnosed 3 years prior to presentation) with metastasis to the bone (status post debulking and radiation) and brain (status post radiation therapy). Patient was admitted due to left ankle cellulitis. Endocrinology was consulted due to incidental finding of hypoglycemia serum glucose of 44 mg/dL. Repeat serum levels showed c-peptide 1 ng/dL (normal 1.1 - 4.4) and glucose of 54 mg/dL. She denied a history of diabetes mellitus, alcohol intake, insulin or sulfonylurea use. She had normal renal and liver function. Continuous infusion of D10 started and after 24 hours the patient's hypoglycemia improved. However, hypoglycemia recurred every morning. Following morning hypoglycemia repeat serum labs showed insulin 1.3 (Normal 2.6-24.9), c-peptide 0.9 ng/dL, and serum glucose of 114 mg/dL confirming that her hypoglycemia was not insulin induced. She was not on any medications known to cause hypoglycemia. CT abdomen without contrast showed left upper quadrant heterogeneous hypoattenuating mass with calcifications, measuring approximately 8.5 cm×10.1 cm×2.6 cm.

Conclusion
This is a case of a patient with a high grade non small cell metastatic neuroendocrine tumor who presented with NICTH. This is the first case of a neuroendocrine tumor with non-small cell pathology causing NICTH that has been described to-date. Based on the patient's clinical presentation and available laboratory findings with recurrent fasting hypoglycemia, low insulin and c-peptide levels we confirmed diagnosis of NICTH. This patient`s hypoglycemia was most likely induced by IGF-2 overexpression (Doege-Potter syndrome) which is the most common cause of NICTH.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
PSUN316 Racial Disparities in Diabetes Control and Use of Technology in a High Risk Cohort of Youth with Diabetes
Authors: Carrillo-Iregui Adriana , Bishop Meredith , Granados Andrea , Pagan Pedro , Arteaga Yadmara , Verme Jacquelyn , Alvarez-Salvat Rose , Carrillo-Iregui Adriana 
Published: November 2022

Abstract

Background
Racial and ethnic minority children experience significant disparities in achieving the American Diabetes Association-recommended hemoglobin A1c (HbA1c) levels when compared to non-Hispanic Whites (NHW). Continuous glucose monitoring (CGM) and insulin pump (IP) use are associated with improved glycemic control. Racial and ethnic disparities exist in the use of these technologies in youth with Type 1 diabetes (T1D), which may contribute to the observed poor glycemic outcomes in this population. However, racial and ethnic differences in CGM and IP use have not been examined in children and adolescents with diabetes.

Objective
We describe the differences in glycemic control, CGM and IP use in an ethnically diverse cohort of children and adolescents seen in a multidisciplinary diabetes clinic designed to provide support (i.e., diabetes education, psychology, social work, nutrition) to youth with poorly controlled diabetes.

Methods
Demographic data, HbA1c levels, CGM and IP use were collected from a cohort of high-risk youth with T1D and T2D attending a multidisciplinary diabetes clinic from January to December of 2021.

Results
A total of 125 children and adolescents (age: 4-20 years) diagnosed with diabetes were included. Twenty (16%) were African Americans (AA), 81 (65%) Hispanic (H), 23 (15%) non-Hispanic White (NHW), and 1 (0.8%) Asian (A). The mean HbA1c in the cohort was 9.07%. HbA1c in AA patients was 12.9% (SD + 3.11), in Hispanics 8.64% (SD + 2.28), and 9.00% (SD + 1.84) in NHW. Seventy percent of AA patients had an A1c&gt; 9%, compared to 36% of Hispanics and 48% of NHW. Use of CGM and IP was 40% and 10% in AA, 79% and 36% in Hispanics, and 82% and 57% in NHW, respectively.

Conclusions
Our study describes recent data on glycemic control and use of diabetes technology among a racially diverse cohort of children and adolescents seen in a multidisciplinary diabetes clinic. Consistent with literature on adults, HbA1c was highest and CGM and IP use were lowest in AA as compared to H and NHW youth. Data was collected during the COVID-19 pandemic, which may have disproportionately impacted AA patients’ economic, social, and personal behaviors that may contribute to diabetes care. These data support the need for multidisciplinary interventions using systems-based and culturally tailored approaches to improve access and use of technology for diabetes management. The current multidisciplinary diabetes clinic is designed to identify high-risk factors and reduce barriers to optimal management of diabetes. Future research will focus on the impact of multidisciplinary intervention on diabetes control through the use of technology, especially for African Americans.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
LBSUN310 Developmental Programming: Gestational Bpa Treatment Leads To Pancreatic Beta Cell Compromise
Authors: Ciarelli Joseph , Sun Haijing , Domke Stephanie , Gregg Brigid , Padmanabhan Vasantha 
Published: November 2022

Abstract
Developmental exposure to endocrine disrupting chemicals (EDC) such as bisphenol A (BPA) have been shown to be associated with many metabolic defects in humans. Studies in animals have documented detrimental effects of fetal exposure to BPA on metabolic variables such as insulin resistance, adiposity, and cardiac function. For instance, developmental exposure of sheep to bisphenol A (BPA), a ubiquitously present EDC, causes insulin resistance and compensatory hyperinsulinemia but the underlying mechanism of it is not fully understood. To determine if pancreatic hyperplasia or hypertrophy contributes to the hyperinsulinemic status and the ontogeny of these effects, pregnant Suffolk sheep were administered daily subcutaneous injections of BPA (0. 05, 0 .5 or 5 mg/Kg BW) in corn oil from days (D) 30-90 of gestation (term 147 days). Controls received corn oil during the same period. Pancreas were taken at Day 65 and 90 of gestation from control and 0.5mg/kg BPA (environmental exposure level)-treated female fetuses, and control and prenatal BPA-treated female offspring at 2 years of age (all 3 doses) during synchronized follicular phase of the cycle. Immunohistochemistry was used to determine beta cell number, size, and islet insulin content. In addition, to determine if the pancreas was fibrotic, islet collagen content was determined by Picro Sirius red staining and whole pancreas collagen content was measured with scroll collagen assay. Data were analyzed by ANOVA (Y2) and Students's t-test (D65 and D90), and magnitude of response by Cohen's Effect Size analysis. Findings showed large magnitude reduction of islet insulin content at day 65, significant decrease in islet insulin and beta cell count at D90 along with large magnitude decrease in pancreas/fetal weight. In contrast, in the Y2 sheep prenatal BPA treatment induced a large magnitude decrease in beta cell count (0. 05mg/kg dose group), a large magnitude increase in islet insulin content (5mg/kg dose group) and large magnitude increase in islet collagen content (all 3 BPA doses). The decrease in insulin in the D65 and D90 sheep along with the decrease in beta cells and pancreas/fetal weight at D90 indicates adverse developmental impact of BPA exposure on pancreatic beta cell differentiation. Increase in collagen accumulation in Y2 sheep likely contributes to the beta cell loss reflected as decrease in beta cell number seen in 0. 05 mg/kg dose of BPA. Absence of beta cell loss in 0.5 and 5mg/kg dose in the face of increased collagen is consistent with the nonmonotonic responses these EDCs manifest. Taken together, these results highlight the risks posed by developmental exposure to BPA on beta cell function and the corresponding risk for beta cell loss as animals age. Supported by NIH R01 grants ES016541 and ES030374
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
ODP263 A Nonbiased Single-Cell Transcriptomic Analysis of Mouse Mammary Gland after Low Dose/Long Term vs. High Dose/Short Term Exposure to PBDEs
Authors: Saeki Kohei , Chang Gregory , Mori Hitomi , Ha Desiree , Yoshitake Ryohei , Wang Xiaoqiang , Tzeng Tony , Shim Hyunjeong , Neuhausen Susan , Chen Shiuan 
Published: November 2022

Abstract

Introduction
Polybrominated diphenyl ethers (PBDEs) are persistent environmental contaminants and associated with breast carcinogenesis. In this study, we examined the effects of PBDEs during the menopausal transition in a 4-vinylcyclohexene diepoxide (VCD)-induced mouse menopause model, which presents a follicle-depleted and ovary-intact animal that closely approximate the gradual menopause transition in humans. The aim of this study was to compare the impacts of PBDE exposures on the mammary gland at the macroscopic gland structures and the single-cell resolution under three treatment schedules.

Materials and Methods
We treated nine-week-old female C57BL/6 mice with VCD (160 mg/kg) for 15 days. Then, the animals had high dose PBDE exposure for 1 week during peri- (Perimenopause/High group) or post-menopausal periods (Menopause/High group). The third group was exposed to low dose PBDE (the 1/20th of the high dose) for 20 weeks during the postmenopausal period (Menopause/Low group). In each group, the mice received various combinations of 17B-estradiol and progesterone treatments simultaneously. Our experimental design allowed us to directly compare the effects of PBDE under three potential exposure conditions.

Results
The mammary glands significantly regressed by the VCD treatment, more evident at the postmenopausal period. All PBDE exposures did not augment or compromise the macroscopic ductal reorganization resulting from the VCD and/or hormonal treatments. Single-cell sequencing revealed that the PBDE exposure in the Menopause/High group caused specific transcriptomic changes in the non-epithelial compartment such as Errfi1 upregulation in fibroblasts and AY036118 downregulation in multiple cell types. The PBDE exposure in the Menopause/Low group resulted in similar transcriptomic changes to a lesser extent.

Conclusion
PBDEs may affect the postmenopausal gland through impacts on the non-epithelial compartments. Low dose PBDE exposure, which is presumably equivalent to the maximum environmental exposure in humans, can exert the influences.
Presentation: No date and time listed
ODP265 Bph, Androgenic Alopecia, and Acne - Markers of Progesterone Deficiency
Authors: Kalinchenko Svetlana , Nikiforov Igor , Samburskaya Olga 
Published: November 2022

Abstract

Materials and methods
The study at this stage involves 6 male patients from 21 to 50 years with the diagnosis: BPH. Androgenic alopecia. Acne disease. All patients were examined for vitamin D in the blood by calcidiol 25(OH)D using mass spectrometry and steroid hormone levelsusing a steroid profile in saliva by mass spectrometry. Findings. Vitamin D level in three patients was below 30 ng/ml, in three patients - below 20 ng/ml. The steroid profile in the saliva of all six patients revealed progesterone deficiency, with normal testosterone levels. Patients were prescribed vitamin D in a dose of 20,000 IU daily and progesterone in a dose of 100 mg daily; patients with acne were additionally prescribed topical treatment - progesterone in gel form. As a result, after 6 months of using this therapy, patients have a cessation of hair loss, growth of downy hair and transition of downy hair to terminal hair,improvement in all patients was 80-90%. Two patients with the papulopustular form of moderate acne improved by 90%, a patient with the conglobate form improved by 50% (transition to the papulopustular form of moderate severity). Improvement of clinical picture of symptoms of BPH is also noted: decrease of IPSS questionnaire score to 7-9. Vitamin D level from 70 to 100 ng/ml. On the steroid profile of saliva, the levels of testosterone and progesterone are within normal limits. Interpretation. The main cause of androgenetic alopecia, acne, BPH is thought to be: an excess of DHT (dihydrotestosterone), increased activity of 5-α-reductase enzyme. These three diseases accompany each other. The main drug which is used 5-α-reductase blockers. The side effects of which greatly exceed the benefitsof treating. Vitamin D is involved in regulation of proliferation, differentiation and apoptosis of keratinocytes, regulation of skin immunity, regulation of pro-inflammatory cytokines, stimulation of the expression of antimicrobial peptides, regulation of the integrity and permeability of the lipid barrier, reducing the severity of systemic inflammation, regulation of cellular, humoral, congenital and acquired immunity. Also, in an in vitro study it was found that progesterone can inhibit the activity of 5-α-reductase, so in the skin the activity of this enzyme is reduced by 97±5.3%. And the positive effect was also established in the treatment of prostate diseases, inhibiting 5-α-reductase, progesterone reduces the growth of the prostate gland and the growth of prostate cancer cells.

Conclusion
Laboratory studies have shown vitamin D and progesterone deficiencies in patients with these diseases. Correction of these deficiencies resulted in improvement both in BPH (reduction of clinical manifestations) and in androgenic alopecia (cessation of hair loss and restoration of terminal hair growth) and acne (significant reduction of inflammation).
Presentation: No date and time listed
ODP274 Shift work is associated with normal weight obesity in community-dwelling adults
Authors: Ahn Chul Woo , Hong Namki , Lee Seunghyun , Park Hye-Sun , Rhee Yumie , Shin Sungjae 
Published: November 2022

Abstract

Objective
Shift working is known to be associated with metabolic syndrome and increased cardiovascular risk. In this study, we aimed to investigate whether shift work is associated with normal weight obesity (NWO), defined as normal weight with high body fat percentage. Method: From the national representative Korea National Health and Nutrition Examination Survey dataset (KNHANES 2008-2011), data of 3800 full-time workers with age≥ 19 years and body mass index (BMI)≤ 25 kg/m 2 were analyzed. In this study, we defined NWO was defined as BMI≤25 kg/m 2 and body fat (BF)percentage≥25% in men and≥37% in women according to the most strict threshold from literature review. Working patterns were classified into 'daytime', 'other than daytime', and 'shift time' based on the self-reported survey data. Multivariable logistic regression was performed to evaluate the relationship between shift time workers and NWO. Prespecified subgroup analysis were analyzed to determine the consistency of the result. Result: Shift work was associated with elevated odds of NWO than daytime work (adjusted odds ratio [aOR] 1.47, 95% CI 1. 04-2. 09) and night/evening work (aOR 1.87, 95% CI 1.11-3.14), after adjustment for working form, working hours, age, sex, BMI, vitamin D, homeostatic model assessment for insulin resistance, and other sociodemographic factors. In the subgroup analysis, association between shift work and NWO were consistent, and, those age ≥ 60 years (aOR 2.23, p=0. 043; p for interaction=0. 097) or working hours ≥ 56 hours per week (aOR 2. 00, p=0. 013; p for interaction=0. 057) showed a tendency to increase the risk.

Conclusion
Shift working was associated with NWO in Korean community-dwelling adults, independent of age, sex, BMI, and other covariates. Keywords: Shift work, Obesity, Normal weight obesity, Body fat percentage, KNHANES
Presentation: No date and time listed
PMON12 Effects of Endocrine Disruptors on Autophagy Markers Gene Expression in Immortalized GnRH Neurons and Hypothalami of Adult Male Mice
Authors: Fernandez Marina , Gomez Juan Manuel Riaño , Sorianello Eleonora , Lux-Lantos Victoria 
Published: November 2022

Abstract
Benzophenones (BP) and Bisphenol A (BPA) are endocrine disrupting chemicals (EDC). Previously, we showed that the in-vitro exposure to EDC inhibited Kiss-induced gene expression in GT1-7 and GN11 cells (donated by Pamela Mellon, UCSD), and altered expression of inflammatory markers in GT1-7 cells and hypothalami of adult male mice.In the present study, we evaluated the effects of the in-vivo exposure to BP2 and BP3 (250 µg/kg/day, orally, for 5 days) on the expression of autophagy markers in hypothalamic nuclei in C57Bl/6 adult male mice, and the in-vitro exposure to BPA, BP2 or BP3 in immortalized GnRH neurons. Animals were sacrificed, brains rapidly dissected and conserved -80°C until processed. Micropunches containing Anteroventral Periventricular (AVPV) or Arcuate (ARC) nucleus were obtained. Effects of the in-vitro exposure for 12 or 24 hours to BPA, BP2 or BP3 (1×10-9M, Sigma), or DMSO as control, were evaluated in GT1-7 and GN11 cell lines, mature and immature GnRH neurons. ARN was obtained using Tri-Reagent (Molecular Research Center, Inc), reverse-transcribed and gene expression analyzed by qPCR, using Ppib as control gene. Results were presented as Media±SE and analyzed by ANOVA (Statistica, StatSoft Inc, USA).In-vivo, five-day exposure to BP2 or BP3 did not alter Lamp2 or p62 gene expression in the AVPV or ARC in adult male mice (ANOVA: ns). In GT1-7 cells, Ulk1 was not significantly altered by any of the stimuli (ANOVA: ns; n=5), whereas in GN11 cells, BP3 significantly increased Ulk1 gene expression after 12 and 24 h exposure [DMSO-24h: 0.93±0.21, DMSO-12h: 0.73± 0.19, BPA-24h: 1.78±0.31, BPA-12h: 1.47±0.33, BP2-24h: 1.51±0.49, BP2-12h: 1.06±0.23, BP3-24h: 2.41±0.89, BP3-12h: 2.45±0.82, Repeated Measures ANOVA: Main effect "TREATMENT" p&lt;0.05, BP3 different from DMSO, p&lt;0.05, n=4]. Our results reinforce the notion that the exposure to EDC have different effects depending on the experimental model and time of exposure, with developing cells being more susceptible to disruption that mature cells. We need more experiments to fully understand if exposure to EDC alters other markers of the autophagy process in mouse hypothalamus and GnRH neurons.Funding: CONICET, ANPCYT, International Society for Neurochemistry, Fund. Williams, Fund. R. Barón.
Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.
PSAT161 Effect of Hyperlipidemia and Statin Use on the Risk of Dementia and Functional Dependence in the Vietnamese Immigrants
Authors: Na Kim Yu , Arif Saleena 
Published: November 2022

Abstract
The role of cholesterol in the etiology of dementia is still controversial. Some studies aiming to explore the association between lipids and/or lipid-lowering treatment and dementia indicated a harmful effect of dyslipidemia and a beneficial effect of statin therapy on the risk for dementia. Still, it is not well studied in the Vietnamese population. We sought to evaluate the impact of hyperlipidemia and statin use on the risk of dementia and functional frailty in Vietnamese immigrants.We identified 38(female(F) 26, male(M) 12) community-dwelling Vietnamese patients aged ≥ 55 seen at the cognitive assessment clinic in a community health center 1/2021-8/2021 through chart review. This cohort's mean age(±SD) was 72.3(±9.35). Because lipid panel results were unavailable, 1 patient (F 1) was excluded. We assigned the patients with normal cognitive tests results or a diagnosis of mild cognitive impairment to the control group and those diagnosed with dementia to the study group. To assess function, we obtained ADLs (activities of daily living) and IADLs (instrumental activities of daily living). This study defined hyperlipidemia (HLD) as LDL &gt;100 and functional dependence as dependence in ADLs and/or IADLs.Among 37 patients (F25, M12), 21 patients were diagnosed with dementia (F15, M 6), and 16 patients (F10, M6) were assigned to the control group. In the study group, 19 patients (F13, M 6) were diagnosed with HLD, and 13 patients (F 8, M 5) were taking statins. Fifteen patients (F 10, M 5) were diagnosed with HLD, and 14 patients (F9, M5) were taking statins in the control group. Thirty-three patients (F 23, M 10) were functional dependent. Among them, 31 patients (F 21, M 10) were diagnosed with HLD, and 24 patients (F 15, M 9) were taking statins. Four patients (F 2, M2) were functionally independent, and 3 patients (F 2, M1) were diagnosed with HLD, and all of them were taking statins.The persons with HLD had an about 12% reduction in risk of dementia (RR 0.8382, P=0.6855), but they were about 37% likely to develop functional dependence (RR 1.3676, P=0.4470). Statin users had a nearly 40% reduction in risk of dementia (RR 0.6019, P=0.0462) but the risk for developing functional dependence was not significantly different from non-users (RR 0.9877, P=0.9211). These findings suggested statin treatment has a beneficial effect on decreasing the risk for dementia in patients with HLD, and HLD has a harmful impact on developing functional frailty. This study showed a risk reduction of dementia in patients with HLD, which was different from other study results. More studies with a larger number of patients in this cohort are needed to investigate this further.
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
ODP281 JDP2 Interacts with MDM2 and Decreases MDM2-Mediated p53 Repression
Authors: Yang William , Wang Chiung-Min , Yang Richard , Yang Wei-Hsiung 
Published: November 2022

Abstract
JDP2 and ATF3 belong to the family of AP-1 protein. JDP2, a transcription factor, can bind to AP-1 site as well as cAMP responsive element (CRE) site in numerous cis-elements of the target genes. JDP2 has been shown to be involved in cancer development and cell-cycle regulation. Previously, we had shown that JDP2 activates Mc2r transcriptional activity. Since ATF3 and JDP2 share high similarity in C-terminal domains with identities of 65% and ATF3 can bind to p53 and regulate p53 transcriptional activity and stability, we hypothesized that JDP2 may have ability to regulate p53 and MDM2 (the main regulator of p53). Herein, we demonstrate for the first time the relationship between JDP2 and MDM2. First, we found that JDP2 can directly bind to MDM2. Secondly, though ATF3 dose-dependently increases MDM2 level, JDP2 dose-dependently decreases MDM2 level. Moreover, the C-terminus of JDP2 is required for regulation of MDM2 level. Finally, using p53RE-Luc (14X) for p53 transactivation study, while MDM2 decreases p53 transactivation, JDP2 dose-dependently abolishes MDM2-mediated p53 repression. Taken together, our results demonstrate that JDP2 directly binds to MDM2 and reduces MDM2-mediated p53 repression, suggesting that JDP2 is a novel regulator of MDM2. Since p53-MDM2 pathway is an important regulator in endocrinology and reproduction, our finding provides a new layer of regulatory mechanism for fertility, tumor suppression, and longevity.
Presentation: No date and time listed