bluuebunny/crossref_metadata_2025_split huggingface dataset:
SAT051 The Effect Of High Fat Diet On Insulin Signaling In White Adipose Tissue Of Liver Androgen Receptor Knockout In Male Mice
Authors: O'neil Hill-Dick Johvan , Young Demarrius , Curry Dwight , Bolarinwa Elizabeth , Qutab Rabia , Carr Kiana , Falzarano Claire , Andrisse Stanley 
Published: October 2023

Abstract
Disclosure: J.O. Hill-Dick: None. D. Young: None. D. Curry: None. E. Bolarinwa: None. R. Qutab: None. K. Carr: None. C. Falzarano: None. S. Andrisse: None.
Insulin resistance affects up to 33% of the US adult population and polycystic ovary syndrome affects up to 10% of reproductive-age adult women. The liver and white adipose tissue play an essential role in the metabolism of insulin and androgen signaling. Hyperandrogenism in females can increase their predisposition to insulin resistance. It has been previously shown that deleting the liver androgen receptor (LivARKO) prevented female mice from developing hyperandrogenemia (HA)-induced insulin resistance. The goal of this research was to determine if LivARKO prevents high fructose diet (HFrD) induced insulin resistance. It was hypothesized that HFrD LivARKO male mice would display impaired insulin action in white adipose tissue in comparison to the control diet-fed LivARKO female mice, suggesting that AR does not play a significant role in regulating HFrD-induced insulin resistance. Male LivARKO mice were placed on either a control (Research Diets Inc, RDI D12450J) or High Fructose (HFrD, RDI D02022704) diet and sacrificed after 1 month. Half of the mice were given 0.5 U/kg of insulin before being sacrificed to investigate the effects of the diets on insulin signaling. Western blots were used to determine protein expression in tissue from the white adipose tissue (WAT) standardized using BCA assays. LivARKO male mice fed a chow or control diet for 1 month displayed no or low expression of p-AKT in the basal and insulin-stimulated state, suggesting that LivARKO had an indirect effect on insulin-stimulated signaling in WAT. Oddly, LivARKO male mice fed a HFrD displayed increased insulin-stimulated p-AKT compared to basal, suggesting functional insulin-stimulated p-AKT. This increased p-AKT may be a compensatory mechanism as HFrD is known to disrupt glucokinase and glycogen synthase. In normal physiology, on a chow diet, insulin should increase p-AKT. The data shows that in male LivARKO mice, insulin did not increase p-AKT in chow, control, or HFrD, suggesting that the male LivARKO mice are experiencing insulin resistance at the level of p-AKT in WAT. Additionally, HFrD is known to cause insulin resistance, however, it is not known to alter p-AKT levels. Thus, the change in p-AKT levels is presumably associated with the LivARKO. Further research is required into what components of the Control Diet are prompting this difference in insulin action and if it only takes place in the LivARKO mouse model.
Presentation: Saturday, June 17, 2023
SAT060 Hyperosmolar Hyperglycemic State Presenting As Seizures
Authors: Faber Alexis , Levy Shiri 
Published: October 2023

Abstract
Disclosure: A. Faber: None. S. Levy: None.
Introduction: Hyperosmolar hyperglycemic state (HHS), also known as hyperosmotic hyperglycemic nonketotic state (HHNK), is one of the most severe complications of diabetes mellitus. HHS is a medical emergency defined by high serum osmolality and hyperglycemia as well as the absence of ketoacidosis in most cases. We present an unusual case of a young man presenting with seizures who on further investigation was found to have HHS. Case Description: A 44-year-old man presented to the hospital for a possible seizure at home. His medical history is significant for EBV+ B-cell lymphoma receiving chemotherapy, HIV on HAART therapy, and prior history of cryptococcus meningitis in 2019. He did not have history of seizures or diabetes mellitus. He reported that five days prior to admission, he began experiencing polydipsia and polyuria, which later progressed to lethargy. The day of admission his mother found him on the floor with generalized body shaking with significant shaking of the right arm, urinary incontinence, and blood in his mouth from tongue biting. He was taken to the hospital due to concern for seizure. Workup revealed elevated blood glucose of 972 and elevated serum osmolality of 322. He did not present with overwhelming ketosis; his beta-hydroxybutyrate was 0.57, he did not have an anion gap, and ketones were not present in his urine. His A1c was elevated at 9.9%. The differential diagnosis for this patient’s seizure included chemotherapy side effect, intracranial pathology, infectious etiology in the setting of known HIV, or HHS. Hematology evaluated the chemotherapy regimen and stated it was not likely the cause of his seizures. Neurology assessed the patient with a CT head, MRI brain, EEG, and lumbar puncture, all of which were negative. The CSF from the lumbar puncture underwent intensive testing, which was negative for HSV, VDRL, CMV, EBV, VZV, Lyme disease, and JC virus. Neurology initially started the patient on anti-seizure medication, however later stated his seizure was likely provoked from hyperglycemia and discontinued the medication. Infectious workup included chest X-ray, blood cultures, and urinalysis, all of which were negative. Endocrinology was consulted and recommended initiating basal and bolus insulin as well as testing for GAD antibodies. Unfortunately, the patient left the hospital against medical advice and GAD antibody testing was not completed. Discussion: The most common symptoms of HSS include hyperglycemia, polyuria, and polydipsia. Though neurological symptoms can occur, they are not common. The neurologic symptoms are typically not seen until the serum osmolality reaches 320 - 330 mOs/kg, and this patient’s serum osmolality was elevated at 322 mOs/kg. Though seizure is not well understood in hyperglycemia, treatment for HHS-induced seizures focuses on aggressive management of the underlying hyperglycemic state.
Presentation: Saturday, June 17, 2023
SAT072 Choline Deprivation Aggravates Hyperglycemia And Fatty Liver In Non-obese Streptozocin-induced Diabetic Rats
Authors: Liapi Charis , Kyriakaki Argyro , Al Humadi Hussam , Al-Saigh1 Rafal , Al Humadi Ahmed , Lazaris Andreas 
Published: October 2023

Abstract
Disclosure: C. Liapi: None. A. Kyriakaki: None. H. Al Humadi: None. R. Al-Saigh1: None. A. Al Humadi: None. A. Lazaris: None.
Background: Choline deprivation (CD) is an established model of steatohepatitis. There is a strong association between non-alcoholic fatty liver disease and diabetes mellitus that has a significant impact on the global health system. The combined state of CD and diabetes can resemble common cases in clinical practice including parenteral nutrition, pregnancy, chronic liver disease malnutrition and/ or alcoholism in diabetic individuals. The aim of this study was to investigate the effects of choline deprivation on glycemic control, insulin signaling pathway and lipid metabolism in non-obese streptozocin-induced diabetic rats. Methods: Thirty-two male adult Wistar rats were divided into four groups; control, diabetes (DM), choline-deprived diet (CDD), and combined group (DM+CDD); DM was induced by intraperitoneal streptozotocin administration. Body weight, fasting blood glucose and plasma insulin levels, lipid profile, liver biochemistry, liver histopathology and gene expression of insulin receptor (IR), insulin receptor substrate-1 (IRS-1), glucose transporters 2 & 4 (GLUT-2 & -4) in hepatic tissue, were assessed. Results: The combination group (CDD+DM) showed a significant increase in blood glucose associated with a significant decrease in plasma insulin level and evidence of dyslipidemia with a significant increase in liver enzymes, histopathology showed extensive micro- and macrovesicular steatosis and a significant decrease in weight gain versus the control, CDD and DM group. A significant increase was observed in gene expression of IR, IRS-1, GLUT-2, and GLUT-4 in all the experimental groups versus the control. Conclusion: The combination of choline deficiency and diabetes has drawn some new scenarios on insulin and some hepatic metabolic pathways: (i) plasma insulin resistance with progressive hyperglycemia and hyperlipidemia.(ii) attenuation of hepatic insulin resistance or sensitization of insulin signaling pathways in the liver, due to the hepatotoxic effects of choline deficiency that could ultimately simulate features of the metabolic syndrome, and (iii) experimentally simulation of metabolic conditions seem to act synergistically, leading to poor glycemic control along with aggravation of hepatic steatosis.
Presentation: Saturday, June 17, 2023
SAT073 β Cell FFA2 Deficiency Suppresses Multiple Low Dose Streptozotocin (MLDS) Induced Diabetes
Authors: Xu Kai , Priyadarshini Medha , Kumar Prabhakaran , Electricwala Husena M , Prabhakar Bellur S , Layden Brian T 
Published: October 2023

Abstract
Disclosure: K. Xu: None. M. Priyadarshini: None. P. Kumar: None. H.M. Electricwala: None. B.S. Prabhakar: None. B.T. Layden: None.
Gut microbiome is recently recognized environmental factor in pathogenesis of type 1 diabetes (T1D). Reduced short chain fatty acid (SCFA) producing gut bacteria and also SCFA levels correlate with T1D risk (TEDDY study). We have previously shown that FFA2 is one of the main SCFA receptors, which is expressed on the β cell and mediates gut microbiome-β cell crosstalk. Based on these data, we hypothesized that β cell FFA2 may play a role in T1D β cell pathology. To examine this, we followed our novel tamoxifen induced β cell FFA2 knockout mice (FFA2 fl/fl; MIP CreERT+, FFA2 BKO) and wildtype littermates (FFA2 fl/fl) after multiple low dose streptozotocin (MLDS) induced T1D. Comparing to wildtype littermates, FFA2 BKO were significantly protected from MLDS insult and exhibited normal glycemic control owing to higher β cell mass. To understand the mechanism of this protective effect, we mined islet transcriptome data from our FFA2 global knockout mice and identified markedly upregulated type 1 interferon pathway in FFA2 global knockout. Accordingly, wildtype islets treated with high dose IFNα (mimicking T1D like conditions) showed significant upregulation of IFNαtargets while FFA2 BKO islets were unresponsive. Using pharmacological inhibition in isolated islets, we identified FFA2 mediated inhibition of NF-κB activation as a critical event in FFA2 mediated regulation of IFNαsignaling. In vivo studies with IFNAR1 antibody showed partial rescue of wildtype mice in the early stages of MLDS induced T1D. Thus, we propose a key role of β cell FFA2 in preserving β cell mass from IFNα signaling mediated damage in T1D. Further studies are needed to test this model.
Presentation: Saturday, June 17, 2023
SAT082 Utility Of A MODY Probability Calculator As A Systemwide Surveillance Tool
Authors: Awad Dana , Hashmi Sulman , Kunwar Sandeep , Desouza Cyrus V 
Published: October 2023

Abstract
Disclosure: D. Awad: None. S. Kunwar: None. C.V. Desouza: None.
Introduction: Maturity-onset diabetes of the young (MODY) is often misdiagnosed as type 1 or type 2 diabetes and is estimated to occur between 1-3% of all cases of diabetes. This leads to unnecessary treatments. There are no systemwide surveillance tools to identify these patients.Methods: This is a single center, cross sectional probable prevalence study of MODY in University of Nebraska medical center (UNMC). The medical records for all outpatients seen at UNMC within the past 5 years with the diagnosis of type 2 DM were reviewed. We included those with a diagnosis of type 2 DM who were &lt;35 years old at the time of diagnosis, had A1C of &lt; 7.6% and had a body mass index (BMI) &lt; 30. We identified a total of 129 patients. 61 were excluded as they did not meet criteria. On the 68 remaining patients, the risk of MODY was calculated using the MODY probability calculator, which was developed by Exeter university. The calculator has the following variables: Age at diagnosis, current age, A1C, BMI, current diabetes treatment, time to insulin treatment, family history of diabetes, ethnicity, other associated features like renal cysts, deafness, lipodystrophy or other syndromic features. Results: Of the 68 included patients, 48% were females and 52% were males. Mean A1C was 6.3%, mean age at diagnosis was 28, mean BMI was 27. Thirty-four had at least one parent with diabetes. 54 were on diabetes treatment (17 on insulin and 37 on oral hypoglycemic agents). On the MODY calculator, 10 patients had a probability score of 75.5%, 3 had a score of 62.4%, 2 had a score of 58%, 3 had a score of 49%, and 3 had a score of 45.5%. The rest had a low probability score. The primary care physicians were informed of these results. The next step is to see how many of the primary care physicians utilize this information to screen patients. Conclusion: The MODY probability calculator is a good systemwide surveillance tool to identify patients with possible MODY and thereby inform providers taking care of those patients, which may result in management changes.
Presentation: Saturday, June 17, 2023
SAT084 Maternally Inherited Diabetes With Deafness: A Rare And Challenging Diagnosis Of Diabetes
Authors: Cuan Katherine , Bass Ilana R 
Published: October 2023

Abstract
Disclosure: K. Cuan: None. I.R. Bass: None.
Introduction: Maternally inherited diabetes with deafness (MIDD) is a rare mitochondrial disease with variable phenotypic expression characterized by a defect in insulin secretion and sensorineural hearing loss. Other potential features of MIDD include proximal myopathy, macular retinal dystrophy, and renal focal segmental glomerulosclerosis. Mitochondrial diseases are difficult to recognize given their heterogeneous presentation, however accurate diagnosis of MIDD is important as there are implications for management. DESCRIPTION: A 38-year-old adopted woman with previously diagnosed type 1 diabetes (T1DM), congenital deafness, and chronic kidney disease presented to our endocrinology clinic with concerns for difficulty controlling her blood glucose levels. She was diagnosed with T1DM at age 21 based on age and normal body habitus and was started on insulin. Due to insurance issues, she discontinued insulin use for several years and her diabetes was poorly controlled during that time, however, she never experienced diabetic ketoacidosis (DKA). Upon resuming insulin, she experienced multiple unpredictable episodes of hypoglycemia and subsequently self-discontinued insulin and presented 8 months later for further care. Past history was notable for muscle weakness with walking upstairs and vision loss in her left eye, which led to a diagnosis of retinopathy in her early twenties. Her family history was unavailable as she was adopted. Her physical exam was significant for a normal body mass index of 24. Labs showed a hemoglobin A1C of 10.8% and detectable c-peptide, 2.7 ng/mL (1.1-4.4 ng/mL) with a glucose of 192mg/dL. Glutamic acid decarboxylase, zinc transporter 8, IA-2 and islet-cell antibodies were all negative. Her creatinine was 1.23 ng/dL with a severely increased microalbumin to creatinine ratio (638, 0-29 mg/g). In view of her congenital deafness, non-diabetic retinopathy, absence of DKA while off insulin, negative antibody testing, and chronic kidney disease, mitochondrial diabetes was considered. She was referred to a geneticist for mitochondrial genome sequencing, of which the results are pending. Dietary modification and oral agents were recommended for her diabetes management, rather than insulin therapy. DISCUSSION: MIDD can be challenging to diagnose and patients may be incorrectly labeled as having type 1 diabetes. The presence of maternal transmission can aid in the diagnosis of MIDD, however, our patient was adopted and this information is unavailable. Additionally, retinal and renal features of MIDD can be misconstrued as microvascular complications of diabetes. In patients with deafness and poorly controlled diabetes with negative antibody testing, MIDD should be considered as an alternative diagnosis. MIDD can be managed with dietary modification, oral agents, and insulin if appropriate.
Presentation: Saturday, June 17, 2023
SAT097 Investigation Of The Minimum Duration Needed To Estimate The Percentile Values For Target Duration In Ambulatory Glucose Profile
Authors: Takeishi Soichi , Inoue Tatsuo 
Published: October 2023

Abstract
Disclosure: S. Takeishi: None. T. Inoue: None.
Ambulatory glucose profile (AGP) is effective in grasping glycemic variability and determining therapeutic strategy. In AGP for intermittently scanned continuous glucose monitoring (isCGM), it is common for patients to intervene at the time when the interquartile range of glucose levels deviates from the target range. It is important to consider the cases having glucose levels with missing values measured using isCGM. There are limited investigations regarding the “minimum duration needed to estimate percentile values of glucose levels for target duration” (MDpercentile). This is a cross-sectional study. In Analysis 1, we analyzed the glucose levels without missing values measured using CGM (FreeStyle Libre Pro) over 24 h for 13 days (from 00:00 on Day 2 to 00:00 on Day 15; CGM attachment: Day 1) for 100 outpatients with type 2 diabetes, who did not change their diabetic treatment through the CGM-wearing duration. In Analysis 2, we analyzed the glucose levels with missing values measured using isCGM (FreeStyle Libre) over 24 h for 60 days (from 00:00 on Day 31 to 00:00 on Day 91; isCGM attachment: Day 1) for 50 outpatients with type 2 diabetes, who did not change their diabetic treatment through the isCGM-wearing duration. In Analysis 1, MDpercentile for the 2-h mean glucose level for 13 days (MDpercentile2h13days) was provided by correlation coefficient analysis using R2=0.9 as the threshold. In Analysis 2, MDpercentile for the 24-h mean glucose level for 60 days (MDpercentile24h60days) was provided by correlation coefficient analysis using R2=0.9 as the threshold. The Pearson’s product-moment correlation coefficient was used for the statistical analysis. In Analysis 1, the average of 12 MDpercentile2h13days in 24 h for 5 percentile values, 25 percentile values, 50 percentile values, 75 percentile values, and 95 percentile values was 7.4, 7.3, 6.9, 6.9, and 5.9 days, respectively. In Analysis 2, the MDpercentile 24h 60 days for 5 percentile values, 25 percentile values, 50 percentile values, 75 percentile values, and 95 percentile values was 26, 17, 15, 13, and 45 days, respectively. In Analysis 1, the lower percentile values needed more days to predict the percentile values. However, in Analysis 2, the 95 percentile value needed the most days to predict the percentile value. Lower percentile values may need more days to predict the percentile values in the calculation using glucose levels without missing values. Quite high percentile values may need many days to predict the percentile value in the calculation using glucose levels with missing values.
Presentation: Saturday, June 17, 2023
SAT112 Ad Libitum Ketogenic Diet Reverts WD-pathological Effects In Liver, But Not In Skeletal Muscle In Mice
Authors: Antonioli Alessandro , Provera Alessia , Reano Simone , Gadipudi Laila Lavanya , Tini Sabrina , Zaggia Ivan , Raiteri Tommaso , Scircoli Andrea , Colasanto Antonio , Raineri Davide , Filigheddu Nicoletta , Sutti Salvatore , Prodam Flavia 
Published: October 2023

Abstract
Disclosure: A. Antonioli: None. A. Provera: None. S. Reano: None. L. Gadipudi: None. S. Tini: None. I. Zaggia: None. T. Raiteri: None. A. Scircoli: None. A. Colasanto: None. D. Raineri: None. N. Filigheddu: None. S. Sutti: None. F. Prodam: None.
Western diet (WD), rich in sugars and saturated fats, is a critical factor contributing to obesity and its comorbidities. Since its effects on insulin resistance and inflammation, WD has been associated with many diseases, such as type 2 diabetes mellitus (T2DM), metabolic fatty liver disease (MAFLD) and steatohepatitis (NASH), and metabolic syndrome (MetS) in both animal and humans. Ketogenic diets (KDs) are nutritional regimens characterized by very low carbohydrate intake, high-fat amounts, and adequate protein content, with or without caloric restriction. Energy is provided by ketone bodies from lipid oxidation and protein metabolism. Since growing evidence suggests that KDs are able to reduce inflammation, oxidative stress, and improving mitochondrial function, we hypothesized that it could be a promising strategy to treat obesity related diseases, including MAFLD and sarcobesity. To demonstrate these effects, after 16 weeks of WD diet, we switched mice to standard diet (SD), ad libitum cholesterol-free KD, or maintained in WD for further 2 and 4 weeks. We demonstrated that both KD and SD are able to revert detrimental effects induced by WD in mouse liver, improving the pathological features and lowering the hepatic inflammatory responses associated with NASH. KD resulted in ketosis and mimicked fasting conditions promoting body weight loss and glycaemic control. However, KD did not have positive effects on skeletal muscle strength, mass, and histologic morphology after WD-induced muscle atrophy. Despite the positive effect on WD-induced liver damage and increased body weight, ad libitum KD does not seem to have protective effects against WD-associated loss of muscle mass and functionality. However, we cannot rule out that muscle might need a longer recovery period than the liver.
Presentation: Saturday, June 17, 2023
SAT115 Diabetes In Pregnancy: Evaluating Access And Usage Of Continuous Glucose Monitors (CGM) In A Medicaid Population
Authors: Chilukuri Pranaya , Llanora Josie , Schadler Aric , Playforth Karen , Naseman Kristina 
Published: October 2023

Abstract
Disclosure: P. Chilukuri: None. J. Llanora: None. A. Schadler: None. K. Playforth: None. K. Naseman: None.
Objective: Diabetes complicates up to 17% of pregnancies in the United States annually. Self-monitoring of blood glucose for diabetics requires supplies, knowledge, and support. Continuous glucose monitor (CGM) use for self-monitoring improves clinical outcomes and patient satisfaction. Despite identified benefits, patient access to CGM is variable. Identifying barriers to CGM access is important to promote health equity. Our objective was to describe CGM prevalence in a pregnant population with diabetes. Study Design: This was a single-center, retrospective observational cohort study using electronic health record review of pregnant patients with diagnoses of Type 1 Diabetes (T1DM), Type 2 Diabetes (T2DM), or gestational diabetes (GDM). Patients ages 18 to 50 years with state Medicaid insurance, for whom CGM is a covered benefit, were considered if seen in any of our institution’s obstetrics clinics within a one-year period. Type of diabetes, race/ethnicity, primary language, home county, medication use, and CGM orders were abstracted. Pearson’s Chi-square, Fisher’s exact, and independent samples t-tests were used for analysis. Results: Of 297 total patients, 7.7% (n=23) had T1DM, 22.2% (n=66) had T2DM, 68.4% (n=203) had GDM, and 1.7% (n=5) had another type. Overall, 19% (n=55) had reported CGM use. There was no difference in CGM use for non-white vs. white race (p=0.081) and urban vs. rural home county (p=0.138). Significantly less non-English speaking patients (p=0.001), Hispanic patients (p=0.026), Metformin users (p=0.03), and those not taking medications (p&lt; 0.001) used CGM. Significantly more T1DM (p&lt; 0.001), T2DM (p=0.007), and insulin-using patients (p&lt;0.001) were in the CGM group. Conclusion: In patients with insurance coverage of CGM, awareness of actual usage is key. Social factors of ethnicity and primary language and clinical factors of diabetes type and medication use may affect CGM use. Obstetricians should advocate for equal CGM access for high-risk patients to improve patient outcomes and satisfaction.
Presentation: Saturday, June 17, 2023