bluuebunny/crossref_metadata_2025_split huggingface dataset:
1288-PUB: Acute Inflammatory Response of Breaking Up Prolonged Sitting with Stair Climbing Exercise Snacks
Authors: CABRAL-SANTOS CAROLINA , RAFIEI HOSSEIN , LIRA FABIO S. , LITTLE JONATHAN P. 
Published: June 2021

Understand the acute inflammatory disturbances is important for preventing early diabetes and obesity-related complications. This study aimed to determine whether breaking up prolonged sitting into brief several shorter bouts spread throughout the day (“exercise snacks”) associated a short-term dietary intervention (low- or high-carbohydrate) have the potential to alter the acute inflammatory response. Ten male and female healthy weight (Lean) and overweight-obese (OW) participants were randomized to non-training control group with either low-carbohydrate snack (9h sitting; LC) or matched for total energy high-carbohydrate snacks consumption (9h; sitting) and a high-carbohydrate snacks consumption plus stair-climbing intervention (8X15-30seconds; ACTIVE). The same high-glycemic index meals were consumed at 0, 3 and 6h at each condition. Blood samples were collected at baseline, 180, 360 and 540 minutes to assess Interleukin-6 (IL-6), Tumor necrosis factor-α (TNF-α) and Salivary Immunoglobulin A (SIgA) levels. Mixed models for repeated measures were undertaken to examine differences according to condition x time and with Bonferroni post-hoc test. Change in TNF-α levels was not different within or between conditions from both Lean and OW group (p=0.512). For IL-6 there were a main effect of time at 540min [X2(11)=23.15; p=0.01] only in HC condition for OW group. Regarding to SIgA, Lean group showed higher level of SIgA on Active compared to LC and HC condition in all time-points (p=0.001). In addition, adults with OW showed elevated SIgA levels on LC and HC condition (p=0.001) when compared with same condition from Lean group. Our data suggests that breaking up nine hours of prolonged sitting implicated in reduction of acute inflammatory IL-6 plasma levels. In addition, acute manipulation on diet (low- and high-carbohydrate) resulted in alterations in the response of SIgA, increasing its levels in overweight/obese adults.

Disclosure
C. Cabral-santos: None. H. Rafiei: None. F. S. Lira: None. J. P. Little: None.

Funding
Natural Sciences and Engineering Research Council of Canada; Fundação de Amparo a Pesquisa do Estado de São Paulo (2018/17648-7)
155-LB: Counterregulatory Response to Hypoglycemia after Short-Term Use of Low and Very Low Carbohydrate Diets in Children with Type 1 Diabetes (T1D)
Authors: FOX LARRY , PERMUY JOSEPH W. , SANTIAGO DELIAMILLE PEREZ , FOX MARY LOUISE , HOSSAIN MD JOBAYER 
Published: June 2021

Background: Low carbohydrate (CHO) diets are used to improve diabetes control, but the safety of these diets has not been studied in children. We assessed counterregulatory response to hypoglycemia after short-term low (LC) or very low (VLC) CHO diets in children with T1D.
Methods: Epinephrine (epi), norepinephrine (NE), glucagon (gluc), and beta-hydroxybutyrate (BOHB) were measured before and immediately after becoming hypoglycemic at baseline and after 3 months on a LC or VLC diet (CHO made up 30-39% or 20-29% of total daily calories, respectively). 13 children were enrolled, mean (±SE) A1c 7.8±0.2%, diabetes duration 6.3±1.0 yrs. Participants were given sufficient insulin to decrease glucose to &lt;60 mg/dL (&lt;3.3 mmol/L). Continuous glucose monitoring (Dexcom® G5 or G6) was used to monitor glucose trends. Hypoglycemia was confirmed using a plasma glucose analyzer.
Results: Mean age (±SE) for LC and VLC, 10.5±1.7 (n=7) and 15.0±0.6 yrs (n=6), respectively. Epi increased in response to hypoglycemia at baseline in both groups (mean±SE increase, pg/mL) (LC 130.9±60.1, p=0.072; VLC 412.6±84.0, p= 0.008). At 3 mos Epi increased in LC (181.6±66.7, p=0.053) but not significantly in VLC (100.2±67.9, p=0.214). The change in Epi in response to hypoglycemia was significantly less at 3 mos vs. baseline in VLC (100.2±67.9 vs. 412.6±84.0, p=0.019) but not in LC (181.6±66.7 vs. 191.4±61.7, p=0.935). Change in NE, gluc and BOHB during hypoglycemia was similar in both groups when comparing 3 months of diet with baseline. There was no effect of diet when comparing baseline and 3-month changes in Epi, NE, gluc and BOHB in response to hypoglycemia.
Conclusion: Short-term use of a diet very low in CHO in children with T1D may adversely affect counterregulatory response to hypoglycemia, whereas LC diet did not affect response. Further studies are needed to confirm these findings and to assess whether these diets affect growth and development in young children.

Disclosure
L. Fox: None. J. W. Permuy: None. D. Perez santiago: None. M. Fox: None. M. Hossain: None.

Funding
Nemours Research Programs; Dexcom, Inc.
168-LB: Latent Autoimmune Diabetes in Youth (15–29 Years Old): The Heavier End of an Autoimmune Disease Spectrum
Authors: CHENG JIN , TANG XIAOHAN , YAN XIANG , LUO SHUOMING , LI XIA , ZHOU ZHIGUANG 
Published: June 2021

Context: Latent autoimmune diabetes in youth (LADY) falls in a grey zone of the current diabetes scheme due to the lack of established definition and diagnosis criteria.
Objective: To investigate the prevalence and clinical features of LADY patients between 15-29 years old as a component of an age-related continuous diabetes spectrum.
Methods: This nationwide, multi-center, cross-sectional study included 1803 newly diagnosed diabetic youth of 15-29 years old across China from April 2015 to October 2017. Glutamic acid decarboxylase autoantibody (GADA) was screened in 1508 phenotypic T2DM subjects and those with positive GADA were defined as LADY. Metabolic status, insulin resistance and residual β-cell function of LADY were investigated and compared with other 658 adult-onset latent autoimmune diabetes (LADA) patients enrolled at the same time. The age-related characteristics of the latent autoimmune diabetes spectrum were explored.
Results: LADY accounted for 7.9% (119/1508) of the phenotypic T2DM youth. Compared with GADA-negative T2DM youth, LADY patients had better metabolic control, less insulin resistance, and lower levels of β-cell function, which were closely related to their GADA levels (all P &lt; 0.05). After stratifying LADA patients according to their age of onset, the GADA level decreased across the LADY, ‘Y-LADA’ (young LADA, age of onset &lt;60 years old) and ‘E-LADA’ (elderly LADA, age of onset ≥60 years old) groups, with the prevalence of metabolic syndrome, levels of insulin resistance and residual β-cell function presenting an increasing trend (all P &lt;0.05).
Conclusions: A high prevalence of LADY exist in phenotypic T2DM youth. The latent autoimmune diabetes occurred at different ages formed a continuous clinical spectrum from LADY to LADA, in which the LADY patients carried heavier autoimmune load.

Disclosure
J. Cheng: None. X. Tang: None. X. Yan: None. S. Luo: None. X. Li: None. Z. Zhou: None.

Funding
National Science and Technology Infrastructure Program (2013BAI09B12, 2015BAI12B13); National Key R&D Program of China (2016YFC1305000, 2017YFC1309604)
169-LB: Type 1 Diabetes Mellitus and Stiff-Person Syndrome
Authors: ARAÚJO CÁTIA A. , BAPTISTA CARLA , PAIVA ISABEL , MORGADINHO ANA 
Published: June 2021

Introduction: Type 1 diabetes mellitus (T1DM) is often associated with other autoimmune diseases. One of them is Stiff-Person Syndrome (SPS), a rare neurological disorder characterized by muscle spasms and progressive muscle stiffness, which most often affects females. Glutamic acid decarboxylase antibodies (anti-GAD) are associated with the pathogenesis of this disease as well as T1DM. These antibodies cause a deficit in the synthesis of γ-aminobutyric acid (GABA) that is essential both in the function as neurotransmitter and in the secretion of insulin in pancreatic β cells.
Clinical case: We present the case of a 32-year-old female patient diagnosed with T1DM at 18 years old. Currently under intensive functional insulin therapy and flash glucose monitoring (FGM). Since 2019 with subcutaneous insulin infusion system. At the age of 26, the patient reports dystonia in the left lower limb with subsequent involvement of the contralateral lower limb, upper limbs, trunk and face. Collaboration was made with the Neurology department. Among the laboratory findings, of note: positive serum anti-GAD65 (5437 U/mL; &lt;1) and positive cerebrospinal fluid anti-GAD65 (126.23 U /mL; &lt;1). The diagnosis of SPS was made. The patient started human immunoglobulin therapy with progressive clinical improvement. Estimated HbA1c from FGM was 6,8 % at February, 2021.
Discussion: The association between T1DM and SPS is frequent. In this case, a patient with a known history of T1DM was presented, but cases of diagnosis of T1DM in patients with SPS have also been described. About 43% of patients have T1DM at the time of diagnosis of SPS. Anti-GAD are involved in the pathophysiology of these two diseases and anti-GAD titers are much higher in cases of association with SPS (about 50 to 100 times). In the treatment of patients with T1DM, physicians should be alert to the onset of other autoimmune diseases and active surveillance is essential for early diagnosis.

Disclosure
C. A. Araújo: None. C. Baptista: None. I. Paiva: None. A. Morgadinho: None.
171-LB: Stress Hyperglycemia Is Associated with Higher Preadmission Glucose and Post-Discharge Diabetes Incidence
Authors: FANG SHUYANG , AIYEDIPE SAMUEL , KHAKHARIA ANJALI , GIRALDI ERICA , EASLEY KIRK A. , PHILLIPS LAWRENCE S. , RHEE MARY K. 
Published: June 2021

Stress hyperglycemia is associated with worse outcomes, but its associated risks and contributors are not well known. We evaluated characteristics associated with high inpatient random plasma glucose levels (RPG) in a retrospective cohort of the national VA Health Care System. Patients were age ≥18 yrs, without diagnosed diabetes (DM), hospitalized ≥3 days in 2002-2014 with ≥2 RPGs, and had regular care ≥2 yrs before and ≥3 yrs after hospitalization. In 205,270 pts, mean age was 73.8 yrs and BMI 28.0 kg/m2; 96% were male, 75% white, 16% black. Second highest inpatient RPG levels (iRPG-2max) of &lt;130, 130-139, 140-159, 160-179, 180-199, and ≥200 mg/dl were found in 63%, 10%, 13%, 6%, 3%, and 4% of patients, respectively, without demographic differences between groups. Those with higher iRPG-2max had longer lengths of stay (LOS; median 5 days with &lt;130 mg/dl vs. 10 days with ≥200, p&lt;0.001), and higher rates of acute kidney injury (AKI; 9.3% with &lt;130 vs. 29.3% with ≥200 group; OR 3.8, 95% CI 3.6-4.0) but no differences in rates of infection. Before admission, higher iRPG-2max groups were more likely to have ≥2 outpatient RPGs (oRPG) ≥130 mg/dl (7.2% with &lt;130 mg/dl vs. 15.2% with ≥200, p&lt;0.001). After discharge, higher iRPG-2max groups had more incident DM within 1 and 3 yrs (1.3% and 3.4%, respectively, with &lt;130 vs. 14.9% and 18.4% with ≥200, both p&lt;0.001). In multivariate analysis, higher iRPG-2max was more likely with oRPG ≥130 mg/dl vs. oRPG &lt;110 (adj OR 1.81, 95% CI 1.75-1.87), and with DM in 3 yrs post-discharge vs. no DM (adj OR 2.52, 95% CI 2.49-2.70).
Conclusion: Patients with outpatient random plasma glucose (RPG) ≥130 mg/dl have a higher risk of stress hyperglycemia, which is associated with longer length of stay, more acute kidney injury, and higher incidence of diabetes after discharge. Thus, patients with ≥2 pre-admission RPGs ≥130 should have inpatient RPGs monitored carefully, and those with high inpatient RPGs should be screened for diabetes for up to 3 years after discharge.

Disclosure
S. Fang: None. S. Aiyedipe: None. A. Khakharia: None. E. Giraldi: None. K. A. Easley: None. L. S. Phillips: Other Relationship; Self; Diasyst Inc., Research Support; Self; AbbVie Inc., Eli Lilly and Company, GlaxoSmithKline plc., Janssen Pharmaceuticals, Inc., Kowa Pharmaceuticals America, Inc., Novartis Pharmaceuticals Corporation, Novo Nordisk Pharma Ltd., Pfizer Inc., Sanofi-Aventis. M. K. Rhee: None.
176-LB: The Impact of COVID-19 Infection on Subsequent Glycemic Control
Authors: THURBER EMILIA G. , MCDONNELL MARIE E. , CROMWELL GRACE , JOHNSON MATTHEW , SIMONSON DONALD C. , PALERMO NADINE E. 
Published: June 2021

Recent studies suggest COVID-19 infection has a detrimental effect on glycemic control in patients with diabetes in the acute care setting. However, there is limited information about the impact of COVID-19 on glycemic control in the months following infection. In this retrospective observational study, we examined the correlation between COVID-19 infection and glycemic control in adult patients with elevated A1c in a single health system (n=3,295). Patients were selected from a cohort of those age 18 years or older who were tested for COVID-19 between 3/1/2020 and 11/1/2020. COVID positive patients were identified through positive SARS-CoV-2 PCR or a COVID flag in the EMR. COVID negative patients were randomly selected in a 3:1 ratio from all patients who had a negative COVID test in the same week as each positive patient. Patients from this cohort were included if they had a baseline A1c ≥ 5.7% measured in the preceding six months and at least two weeks prior to their COVID positive (n=670) or COVID negative (n=2,625) test date, as well as an endpoint A1c ≥ 5.7% at least three months after this date. The study population was 54% female, 60% White, 20% Hispanic, and 13% Black with a mean BMI 32 ± 7.3 kg/m2, age 64.1 ± 13.6 yrs, and baseline A1c of 7.7± 1.6 %; 81% of patients had a diagnosis of type 2 diabetes. In a linear regression model, COVID-19 infection was significantly associated with increased endpoint A1c (coefficient = 0.14, 95% CI [0.03 - 0.25], p = 0.01). Baseline A1c, male sex, and Hispanic ethnicity were also significantly associated with increased A1c, while age and median income based on zip code were associated with decreased A1c. In conclusion, prior COVID-19 infection appears to be associated with worse glycemic control at least 3 months post-infection compared to patients who did not contract COVID-19. Additional research is needed to determine if this association is present in other patient populations as well as the physiologic and socio-demographic causes for this finding.

Disclosure
E. G. Thurber: None. M. E. Mcdonnell: Stock/Shareholder; Spouse/Partner; Abbott Diabetes. G. Cromwell: None. M. Johnson: None. D. C. Simonson: Stock/Shareholder; Spouse/Partner; Phase V Technologies, Inc. N. E. Palermo: None.
190-LB: Using Genetics to Uncouple Higher Adiposity from Its Adverse Metabolic Effects
Authors: MARTIN SUSAN , TYRRELL JESSICA , THOMAS ELIZABETH L. , BOWN MATTHEW , ELDER JAMES T. , KABRHEL CHRISTOPHER , PAPADIMITRIOU NIKOS , GUNTER MARC , VINCENT EMMA E. , BELL JIMMY D. , FRAYLING TIMOTHY M. , YAGHOOTKAR HANIEH 
Published: June 2021

Type 2 diabetes is linked to higher risk of many non-metabolic conditions (e.g. cancers, neuropsychiatric and musculoskeletal disease) which all share a common risk factor: obesity. The causal pathways from excess weight to disease are unknown. We aimed to use specific genetic variants to separately test the causal roles of higher adiposity with and without its adverse metabolic effects. Using metabolic biomarkers from 442,278 UK Biobank individuals, we identified two clusters of body fat % increasing alleles: a) 36 “favourable adiposity” (FA) alleles associated with a favourable metabolic profile (higher HDL and SHBG and lower triglyceride and liver enzymes); b) 38 “unfavourable adiposity” (UFA) alleles associated with an unfavourable profile (lower HDL and SHBG and higher triglyceride and liver enzymes). We used two-sample Mendelian randomization with 43 diseases from non-UK Biobank GWASs. We identified two sets of diseases. 1) Those where the metabolic effect of higher adiposity is the likely primary cause of the disease. Here the FA and UFA clusters had an opposing effect on the risk of disease: type 2 diabetes (FA: 0.11 OR per 1 standard deviation higher body fat % [95%CI: 0.08, 0.16] vs. UFA: 5.50 [4.29, 7.05]), stroke (0.65 [0.52, 0.83] vs. 1.43 [1.23, 1.67]), gout (0.44 [0.29, 0.68] vs. 2.49 [1.88, 3.29]), breast cancer (1.12 [0.64, 1.94] vs. 0.52 [0.39, 0.68]) and colorectal cancer (0.67 [0.52, 0.85] vs. 1.20 [1, 1.50]). 2) Those where the mechanical excess weight (or other non-metabolic effects) is likely a cause of the disease. Here the FA cluster, despite having lower metabolic risk, and the UFA cluster were both associated with higher disease risk: venous thromboembolism (2.52 [1.82, 3.47] vs. 1.63 [1.25, 2.13]), osteoarthritis (1.45 [1.19, 1.76] vs. 2.20 [1.64, 2.95]), depression (2.85 [1.38, 5.89] vs. 2.59 [1.60, 4.21]). Our results assist in understanding the consequences of higher adiposity uncoupled from its adverse metabolic effects in non-metabolic diseases pathophysiological mechanisms.

Disclosure
S. Martin: None. J. D. Bell: None. T. M. Frayling: None. H. Yaghootkar: None. J. Tyrrell: None. E. L. Thomas: None. M. Bown: None. J. T. Elder: None. C. Kabrhel: Research Support; Self; Diagnostica Stago, Grifols. N. Papadimitriou: None. M. Gunter: None. E. E. Vincent: None.

Funding
Diabetes UK (17/0005594)
200-LB: Circadian Regulation of the MRTF-SRF Signaling Promotes Beige Adipocyte Development
Authors: XIONG XUEKAI , LIU RUYA , YECHOOR VIJAY , SAHA PRADIP , MA KE 
Published: June 2021

The adipogenic progenitor transformation into mature adipocytes requires dissolution of intracellular actin cytoskeleton, and the cytoskeleton-MRTF/SRF signaling blocks adipogenesis. The circadian clock confers temporal control in metabolism, with tissue-intrinsic clock circuits contributing to metabolic homeostasis. In the current study, we identify a novel clock-MRTF/SRF regulatory axis that suppresses beige adipogenesis that is required for whole-body glucose metabolism. Key components of the cytoskeleton-MRTF/SRF signaling cascade display circadian oscillations in beige fat depot mediated by Bmal1 transcriptional activity. Genetic loss- or gain-of-functions of Bmal1 in adipogenic precursors markedly altered actin cytoskeleton organization, with silencing of Bmal1 inhibiting F-actin formation and MRTF/SRF activity whereas its forced expression augmenting actin architecture. Furthermore, we show that Bmal1 circadian control of the MRTF/SRF pathway drives beige thermogenic capacity in vivo. Prrx1-Cre-mediated beige fat-selective Bmal1 ablation induced beige depot browning with augmented mitochondrial metabolism, resulting in improved whole-body insulin sensitivity and resistance to obesity. Conversely, beige fat-specific overexpression of Bmal1 suppressed beige thermogenic program leading to impaired glucose tolerance and adipose expansion. Mechanistically, we show that Bmal1 deficiency enhanced beige precursor differentiation and thermogenic induction. Collectively, our findings uncover a temporal regulation of the cytoskeleton-MRTF/SRF signaling that modulates beige thermogenic capacity to maintain metabolic homeostasis.

Disclosure
X. Xiong: None. R. Liu: None. V. Yechoor: None. P. Saha: None. K. Ma: None.

Funding
National Institutes of Health (DK112794, DK097160-01); American Heart Association (17GRNT33370012)
204-OR: ADA Presidents’ Select Abstract: Cardiovascular Autonomic Neuropathy Is Associated with Rapid Kidney Function Decline in Type 2 Diabetes: Findings from the ACCORD Trial
Authors: TANG YALING , JUNIOR CARLOS BUENO , SHAH HETAL , ANG LYNN , POP-BUSUI RODICA , DORIA ALESSANDRO 
Published: June 2021

Cardiovascular autonomic neuropathy (CAN) has been shown to predict progressive kidney function decline among persons with type 1 diabetes. We aimed to determine whether CAN has a similar effect on kidney function decline in type 2 diabetes (T2D). To this end, we investigated the association between measures of CAN obtained at baseline and GFR decline during a 5-year follow-up among T2D participants in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial. CAN was defined as ECG-derived heart rate variability indices being below the 5th percentile of the normal distribution (standard deviation of all normal-to-normal R-R intervals [SDNN] &lt;8.2 ms and root mean square of successive differences between normal-to-normal R-R intervals [rMSSD] &lt;8.0 ms). eGFR slopes were estimated by linear regression among participants with ≥3 eGFR measurements during follow up. Of the 6,805 ACCORD participants who had valid measures of CAN and eGFR slope, 1,327 (19.5%) had evidence of CAN at baseline. CAN independently predicted a steeper eGFR decline during follow-up (beta=-0.44 ml/min/1.73m2/year, P=0.0007); 24.6% of participants with CAN at baseline experienced subsequent eGFR loss ≥5 ml/min/1.73m2 per year as compared to 18.6% of participants without CAN (OR=1.39 [1.18 - 1.64], P&lt;0.0001, after adjustment for age, sex, duration of diabetes, BMI, HbA1c, eGFR, urinary albumin-creatinine ratio, and positive CVD history at baseline). Consistent with these findings, in a time-to-event analysis, baseline CAN was associated with a 40% increase in the risk of experiencing a ≥40% eGFR loss during follow-up (adjusted HR=1.40 [1.20-1.63], P&lt;0.0001).
In summary, CAN was an independent predictor of kidney function loss in T2D participants. Further studies are needed to understand whether this association reflects a shared etiology of CAN and diabetic kidney disease or a direct deleterious effect of autonomic nervous system alterations on kidney function.

Disclosure
Y. Tang: None. C. Bueno junior: None. H. Shah: None. L. Ang: None. R. Pop-busui: Advisory Panel; Self; Novo Nordisk, Consultant; Self; Averitas Pharma, Bayer Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Nevro Corp., Regenacy. A. Doria: None.

Funding
National Heart, Lung, and Blood Institute N01-HC-95178, N01-HC-95179, N01-HC-95180, N01-HC-95181, N01-HC-95182, N01-HC-95183, N01-HC-95184, IAA-Y1-HC-9035, IAA-Y1-HC-1010)
210-LB: Exploring Mechanisms of Insulin Resistance in Mental Illness: Antipsychotic Drugs Alter Metabolic, Inflammatory, and Nonalcoholic Fatty Liver Disease (NAFLD)–Associated Human and Mouse Proteomes in the Absence of Weight Gain
Authors: MAY MEGHAN , BEAUCHEMIN MEGAN , VARY CALVIN , BOUCHARD CELESTE , HOUSEKNECHT KAREN L. 
Published: June 2021

Atypical antipsychotic drugs (AA) can cause rapid onset weight gain, insulin resistance, dyslipidemia and NAFLD. Although AA metabolic effects are often associated with obesity, acute AA treatment can cause whole body and hepatic insulin resistance in the absence of weight gain pre-clinically, indicating mechanisms distinct from chronic obesogenic effects of AA. Our aim was to identify pathways involved in AA-associated side effects by correlating differentially expressed traits common to acute AA-exposed mice and drug-exposed human cells using a multi-omic approach. C57BL/6J mice fed chow were treated daily with low, clinically relevant doses of risperidone (RIS; 1 mg/kg BW), olanzapine (OLAN; 5 mg/kg BW) or drug vehicle (VEH; 0.1% acetic acid) for 28 days. Drug treatment had no effect on body weight gain vs. VEH (P&gt;0.05); however, hepatic steatosis was readily observed. Proteomic signatures were generated from hearts and livers of each treatment group, and differentially expressed (DE) proteins (P&lt;0.05; RIS or OLAN vs. VEH) were catalogued. Drug-associated expression signatures consistent with immune disruption, insulin resistance, NAFLD, type 1 and type 2 diabetes occurred with both drugs. Significant (P&lt;0.05) transcriptomic changes between human neuroblastoma cells exposed to 100 nM RIS or VEH were accessed from the Gene Expression Omnibus Database (GSE149611), and overlaid onto proteomic changes of RIS- and OLAN-treated mice. Over 65 pathways associated with metabolic and immune function, insulin resistance, and diabetes were disrupted in both the human and murine systems in the absence of weight gain. These data indicate that AA medications contribute directly to drug-induced immune dysregulation, NAFLD, and metabolic syndrome in patients, potentially via universal mechanisms of systemic dysregulation conserved across species.

Disclosure
M. May: None. M. Beauchemin: None. C. Vary: None. C. Bouchard: None. K. L. Houseknecht: None.

Funding
National Institutes of Health (DK095143)