bluuebunny/crossref_metadata_2025_split huggingface dataset:
351-OR: Six-Day Subcutaneous GIP Infusion Increases Glycemic Time-in-Range in Patients with Type 1 Diabetes
Authors: NGUYEN HEIMBÜRGER SEBASTIAN M. , HOE BJØRN , NIELSEN CHRIS N. , BERGMANN NATASHA C. , HARTMANN BOLETTE , HOLST JENS J. , STØRLING JOACHIM , VILSBØLL TINA , DEJGAARD THOMAS F. , CHRISTENSEN MIKKEL B. , KNOP FILIP K. 
Published: June 2020

The glucagonotropic effect of glucose-dependent insulinotropic polypeptide (GIP) during insulin-induced hypoglycemia in patients with type 1 diabetes (T1D) prompted us to investigate the effect of a 6-day subcutaneous (sc) GIP infusion on glucose variability in patients with T1D. In a randomized, placebo-controlled, double-blinded, crossover study, 20 men with T1D (age [mean± SD] 26±8 years, BMI 23.8±1.8 kg/m2, HbA1c 51±10 mmol/mol), underwent 2 × 6 days of continuous sc GIP (6 pmol/kg/min) and placebo (saline) infusion, respectively, with an interposed 7-day washout period. Participants wore a continuous glucose monitoring system. GIP significantly increased daytime time in range (3.9-7.8 mmol/L) by [mean±SEM] 104±69 min/day (P=0.035) without statistically significant effects on time below range (&lt;3.9 mmol/L), time above range (&gt;10.1 mmol/L), mean glucose or hypoglycemic events. Compared to placebo, GIP increased hepatic fat content by 12.6±4.2 percentage points (assessed by FibroScan®) (P=0.006), decreased 24-hour systolic and diastolic blood pressure by 4.6±2.8 (P=0.001) and 2.6±1.3 mmHg (P=0.028), respectively, and increased heart rate by 4.4±2.0 beats per minute (P=0.002) (Figure). Compared to placebo, a 6-day sc GIP infusion in patients with T1D increased glycemic time in range and hepatic fat content and reduced systolic and diastolic blood pressure while increasing heart rate.

Disclosure
S.M. Nguyen Heimbürger: None. B. Hoe: None. C.N. Nielsen: None. N.C. Bergmann: Employee; Self; Zealand Pharma A/S. B. Hartmann: None. J.J. Holst: Advisory Panel; Self; AstraZeneca, Merck Sharp & Dohme Corp., Novo Nordisk A/S, Zealand Pharma A/S. Other Relationship; Spouse/Partner; Antag Therapeutics. J. Størling: None. T. Vilsbøll: Advisory Panel; Self; AstraZeneca, Mundipharma International, Novo Nordisk A/S, Sun Pharmaceutical Industries Ltd. Consultant; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Lilly Diabetes, Medscape, Merck Sharp & Dohme Corp., Sanofi. T.F. Dejgaard: Advisory Panel; Self; Novo Nordisk A/S. Consultant; Self; Boehringer Ingelheim International GmbH, Novo Nordisk A/S. Speaker’s Bureau; Self; AstraZeneca, Boehringer Ingelheim International GmbH, Novo Nordisk A/S. M.B. Christensen: None. F.K. Knop: Advisory Panel; Self; AstraZeneca, Merck Sharp & Dohme Corp., Mundipharma International, Novo Nordisk A/S, Sanofi. Consultant; Self; Carmot Therapeutics, Inc., Eli Lilly and Company, Novo Nordisk A/S. Research Support; Self; AstraZeneca, Gubra, Novo Nordisk A/S, Sanofi, Zealand Pharma A/S. Speaker’s Bureau; Self; AstraZeneca, Lupin Pharmaceuticals, Inc., Merck Sharp & Dohme Corp., Norgine B.V., Novo Nordisk A/S.

Funding
The Leona M. and Harry B. Helmsley Charitable Trust (2018PG-T1D037)
359-OR: a- or ß-Adrenergic Blockade Does Not Affect Transplanted Islet Responses to Hypoglycemia in Type 1 Diabetes (T1D)
Authors: RICKELS MICHAEL R. , BELLIN MELENA , STEFANOVSKI DARKO , PELECKIS AMY J. , DALTON-BAKES CORNELIA V. , MARKMANN EILEEN , NGUYEN HUONG-LAN T. , NAJI ALI 
Published: June 2020

Recipients of intrahepatic islet transplantation for T1D exhibit appropriate suppression of endogenous insulin and activation of glucagon secretion in response to insulin-induced hypoglycemia with restored glucose counterregulation and protection against clinically significant hypoglycemia. Whether sympathetic activation of adrenergic receptors on transplanted islets is required for these responses is not known. To evaluate the adrenergic contribution to post-transplant glucose counterregulation, we performed a randomized, double-blind crossover study of responses during a hyperinsulinemic (1 mU·kg-1·min-1) euglycemic (EU, ∼90 mg/dL)-hypoglycemic (HYPO, ∼50 mg/dL) clamp conducted under phentolamine (0.95 µg·kg-1·min-1; α-adrenergic blockage), propranolol (0.48 µg·kg-1·min-1; β-adrenergic blockage), or placebo infusion. Subjects were 5F/4M with median (range) age 53 (34 - 63) years, T1D duration 29 (18 - 56) years, post-transplant 7 (2 - 8) years, HbA1c 5.8 (4.5 - 6.8) %, insulin in-/dependent 5/4, on tacrolimus-based immunosuppression, and spent 97 (76 - 99) % time in range 70 - 180 mg/dL and 1 (0 - 3) % time with hypoglycemia &lt; 70 mg/dL by CGM. During the EU-HYPO clamp, blood pressure was lower with phentolamine and heart rate lower with propranolol vs. placebo (P &lt; 0.05). There was no difference in suppression of C-peptide or activation of glucagon with phentolamine or propranolol vs. placebo. Pancreatic polypeptide was greater with phentolamine vs. placebo during EU (P &lt; 0.05), and free fatty acids were lower and the glucose infusion rate higher with propranolol vs. placebo during HYPO (P &lt; 0.05) with no differences seen for endogenous glucose production. These results indicate physiologic α- and β-adrenergic blockage had no effect on transplanted islet responses to hypoglycemia. Sympathetic re-innervation, as occurs with re-vascularization of intrahepatic islets, may not be necessary for post-transplant recovery of glucose counterregulation in T1D.

Disclosure
M.R. Rickels: Consultant; Self; Semma Therapeutics, Inc. Research Support; Self; Xeris Pharmaceuticals, Inc. M. Bellin: Research Support; Self; Dexcom, Inc., Viacyte, Inc. Other Relationship; Self; Insulet Corporation. D. Stefanovski: None. A.J. Peleckis: None. C.V. Dalton-Bakes: None. E. Markmann: None. H.T. Nguyen: None. A. Naji: None.

Funding
National Institutes of Health (R01DK091331, UL1TR001878, P30DK19525)
36-OR: Comparative Effectiveness of SGLT2 Inhibitors vs. GLP-1 Agonists
Authors: POONAWALLA INSIYA , BOWE ANDY , TINDAL MICHAEL , MEAH YUNUS A. , SCHWAB PHIL 
Published: June 2020

This retrospective cohort study compared sodium-glucose co-transporter-2 (SGLT2) inhibitor and glucagon-like peptide-1 (GLP-1) agonist therapeutic drug classes on cardiovascular (CV) outcomes, treatment persistence/discontinuation, healthcare utilization and costs. Using medical and pharmacy claims data from the Humana Research Database, new users of SGLT2 inhibitors or GLP-1 agonists from January 2015 to June 2017 were identified. Eligible patients were 19-89 years, enrolled in a Medicare Advantage Prescription Drug or fully-insured commercial health plan, with at least 12 months of continuous enrollment pre- and post-index date (i.e., date of first new prescription). Propensity score matching (1:1) was used to balance baseline characteristics. Cox proportional hazards models were used to compare CV outcomes and treatment discontinuation. Healthcare resource utilization and costs were compared using Wilcoxon signed rank test. A total of 5,507 patients were included in each treatment group. Patients indexed to use GLP-1 agonists were more likely to discontinue treatment (hazard ratio 1.15, 95% confidence interval 1.10-1.21) and more likely to encounter an inpatient hospitalization (14.4% vs. 11.9%, P&lt;0.001) or emergency department visit (27.4% vs. 23.5%, P &lt;0.001) compared to patients indexed on SGLT2 inhibitors. The risk of primary composite CV outcome (myocardial infarction or stroke or mortality) and secondary CV outcome (heart failure or death) was similar across cohorts. The average per-person per-month total cost ($1,796 vs. $1,617, P&lt;0.001), medical ($904 vs. $834, P&lt;0.001) and pharmacy costs ($891 vs. $783, P&lt;0.001) were higher for the GLP-1 agonist cohort compared to the SGLT2 inhibitor cohort. Although differences in extra-glycemic CV benefits were not established, these findings may be useful to providers and payers, as this real-world data showed SGLT2 inhibitors were associated with longer treatment persistence and reduced healthcare utilization and costs relative to GLP-1 agonists.

Disclosure
I. Poonawalla: None. A. Bowe: Employee; Self; Humana. M. Tindal: None. Y.A. Meah: None. P. Schwab: Employee; Self; Humana. Employee; Spouse/Partner; Humana.
361-OR: BETA-2 Score Is Highly Predictive of Graft Function after Islet Transplant: Analysis of Clinical Islet Transplant Consortium Trials
Authors: SENIOR PETER A. , RICKELS MICHAEL R. , EGGERMAN THOMAS , BAYMAN LEVENT , QIDWAI JULIE , ALEJANDRO RODOLFO , MARKMANN JAMES F. , HUNSICKER LAWRENCE G. ,   CLINICAL ISLET TRANSPLANT CONSORTIUM
Published: June 2020

The safety and efficacy of islet transplant for type 1 diabetes complicated by severe hypoglycemia was tested in a series of trials by the Clinical Islet Transplant (CIT) consortium. We sought to validate BETA-2 score and its utility to track change in graft function over time. 128 subjects (age 48.2 ± 10.9 years, 61.3% female) participated in 7 trials testing different approaches to immunosuppression, with 58 subjects enrolled in a follow-up observational study for up to 8 years. All subjects received 1-3 islet infusions of &gt;4000 IE/kg at least 75 days apart. BETA-2 was calculated at 2.5, 6, 9, 12 months and then annually. Mean follow up was 45.0 months. Graft failure was defined as stimulated C-peptide &lt; 0.3 ng/ml. The effect of time dependent BETA-2 on hazard of subsequent graft loss was estimated by joint analysis. In 120/128 subjects with graft function at day 75, CIT led to a rapid increase in BETA-2 to 24.3 ± 16.4 and remained stable for up to 8 years. 21 subjects who lost graft function after day 75 had lower BETA-2 than subjects who maintained graft function (D75: 14.5 ± 10.0 vs. 21.8 ± 11.1, p = 0.006). Joint analysis showed time dependent BETA-2 was highly predictive of graft loss (a 1 point drop in BETA-2 increased hazard of subsequent graft loss by 17% (eta = -0.19 ± 0.05, p = 0.0001). BETA-2 is a simple, yet powerful tool to describe and predict clinically important changes in graft function.

Disclosure
P.A. Senior: None. M.R. Rickels: Consultant; Self; Semma Therapeutics, Inc. Research Support; Self; Xeris Pharmaceuticals, Inc. T. Eggerman: None. L. Bayman: None. J. Qidwai: None. R. Alejandro: None. J.F. Markmann: None. L.G. Hunsicker: Advisory Panel; Self; Allergan plc., Bristol-Myers Squibb.
364-OR: Igls Classification for Islet Autotransplantation
Authors: MCEACHRON KENDALL R. , YANG YI , PRUETT TIMOTHY L. , BELLIN MELENA 
Published: June 2020

Background: The Igls criteria for assessing islet function after allotransplantation cannot be directly applied to islet autotransplantation (IAT) patients due to differences in baseline characteristics of IAT patients (insulin independent and C-peptide positive).
Methods: We tested modified criteria (Auto-Igls) for assessing islet function in a large cohort of total pancreatectomy-IAT (TPIAT) patients from 2010-2018 (n=379). Metabolic outcomes post-IAT were assessed (Table 1). We assigned an Auto-Igls class to each patient as able, and evaluated the utility, validity, and perioperative predictors of Auto-Igls at 1 year post-IAT. We associated Auto-Igls with independent measures of islet graft function where available: continuous glucose monitoring (CGM) data or acute c-peptide response to glucose (ACRglu) from intravenous glucose tolerance tests.
Results: Auto-Igls class was assigned to 264 patients (69%). Of the 115 patients who could not be classified, most (74%) were missing exact insulin u/kg/day. The only significant predictor of Auto-Igls class was the islet mass transplanted (p&lt;0.0001). Higher percent time in range (70-140 mg/dL) on CGM and higher ACRglu were associated with a better Auto-Igls class (p=0.02 and p&lt;0.0001, respectively).
Discussion: The modified Igls criteria for IAT permit a simple, comprehensive assessment of metabolic outcomes after TPIAT, and is associated with other measures of islet function.

Disclosure
K.R. McEachron: None. Y. Yang: None. T.L. Pruett: None. M. Bellin: Research Support; Self; Dexcom, Inc., Viacyte, Inc. Other Relationship; Self; Insulet Corporation.

Funding
National Institutes of Health (T32DK108733, R01DK109124)
369-OR: [1,2-13C2]-L-Glutamine Mass Isotopomers Map Hepatic Mitochondrial Metabolism without Tracer Interference
Authors: SIEBEL STEPHAN , CARDONE REBECCA L. , ABULIZI ABUDUKADIER , RAAISA RAAISA , WILLIAMS RICHARD M. , SEHGAL RAGHAV , BUTRICO GINA MARIE , CLINE GARY , ROTHMAN DOUGLAS L. , MASON GRAEME F. , KIBBEY RICHARD 
Published: June 2020

Background: Tracers should be maximally descriptive with minimal interference to the metabolic system of interest. Divergent concepts of in vivo hepatic metabolism (e.g., anaplerosis) may have emerged, in part, from invalid assumptions and/or perturbations associated with common tracers.
Aim: We evaluated three common substrate tracers for intrahepatic metabolism vis-à-vis a novel independent [1,2-13C2]-L-glutamine strategy.
Methods: Overnight fasted Sprague-Dawley rats underwent primed, continuous infusions of reported tracer rates for lactate, propionate, acetate or glutamine. Plasma/freeze-clamped livers were obtained at 0, 5, 15, 30, 60, and 120 min. Plasma/tissue isotopomers were subject to steady state and kinetic Mass Isotopomer MultiOrdinate Spectral Analysis (MIMOSA) and reported relative to citrate synthase (CS).
Results: In contrast to glutamine infusion, plasma insulin ([i]) glucose concentration ([g]), and/or plasma glucose turnover (Ra) were increased by acetate ([i] = 1.5 fold, p = 0.015; [g] = 129 mg/dl, p=0.021), lactate ([i]= 2.03 fold, p = 0.0001; [g] = 156mg/dl, p = 0.0001, Ra = 7.2 mg/kg/min, p=0.006), and propionate ([i]= 1.7 fold, p = 0.0013; [g] = 165 mg/dl, p = 0.0001, Ra = 7.8 mg/kg/min, p = 0.0017). [1,2-13C2]-L-glutamine quickly reached isotopic equilibrium without impacting mitochondrial metabolite concentration or glutamate anaplerosis. Transaminase exchange (Vx) was &gt;&gt;CS. PEPCK was 1.6 x CS with pyruvate only accounting for 76% of anaplerosis (remainder from propionate and glutamate anaplerosis). PK was less than CS while ATP citrate lyase (ACLy) was 18% of CS.
Conclusion: Direct in vivo measurements of pyruvate cycling rates were low relative to CS while ACLy, IDH exchange, and non-pyruvate anaplerosis contributed substantially to hepatic metabolism. [1,2-13C2]-L-glutamine MIMOSA delivered an unencumbered, direct assessment of hepatic mitochondrial metabolism.

Disclosure
S. Siebel: None. R.L. Cardone: None. A. Abulizi: None. R. Raaisa: None. R.M. Williams: None. R. Sehgal: None. G. Butrico: None. G. Cline: None. D.L. Rothman: None. G.F. Mason: None. R. Kibbey: None.

Funding
National Institutes of Health (2K12DK094714-06, R01DK108283)
371-OR: Reduced Hepatic Expression of the Mitochondrial Quality Control Factor PARKIN Hastens the Progression of NAFLD in Mice and Is Associated with NASH in Patients
Authors: UNDAMATLA RAMYA , EDMUNDS LIA R. , XIE BINGXIAN , MILLS AMANDA , SIPULA IAN J. , MONGA SATDARSHAN P. , JURCZAK MICHAEL J. 
Published: June 2020

Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of pathologies, including steatosis, steatohepatitis (NASH) and fibrosis and is strongly associated with type 2 diabetes. Changes in mitochondrial function are implicated in the pathogenesis of NAFLD. Mitophagy is a mitochondrial quality control mechanism that allows for selective removal of damaged mitochondria from the cell. Whether changes in mitophagy occur during and contribute to NAFLD is unknown. PARKIN is a ubiquitin E3 ligase that regulates mitophagy by generating a ubiquitin signaling motif on the outer membrane of damaged mitochondria, marking them for degradation. We undertook the studies described to determine effects of genetic inhibition of mitophagy via conditional deletion of PARKIN in liver on progression of NAFLD. Twelve-week old male liver-specific PARKIN knockout (LKO) and wild type (WT) mice were fed a diet previously demonstrated to induce NAFLD that consisted of high-fat (45%), cholesterol (0.15%) and high-fructose corn syrup drinking water (42g/L) for 8 weeks. There was no difference in body weight or composition between groups. Plasma ALT and AST levels were increased 2-fold (p=0.18) and 1.7-fold (p&lt;0.05), respectively, in LKO compared with WT mice, while plasma cholesterol and insulin levels were not different and plasma fatty acid levels were reduced by 27% (p&lt;0.05). NAFLD activity score was increased 2-fold (p&lt;0.05) in LKO mice reflecting an increase in steatosis, ballooning and inflammation. Gene expression markers of NAFLD progression including markers of inflammation (Ccl2, Cd68, Il-1b, ll-6) and fibrosis (Col1a1, Col3a1) were significantly increased in LKO mice. Consistent with these mouse data, we found PARKIN protein expression to be reduced in liver biopsies from patients with NASH compared with healthy controls. These data suggest that loss of PARKIN-mediated mitophagy may contribute to the progression of NAFLD.

Disclosure
R. Undamatla: None. L.R. Edmunds: None. B. Xie: None. A. Mills: None. I.J. Sipula: None. S.P. Monga: None. M.J. Jurczak: None.

Funding
National Institutes of Health (DK114012)
372-OR: Ablation of the Hepatokine TSK Protects Mice against Obesity and Metabolic Disorders Caused by MC4R Deficiency
Authors: WANG QIUYU , LIN JIANDIE 
Published: June 2020

Endocrine hormones released by peripheral tissues, such as adipose tissue, skeletal muscle and the liver, play an important role in metabolic crosstalk and homeostasis and contribute to disease pathogenesis. We recently identified Tsukushi (TSK) as a liver-enriched secreted factor that is highly inducible in response to increased energy expenditure. TSK null mice were resistant to diet-induced obesity, insulin resistance, and diet-induced NASH as a result of enhanced sympathetic activation and brown fat thermogenesis. However, the mechanisms underlying TSK action remain incompletely elucidated. Melanocortin 4 receptor (MC4R) is a key regulator of energy balance and its mutations represent the most common monogenic cause of obesity in human. In this study, we generated TSK/MC4R double knockout mice to explore potential crosstalk between the TSK and MC4R signaling pathways. While MC4R-null mice developed severe obesity when fed standard rodent chow, TSK inactivation nearly completely abolished the defects of energy balance caused by MC4R deficiency. Remarkably, ablation of TSK normalized food intake and corrected hepatic steatosis, adipose tissue inflammation, and insulin resistance in MC4R null mice. TSK deficiency also rescued the impairments of thermogenic gene expression caused by MC4R deficiency. Those results suggest that TSK likely acts downstream or in parallel to MC4R signaling to regulate feeding behavior and energy expenditure. Our work supports a rationale for therapeutic blockade of TSK for the treatment of obesity and metabolic disease caused by MC4R mutations.

Disclosure
Q. Wang: None. J. Lin: None.

Funding
National Institutes of Health (DK102456, AG055379, DK114220)
373-OR: Paternal SGLT2 Inhibition Upregulates Hepatic Expression of Oxidative Phosphorylation Genes in Both Fetal and Adult Offspring
Authors: SU LEI , OSATAPHAN SORAVIS , MACCHI CHIARA , CHIMENE-WEISS JEREMY I. , DREYFUSS JONATHAN , PAN HUI , PATTI MARY-ELIZABETH 
Published: June 2020

Paternal obesity has a detrimental impact on metabolic health of his offspring, suggesting an opportunity for preventive strategies prior to conception. Indeed, treatment of male mice with the SGLT2 inhibitor canagliflozin (CANA, 25mg/kg/d) for 4 weeks prior to breeding reduces obesity, hepatic steatosis, and glycemia in offspring. To identify molecular mediators, we analyzed mRNA-seq in fetal and adult liver from male offspring of fathers treated with chow (pCHOW), 60% high-fat diet (pHFD), or HFD+CANA (pCANA). Differentially expressed genes were identified using Limma (R). In adult offspring, paternal SGLT2 inhibition altered the expression of 213 genes (FDR&lt;0.05, 137 upregulated, 67 downregulated with FC ≥|1.5|, vs. paternal HFD, n=5/group). Pathway analysis revealed enrichment of oxidative phosphorylation and ribosome in upregulated genes, including 11 subunits of complex IV (Cox6b2), complex III (Uqcrq, Uqcr10), complexI(Ndufs7, Ndufa1, Ndufa2/3/7/11) and complex V(Atp5mpl, Atp5e), with similar trend for complex II Sdhb (FC=1.32, FDR=0.07). Mitochondrial DNA (quantitated by NADH dehydrogenase 1 relative to β-globin DNA) did not differ between pCANA and pHFD. To determine whether this pattern was present early in life, before emergence of offspring metabolic phenotypes, we analyzed E16.5 fetal liver. 95 genes were differentially expressed in pCANA vs. pHFD (p&lt;0.05, 55 upregulated, 40 downregulated with FC ≥|1.5|, n=5 vs. n=3); of these, 99% were also inversely regulated by pHFD vs. pChow. 16 OXPHOS genes were downregulated by pHFD but upregulated by pCANA (FC≥|1.2|). ETFB was downregulated by pHFD (FC -1.6), but upregulated by pCANA in both fetal (FC 1.3) and adult (FC 1.5) liver.
In summary, paternal CANA modulates liver mitochondrial gene expression in his offspring during both embryonic and adult life, suggesting that improvements in oxidative capacity may mediate the protective effects of paternal SGLT2 inhibition.

Disclosure
L. Su: None. S. Osataphan: None. C. Macchi: None. J.I. Chimene-Weiss: None. J. Dreyfuss: None. H. Pan: None. M. Patti: Consultant; Self; Fractyl Laboratories, Inc. Research Support; Self; Dexcom, Inc., Xeris Pharmaceuticals, Inc. Other Relationship; Self; Academy of Nutrition and Dietetics, American Diabetes Association, American Society of Metabolic and Bariatric Surgery, Endocrine Society, Insulet Corporation, King Abdullah International Medical Research Center, SUNY Downstate.

Funding
National Institutes of Health (R01DK106193, P30DK046200)
377-P: Impact of Ramadan-Focused Education Program on Hypoglycemia Risk and Metabolic Control for Patients with Type 2 Diabetes: A Systematic Review and Meta-analysis
Authors: TOURKMANI AYLA , ALHARBI TURKI , ALRASHEEDY ALIAN , ALMADANI WIDAD , RSHEED ABDULAZIZ BIN 
Published: June 2020

Ramadan fasting is regarded as a form of worship among Muslims. However, patients with a high risk of diabetic complications are advised to avoid fasting, as the practice is associated with significant impacts on several health factors for type 2 diabetic patients, including glycemic control. Thus, a lack of adequate education before Ramadan may result in negative health outcomes. To evaluate the impact of a Ramadan-focused education program on hypoglycemic risk and other clinical and metabolic parameters. A systematic literature search was performed using Scopus and PubMed to identify relevant studies meeting the inclusion criteria from inception to November 2018. The PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses Statement and guidelines) were followed when performing the search and identification of appropriate studies. A total of 17 studies were included in this systemic review, with various study designs, including randomized controlled trials, quasi-experimental and non-randomized studies. Overall, the results revealed a significant reduction of hypoglycemia risk (81% reduction) for fasting patients in intervention groups who received Ramadan-focused education compared with patients receiving conventional care (OR 0.19, 95% CI: 0.08-0.46). Moreover, HbA1c was significantly improved among patients who received a Ramadan-focused education intervention, compared with those receiving conventional care. Ramadan-focused education programs had a significant impact on hypoglycemia and glycemic control, with no significant effect on body weight, blood lipids or blood pressure.

Disclosure
A. Tourkmani: None. T. Alharbi: None. A. Alrasheedy: None. W. Almadani: None. A. Bin Rsheed: None.