bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serum Apolipoprotein C-III and Cardiovascular Events in Type 1 Diabetes
Authors: BASU ARPITA , BEBU IONUT , JENKINS ALICIA , STONER JULIE , ZHANG YING , KLEIN RICHARD L. , LOPES-VIRELLA MARIA F. , TIMOTHY GARVEY W. , BUDOFF MATTHEW , LYONS TIMOTHY ,   DCCT/EDIC RESEARCH GROUP
Published: June 2018

Background: Apolipoproteins Apo-B, Apo-C-III, and Apo-E are atherogenic and are associated with diabetic dyslipidemia and cardiovascular disease (CVD). Apolipoprotein-defined lipoprotein subclasses (ADLS) also show associations with CVD, but prospective associations of these detailed metrics with CVD in people with type 1 diabetes (T1DM) have not been explored.
Objective: Prospective associations of serum apolipoproteins and ADLS with CVD and major atherosclerotic cardiovascular events (MACE: composite of CVD death, nonfatal myocardial infraction or nonfatal stroke) in T1DM.
Methods: Serum apolipoproteins and ADLS (14 biomarkers in total) measured in sera (1997-2000) in a subset (n=465) of the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications cohort. Prospective associations of CVD and MACE over 5942 and 6180 patient-years follow-up, respectively, were investigated using Cox proportional hazards models unadjusted and adjusted for risk factors.
Results: During 15 years follow-up, 50 CVD and 24 MACE events occurred. Significant positive univariate associations for CVD were: Lp-B, Apo-B, Apo-C-III (total, heparin precipitate (HP), i.e., Apo-C-III in VLDL, and heparin soluble (HS), i.e., Apo-C-III in HDL) and Lp-B:C; for MACE: Apo-C-III sub fractions (total, Apo-C-III-HP, and Apo-C-III-HS). Adjusting for sex, age, HbA1c, systolic blood pressure, pulse rate, LDL-cholesterol, and triglycerides: for CVD, Apo-C-III-HS remained significant (HR (95% CI): 1.18 (1.03, 1.35); P=0.01). For MACE, total Apo-C-III and Apo-C-III-HS persisted when adjusted for age, HbA1c and LDL [1.11 (1.01, 1.22); P=0.02, and 1.22 (1.02, 1.45); P=0.02, respectively], but not for age, HbA1c and (log) triglycerides. No significant associations of other ADLS, Apo-A-I, A-II and Apo-E with CVD/MACE were observed.
Conclusions: Total serum Apo-C-III and Apo-C-III in HDL and Apo-B-containing lipoproteins may serve as predictive biomarkers for CVD events in T1DM adults.

Disclosure
A. Basu: None. I. Bebu: None. A. Jenkins: Research Support; Self; Medtronic, Mylan, Sanofi-Aventis. J. Stoner: None. Y. Zhang: None. R.L. Klein: None. M.F. Lopes-Virella: None. W. Garvey: Advisory Panel; Self; Novo Nordisk Inc., Merck & Co., Inc.. Research Support; Self; Sanofi, Pfizer Inc., Novo Nordisk Inc., AstraZeneca, Merck & Co., Inc., Elcelyx Therapeutics, Inc., Lexicon Pharmaceuticals, Inc., Eisai Inc. M. Budoff: Speaker's Bureau; Self; Janssen Pharmaceuticals, Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Amarin Corporation. T. Lyons: None.
Praliciguat, a Clinical-Stage sGC Stimulator, Improved Glucose Tolerance and Insulin Sensitivity and Lowered Triglycerides in a Mouse Diet-Induced Obesity Model
Authors: SCHWARTZKOPF CHAD D. , HADCOCK JOHN , JONES JULI E. , CURRIE MARK , MILNE GEORGE T. , MASFERRER JAIME 
Published: June 2018

Background: Praliciguat (IW-1973) is a soluble guanylate cyclase (sGC) stimulator in clinical development. In animal models, praliciguat has broad tissue distribution and enhances nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) signaling, which has been shown to elicit hemodynamic, anti-inflammatory, and anti-fibrotic effects. This study assessed the metabolic effects of praliciguat in a mouse DIO model.
Methods: Male C57BL/6J mice (12 weeks old at the start of treatment) were either maintained on regular chow (lean mice) or switched to a 60% high fat diet (HFD) starting at age 6 weeks (obese mice). At the start of treatment, obese mice received either praliciguat (6 mg/kg) or vehicle in the HFD. The lean mice remained on regular chow. On day 28, an oral glucose tolerance test (OGTT) was performed after a 3-h fast. On day 29, organs and terminal blood were collected for analysis after a 3-h fast.
Results: Praliciguat treatment lowered OGTT glucose area under the curve (-22%, P&lt;0.05), fasting plasma insulin (-53%, P&lt;0.01) and HOMA-IR, an index of insulin resistance (-53%, P&lt;0.01) vs. vehicle treatment. Praliciguat-treated mice also had lower liver (-36%, P&lt;0.05) and fasting circulating triglycerides (-30%, P&lt;0.01) vs. vehicle-treated mice. Furthermore, several fasting biomarkers did not change in treated vs. vehicle including beta-hydroxybutyrate, free fatty acids, plasma glucose, cholesterol, leptin, and adiponectin.
Conclusions: Praliciguat improved insulin sensitivity, glucose tolerance, and yielded lower circulating and liver triglycerides in a mouse diet-induced obesity model.

Disclosure
C.D. Schwartzkopf: None. J. Hadcock: None. J.E. Jones: None. M. Currie: Employee; Self; Ironwood Pharmaceuticals, Inc. G.T. Milne: Employee; Self; Ironwood Pharmaceuticals, Inc.. Stock/Shareholder; Self; Ironwood Pharmaceuticals, Inc.. Employee; Spouse/Partner; Catabasis Pharmaceuticals. Stock/Shareholder; Spouse/Partner; Catabasis Pharmaceuticals. J. Masferrer: Employee; Self; Ironwood Pharmaceuticals, Inc..
Uric Acid and Cardiovascular Disease in Type 1 Diabetes
Authors: BASU ARPITA , BRAFFETT BARBARA , JENKINS ALICIA , BEBU IONUT , KLEIN RICHARD L. , LOPES-VIRELLA MARIA F. , DAGOGO-JACK SAMUEL , ORCHARD TREVOR J. , WALLIA AMISHA , LACHIN JOHN , TIMOTHY GARVEY W. , LYONS TIMOTHY ,   DCCT/EDIC RESEARCH GROUP
Published: June 2018

Background: Serum uric acid (UA) is associated with the pathogenesis of diabetes complications, including cardiovascular disease (CVD) and kidney injury. Current epidemiological evidence is limited regarding the association between UA and the development of CVD in type 1 diabetes mellitus (T1DM).
Objective: To examine associations of serum UA with CVD and major atherosclerotic cardiovascular events (MACE) in T1DM.
Methods: UA was measured in sera (1997-2000) from a subset of participants (n=973; males=540, females=433) in the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) study. Subsequent CVD events were adjudicated by a review committee masked to DCCT assignment and HbA1c levels, and defined as the time to the first of any of the following: non-fatal myocardial infarction (MI) or stroke, CVD death, silent MI on annual ECG, angina confirmed by ischemic changes with exercise tolerance testing, congestive heart failure, or revascularization; MACE were defined as a composite of CVD death, nonfatal MI, or stroke. Cox proportional hazards models were used to evaluate prospectively the effect of UA as a fixed covariate on CVD and MACE, separately by gender, and adjusted for age and HbA1c.
Results: Over 15 years follow-up, there were 201 adjudicated CVD events among 110 participants (HR=1.10 per 1 mg/dl change in UA, 95% CI 0.93-1.30); 61 males experienced 96 events (HR=1.15, 95% CI 0.90-1.46) and 49 females, 105 events (HR=1.17, 95% CI 0.88-1.56). There were 62 adjudicated MACE among 53 participants (HR=1.18, 95% CI 0.93-1.49); 29 males experienced 31 events (HR=1.10, 95% CI 0.77-1.58) and 24 females, 31 events (HR=1.47, 95% CI 1.01-2.14). No significant associations between quartiles of UA and either CVD or MACE were observed in either sex.
Conclusions: Our results show UA may not serve as a predictive biomarker for CVD events in T1DM adults. Sex-specific associations with MACE deserve further investigation.

Disclosure
A. Basu: None. B. Braffett: None. A. Jenkins: Research Support; Self; Medtronic, Mylan, Sanofi-Aventis. I. Bebu: None. R.L. Klein: None. M.F. Lopes-Virella: None. S. Dagogo-Jack: None. T.J. Orchard: None. A. Wallia: Research Support; Self; UnitedHealth Group. Consultant; Self; Glytec Systems, Lexicon Pharmaceuticals, Inc.. Research Support; Self; Eli Lilly and Company. J. Lachin: Board Member; Self; AbbVie Inc., Celgene Corporation. W. Garvey: Advisory Panel; Self; Novo Nordisk Inc., Merck & Co., Inc.. Research Support; Self; Sanofi, Pfizer Inc., Novo Nordisk Inc., AstraZeneca, Merck & Co., Inc., Elcelyx Therapeutics, Inc., Lexicon Pharmaceuticals, Inc., Eisai Inc.. T. Lyons: None.
The Effect of Nutritional Transition on the Differentiation of Bone Marrow Stem Cells and the Therapeutic Effect of GLP-1
Authors: XIA WENFANG , CHEN LULU , ZHANG QING 
Published: June 2018

Background: Catch up growth is associated with glucose and lipid metabolism disorders, that can lead to osteoporosis and related fractures. Glucagon-like peptide-1 receptor agonists, such as liraglutide, exert an anabolic effect on bone in insulin resistant mice, but the mechanism for the action remains unclear. We established an animal model of catch-up growth to explore the actions of GLP-1 on bone mass and structure.
Methods: 30 male C57BL/6 mice were randomly divided into the normal diet (ND, n=10), the catch-up growth model (RH, n=10) and the catch-up growth model +GLP-1 (RH+GLP-1, n=10) groups. Liraglutide was subcutaneously administered (200ug/kg, twice a day, for four weeks). After killing, tibia and fibula were removed for bone histomorphometry, bilateral femoral bone marrow mesenchymal stem cells were collected to evaluate their differentiation ability.
Results: GLP-1 administration decreased weight of visceral fat tissue, body weight, ratio between them, and blood lipids of the RH group. GLP-1 decreased triglyceride levels, and fatty acids in the liver, visceral fat tissue, subcutaneous fat tissue and skeletal muscle tissue. Compared to the ND group, GLP-1 secretion decreased in the RH group, but noticeably increased after GLP-1 administration. The areas under curves of intraperitoneal glucose tolerance test and insulin tolerance test and HOMA-IR in RH+GLP-1 group significantly declined. GLP-1 reversed deteriorated tibial and fibular bone structure in RH mice and induced osteoblastic differentiation.
Conclusion: Decreased ability of osteoblastic/osteogenesis differentiation of MSCs in RH mice led to impaired bone formation and GLP-1 intervention reversed the damage and enhanced insulin sensitivity.

Disclosure
W. Xia: None. L. Chen: None. Q. Zhang: None.
Exercise Is Required to Improve Mitochondrial Respiratory Capacity in Skeletal Muscle of Older Obese Subjects during Calorie Restriction–Induced Weight Loss to Improve Insulin Sensitivity
Authors: DISTEFANO GIOVANNA , STANDLEY ROBERT , CARNERO ELVIS A. , COEN PAUL M. , VEGA RICK B. , GOODPASTER BRET H. 
Published: June 2018

Calorie restriction has been shown to have “anti-aging” effects in animal models, and calorie restriction-induced weight loss (CRWL) and exercise can both improve insulin sensitivity.
The aim of this study was to investigate the effect of 6-month diet-induced weight loss intervention with or without the addition of exercise training on skeletal muscle mitochondrial respiratory capacity and IS.
Methods: Forty-four older adults with obesity were randomized to one of the following 6-month intervention: Health education (CON: n=14, age=70±4 years, BMI=34±5kg/m2), Diet induced weight-loss (DIWL: n=14, age=70±4 years, BMI=36±5kg kg/m2), or Weight-loss and exercise (WLEX: n=16, age=66±3 years, BMI=37±5kg/m2). CRWL and WLEX participants had a goal of 10% weight-loss through calorie restriction. Subjects in the WLEX group completed a supervised exercise program. Mitochondrial respiratory capacity of permeabilized myofibers from biopsies was evaluated by high-resolution respirometry. Complex I+II supported maximal oxidative phosphorylation (OXPHOS), and maximal uncoupled respiration were evaluated. IS was determined by hyperinsulinemic euglycemic clamps.
Results: IS improved in both CRWL (10.4%) and WLEX (50%) compared to CON (0.7%). However, while mitochondrial respiration was unchanged in the CON and CRWL groups after the 6-month intervention (p&gt;0.05), subjects in the WLEX group presented an increased maximal OXPHOS (PRE: 50.7±10.1 vs. POST: 72.6±17.9 pmol/s*mg) and uncoupled respiration (PRE: 57.2±10.5 vs. POST: 79.6±19.3 pmol/s*mg) after the exercise training.
Conclusions: Despite weight loss and exercise both improving insulin sensitivity, exercise is required to improve mitochondrial respiratory capacity in skeletal muscle of older obese human subjects undergoing calorie restriction-induced weight loss.

Disclosure
G. Distefano: None. R. Standley: None. E.A. Carnero: None. P.M. Coen: None. R.B. Vega: None. B.H. Goodpaster: None.
Long-Term Insulin Treatment Alters Muscle-Related Protein in OLETF Rat Skeletal Muscle
Authors: KWON HYUK-SANG , HONG OAKKEE , KWON HEE SUN , KANG YANGGYO , LEE SEONG-SU , KIM SUNG RAE , YOO SOON JIB 
Published: June 2018

Purpose: The objective of this study was to investigate molecular and physiological changes in response to long-term insulin glargine treatment in the skeletal muscle of Otsuka Long-Evans Tokushima Fatty (OLETF) rats.
Methods: Protein changes in the skeletal muscle of type 2 diabetic rats was detected by Western blot analysis, and muscle fiber type composition was assessed by real-time PCR.
Results: Insulin glargine (1 U/kg) treatment in OLETF rats (OLETF-G) for 24 weeks were changed in blood glucose levels in intraperitoneal glucose tolerance tests compared with age-matched, untreated OLETF rats (OLETF-C), and the area under the curve was significantly decreased for OLETF-G rats compared with OLETF-C rats (P &lt; 0.05). The protein levels of myosin heavy chain (MHC) isoforms were altered in gastrocnemius muscle of OLETF rats, and the proportions of MHC type I and II fibers were lower and higher, respectively, in OLETF-G compared with OLETF-C rats. Activation of myokines (interleukin [IL]-6, IL-15, fibronectin type III domain containing 5 [FNDC5]/irisin, and myostatin) in gastrocnemius muscle was significantly inhibited in OLETF-G compared with OLETF-C rats (P &lt; 0.05). Moreover, myogenin determination gene D and myogenin levels were decreased, while insulin-like growth factor-I levels were increased, in the skeletal muscle of OLETF-G rats (P &lt; 0.05). Insulin glargine treatment significantly increased the phosphorylation levels of 5’-AMP-activated protein kinase, sirtuin 1, and peroxisome proliferator-activated receptor γ coactivator 1α.
Conclusions: Our results suggest that long-term insulin glargine treatment can effectively alter protein expression in the gastrocnemius muscle of OLETF rats.

Disclosure
H. Kwon: None. O. Hong: None. H. Kwon: None. Y. Kang: None. S. Lee: None. S. Kim: None. S. Yoo: None.
The Rates of Overtreatment and Deintensification of Antidiabetic and Antihypertensive Medications in Patients with Diabetes Mellitus
Authors: SONMEZ ALPER , TASCI ILKER , DEMIRCI IBRAHIM , HAYMANA CEM , BARCIN CEM , AYDIN HASAN , CETINKALP SEVKI , OZTURK FEYZA YENER , GUL KAMILE , SABUNCU TEVFIK , SATMAN ILHAN , BAYRAM FAHRI ,   TEMD STUDY GROUP
Published: June 2018

Background: Targeting better HbA1c and blood pressure (BP) goals may endanger older adults with type 2 diabetes mellitus (T2DM) for a number of risks. Overtreatment of T2DM and hypertension (HTN) is a trending issue but awareness and attitudes of physicians need to be explored.
Objective: To assess the rates and predictors of overtreatment and undertreatment of glycemia and blood pressure in older adults with T2DM. Treatment deintensification or intensification by the physicians were also investigated.
Method: Data from older adults (≥65 years) enrolled in a large nationwide T2DM survey in 2017 across Turkey were analyzed. Overtreatment was defined as HbA1c &lt;6.5% plus use of ≥2 oral hypoglycemics or insulin, and systolic BP &lt;120 mmHg or diastolic BP &lt;65 mmHg plus use of ≥2 drugs). Undertreatment was defined as HbA1c &gt;9% at all, and SBP &gt;140 mmHg or DBP &gt;90 mmHg plus use of &lt;3 drugs. Deintensification or intensification rates were calculated according to treatment modification by the physicians.
Results: A total of 1276 patients were included. The overtreatment rates for glycemia and BP were 9.8% and 5.9%, whereas undertreatment rates were 14.2% and 17.7%, respectively. In the adjusted model, use of oral hypoglycemics only (OR:3.1, 95% CI:1.9-5.3) and follow-up at a private clinic (OR:2.2, 95% CI:1.2-3.9) were the predictors of glycemia overtreatment. Presence of microvascular complications (OR:2.0, 95% CI:1.1-3.5) was the only predictor of BP overtreatment. The deintensification and intensification rates for glycemia were 25% and 75.7% respectively, and for the BP 10.9% and 9.0% respectively.
Conclusion: The overtreatment rates of diabetes and BP in Turkish older adults with T2DM were consistent with the previous studies, while the undertreatment rates were much higher. Doctors seem to feel more comfortable to intensify glycemic management and largely ignore BP control. The results warrant enforced measures to improve care of older adults with T2DM.

Disclosure
A. Sonmez: None. I. Tasci: None. I. Demirci: None. C. Haymana: None. C. Barcin: None. H. Aydin: None. S. Cetinkalp: None. F. Yener Ozturk: None. K. Gul: None. T. Sabuncu: None. I. Satman: None. F. Bayram: None.
Exogenous Delta-Like 1 Homolog (DLK1)-Fc Treatment Attenuates Muscle Atrophy in Both Dexamethasone and High-Fat Diet–Induced Obesity Mice Models
Authors: LEE JI YOUNG , LEE MINYOUNG , JUNG HYE-IN , LEE JI-YEON , CHO YONGIN , BAE JAEHYUN , LEE YONG-HO , LEE BYUNG-WAN , KANG EUN SEOK , CHA BONG-SOO 
Published: June 2018

Skeletal muscle degeneration is accelerated in elderly patients with diabetes and the imbalance between muscle growth and wasting can lead to metabolic dysfunction. DLK1 is a member of the EGF-like family and essential for skeletal muscle development and regeneration. To identify whether exogenous DLK1 treatment can prevent muscle wasting, we assessed muscle mass as well as muscle differentiation and atrophy markers in two different models: dexamethasone and high fat diet (HFD)-induced obesity mice models (n=7-8 per each group). In the dexamethasone model, mice were divided into (1) control, (2) dexamethasone treatment (1mg/Kg, 2 weeks), and (3) DLK1 (0.8mg/Kg, 2 weeks) and dexamethasone treatment groups. In the HFD model, mice were divided into (1) control, (2) HFD (60% calories from fat, 8 weeks), and (3) HFD with DLK1 treatment (0.8mg/Kg, 8 weeks) groups. The expressions of genes related to muscle differentiation and atrophy were determined using RT-PCR. We observed that dexamethasone reduced muscle mass and markedly increased atrophy makers including atrogin-1 and murf-1. DLK1 treatment attenuated these degenerative changes. Furthermore, the level of myostatin, which inhibits muscle cell growth, was reduced in DLK1 treatment group compared to dexamethasone group. Additionally, compared to HFD group, DLK1 inhibited muscle atrophy by increasing the differentiation marker: myoD, and decreasing the atrophy markers: mysotatin, atrogin-1, and murf-1. Taken together, these results suggest that DLK1 attenuates both dexamethasone and HFD-induced muscle atrophy in mice by suppressing the downstream signaling of myostatin/atrogin-1/murf-1 pathway. The increased expression of myoD indicates that DLK1 treatment can also improve the quality of muscle formation. Our study implies that DLK1 could be a promising candidate in the treatment of aging or diabetes-related sarcopenia, characterized by muscle atrophy and dysfunction.

Disclosure
J. Lee: None. M. Lee: None. H. Jung: None. J. Lee: None. Y. Cho: None. J. Bae: None. Y. Lee: None. B. Lee: None. E. Kang: None. B. Cha: None.
Skeletal Muscle Clock Is Essential for Nutrient-Sensing and Interorgan Metabolic Fuel Partitioning
Authors: MA KE , CHATTERJEE SOMIK , YIN HONGSHAN 
Published: June 2018

The circadian clock exerts temporal control in metabolism and its disruption leads to the development of diabetes and obesity. Tissue-intrinsic clock circuits are integral components of global metabolic homeostasis, although how they sense nutrient signals to orchestrate metabolic flux is not clear. Skeletal muscle is major site for metabolic substrate oxidation, and its utilization of glucose and fatty acid depends on availability of nutrients accompanying feeding-fasting transitions. Interestingly, nearly 30% of rhythmic transcripts in skeletal muscle belongs to metabolism. By generating a mouse model with myocyte-selective ablation of the clock transcription activator Bmal1, here we show that cell-autonomous muscle clock plays an essential role in coordinating nutrient utilization with feeding-fasting induced cycles. Bmal1 in skeletal muscle was robustly induced by feeding, and its loss markedly impaired feeding-induced switch to glucose metabolism from fatty acid utilization. As a result, Bmal1-deficient muscle displays nearly 50% reduction of glucose oxidation whereas fatty acid oxidation was enhanced, resembling a constant fasting state. This metabolic shift was accompanied by muscle fiber type switching to an oxidative phenotype, and led to a remarkable resistance to hepatic lipid accumulation induced by prolonged fasting or high-fat diet feeding. In contrast, systemic fasting glucose levels in muscle Bmal1-deficient mice was elevated, which is due to a failure of suppressing hepatic glucose output as revealed by hyperinsulinemic-euglycemic glucose clamp study. Collectively, our results reveal a novel function of the Bmal1-driven muscle clock as a key metabolic sensor that coordinates metabolic fuel oxidation with oscillatory nutrient availability in fasting-feeding cycles. This temporal mechanism in orchestrating global nutrient flux may contribute to metabolic abnormalities induced by circadian misalignment.

Disclosure
K. Ma: None. S. Chatterjee: None. H. Yin: None.
Effects of Diet/Exercise and Pioglitazone on the Association between Fitness and Intramyocellular FFA Trafficking
Authors: SHADID SAMYAH ,   N ENDOCRINE RESEARCH UNIT, MAYO CLINIC, ROCHESTER, M, JENSEN MICHAEL D. 
Published: June 2018

Background: Intramyocellular (im) triglycerides (TG) are increased in athletes, but also insulin resistant (IR) adults. To elucidate this discrepancy, we studied FFA storage in imTG and im oleyl-carnitine (OC) concentrations in IR humans pre and post 2 methods of insulin sensitization (IS) in the context of fitness (VO2max).
Methods: 39 adults (BMI 28-36 kg/m2) were given a diet/exercise program (DE; 11.7 ± 3.2 kg weight loss) or 30 mg/day pioglitazone (PI) for ∼19 weeks. Blood and muscle samples were taken before and after a 6 hour [U-13C]oleate infusion with either a euglycemic, hyperinsulinemic clamp (n=20) or saline infusion. Plasma oleate storage in imTG (nmol FFA/g muscle/hr) was calculated.
Results: Quantative IS was similar in DE and PI groups. VO2max increased post DE (44 ± 1 to 46 ± 2 ml/kgFFM/min†), but not PI (45 ± 1 ml/kgFFM/min pre and post PI). At baseline, oleate storage in imTG during clamps correlated with VO2max (r=0.51*), but the δVO2max with treatment did not correlate with the δoleate storage in imTG. Following IS, VO2max correlated with imOC (r=0.46*); the latter was true for men (m) (r=0.89*), but not women (r=0.32), and for DE (m: r=0.97*) but not PI (m: r=0.70, p=0.18). δ VO2max correlated with δimOC (m: r=0.92*, f: r=0.57†), both post WL (r=0.91*) and PI (r=0.96*).Summary: In IR adults, IS influences the associations between fitness and markers of imFFA oxidation and storage in imTG during hyperinsulinemia. These relationships are more apparent in men and exaggerated post-IS.
Conclusion: Fitness in men regulates imFFA trafficking towards storage and oxidation. *p&lt;0.05; †p=NS.

Disclosure
S. Shadid: None. M.D. Jensen: Other Relationship; Self; Novo Nordisk A/S. Consultant; Self; Novo Nordisk A/S.