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  • 1
    In: The Lancet Diabetes & Endocrinology, Elsevier BV, Vol. 7, No. 9 ( 2019-09), p. 684-694
    Type of Medium: Online Resource
    ISSN: 2213-8587
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
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  • 2
    Online Resource
    Online Resource
    Elsevier BV ; 2019
    In:  The Lancet Diabetes & Endocrinology Vol. 7, No. 11 ( 2019-11), p. 828-829
    In: The Lancet Diabetes & Endocrinology, Elsevier BV, Vol. 7, No. 11 ( 2019-11), p. 828-829
    Type of Medium: Online Resource
    ISSN: 2213-8587
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
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  • 3
    In: Diabetes, American Diabetes Association, Vol. 68, No. Supplement_1 ( 2019-06-01)
    Abstract: Knockdown of the gene encoding transmembrane 6 superfamily member 2 protein (TM6SF2) in mice increases hepatocellular lipid content (HCL) and decreases very low-density lipoprotein secretion. Humans with TM6SF2 mutations are at higher risk of nonalcoholic fatty liver disease, but lower risk of cardiovascular disease. The relevance of TM6SF2 mutations for HCL and insulin sensitivity in type 2 diabetes is less clear. This study aimed at elucidating the relevance of the E167K (SNP rs58542926) mutation in the gene encoding TM6SF2 for HCL, hepatic insulin sensitivity and whole-body insulin sensitivity in type 2 diabetes. We compared male patients with recently diagnosed type 2 diabetes with (n=16) or without (n=16) E167K mutation, matched for age and BMI (50±1 vs. 48±3 years; 32±1 vs. 32±2 kg/m2) from the German Diabetes Study. Whole-body and hepatic insulin sensitivity were assessed by Botnia-clamp tests with [6,6-2H2]glucose, HCL by 1H magnetic resonance spectroscopy and hepatic fibrosis by the fibrosis-4 index (FIB4). Patients with and without TM6SF2 mutation had comparable levels of HbA1c (6.2±0.2 vs. 5.9±0.1%) and serum triglycerides (136±14 vs. 149±14 mg/dl). Carriers of TM6SF2 mutation had higher HCL (9.0±1.9 vs. 4.6±0.4%, p & lt;0.05) and whole-body insulin sensitivity (7.1±0.6 vs. 5.4±0.2 mg/(kg*min), p & lt;0.05), but similar hepatic insulin sensitivity (1.6±0.1 vs. 1.6±0.1 mg/(kg*min)) and fibrosis score (1.2±0.1 vs. 1.0±0.1). In conclusion, the E167K mutation of the TM6SF2 gene dissociates liver steatosis from whole-body insulin sensitivity. This may result from favored trapping of triglycerides within the liver, which would in turn protect peripheral tissues from insulin resistance induced by liver-derived lipids. Disclosure K. Bodis: None. J. Szendroedi: None. J.M. Ahlers: None. Y. Karusheva: None. O.P. Zaharia: None. S. Antoniou: None. B. Knebel: None. Y. Kupriyanova: None. J. Hwang: None. V. Burkart: None. K. Muessig: None. H. Al-Hasani: None. M. Roden: Advisory Panel; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Poxel SA, Servier. Board Member; Self; Eli Lilly and Company. Research Support; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Sanofi. Speaker's Bureau; Self; Novo Nordisk Inc. D.F. Markgraf: Research Support; Self; Sanofi.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
    detail.hit.zdb_id: 1501252-9
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  • 4
    In: Diabetes, American Diabetes Association, Vol. 69, No. Supplement_1 ( 2020-06-01)
    Abstract: Understanding the role of insulin resistance (IR) in type 1 diabetes (T1D) may help to improve its treatment. Postprandial insulin secretion stimulates amino acid (AA) uptake and protein synthesis. Consequently, impaired insulin-mediated AA clearance could raise postprandial branched-chain AA (BCAA: valine (VAL), leucine (LEU), isoleucine (ILE)) levels and in turn contribute to BCAA-induced IR. We hypothesized that BCAA levels associate negatively with postprandial ß-cell function already in recent-onset T1D. In a cross-sectional study, volunteers of the German Diabetes-Study with T1D (n=10, diabetes duration & lt;1 year) and excellent glycemic control (HbA1C 6.6±0.9%/48±9 mmol/mol), and age-, sex- and BMI- matched glucose tolerant humans (control, CON, n=10, HbA1C 5.1±0.3%/32±3 mmol/mol) underwent a mixed-meal tolerance test (MMT) to assess ß-cell function through disposition index (DI, the product of insulin sensitivity (IS) and acute insulin response to glucose) and postprandial IS (PREDIM index, predicted M-value). Adipose tissue (AT) IR index was calculated as fasting plasma levels of FFA (mmol*l-1) x insulin (pmol*l-1). Postprandial total BCAA, VAL and LEU levels were 25% higher in patients with T1D compared with CON (AUC 11167±5136 vs. 8410±3298, 14363±959 vs. 11754±3890, 11980±4317 vs. 8476±4257 µmol*l-1*3 h-1, p & lt;0.05, respectively). PREDIM was lower in T1D (3.3±1.1 vs. CON 7.0±1.4 ml*min-1*m-2, p & lt;0.01), while fasting and postprandial AT IR were not different. Persons with T1D showed an inverse relationship between BCAA concentrations and C-peptide levels (total BCAA: r=-0.76, p & lt;0.01; VAL: r=-0.80, p & lt;0.01; LEU: r=-0.71, p & lt;0.05; ILE: r=-0.67, p & lt;0.05) and DI (total BCAA: r=-0.71, p & lt;0.05; VAL: r=-0.78, p & lt;0.01; LEU: r=-0.75, p & lt;0.01; ILE: r=-0.69, p & lt;0.05). In conclusion, persons with even well-controlled recent-onset T1D exhibit elevated postprandial BCAA concentrations, likely due to impaired ß-cell function, which contribute to postprandial IR. Disclosure Y. Karusheva: None. K. Strassburger: None. D.F. Markgraf: None. O.P. Zaharia: None. K. Bodis: None. A. Tura: None. G. Pacini: None. V. Burkart: None. J. Szendroedi: None. M. Roden: Advisory Panel; Self; Servier. Board Member; Self; Poxel SA. Consultant; Self; Eli Lilly and Company, Gilead Sciences, Inc., ProSciento, TARGET PharmaSolutions. Research Support; Self; Boehringer Ingelheim International GmbH, Novartis Pharma K.K., Sanofi US. Speaker’s Bureau; Self; Novo Nordisk A/S.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2020
    detail.hit.zdb_id: 1501252-9
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  • 5
    In: Diabetes, American Diabetes Association, Vol. 71, No. Supplement_1 ( 2022-06-01)
    Abstract: Background: The neurofilament light chain (NFL) is a polypeptide abundant in neuronal axons, reflecting ongoing neuroaxonal degeneration when detected in the blood. However, no previous study has explored NFL as a potential biomarker for diabetic sensorimotor polyneuropathy (DSPN) , a neurodegenerative disease of the peripheral nervous system commonly found in individuals with diabetes. We hypothesized that higher serum NFL levels are associated with DSPN. Methods: We used data from the German Diabetes Study, a prospective observational study that includes adults with recent-onset diabetes ( & lt;1 year) . DSPN was assessed using Toronto consensus criteria. Serum levels of NFL were measured using proximity extension assay, and Poisson regression was used to estimate associations between serum NFL and prevalent DSPN. Results: From a total of 423 participants, 66 (16%) had DSPN. Serum NFL was inversely correlated with age, eGFR and nerve conduction velocities in motor and sensory nerves (all P Spearman & lt;0.0001) . After adjustment for age, sex, waist circumference, height, HbA1c, diabetes duration, diabetes type, cholesterol, eGFR, hypertension, cardiovascular diseases, use of lipid-lowering drugs, and NSAIDs, higher serum levels of NFL were associated with prevalent DSPN (RR (95% CI) 1.92 (1.50, 2.45) (P & lt; 0.0001) . Conclusion: NFL might be useful for detecting DSPN in recent-onset diabetes, but validation in other studies will be required. Considering the absence of FDA-approved biomarkers for DSPN, NFL might be a promising biomarker that could improve the management of DSPN. Disclosure H. Maalmi: None. A. Strom: None. S.M. Hauck: None. G.J. Bönhof: None. W. Rathmann: Consultant; IQVIA Inc. Speaker's Bureau; Boehringer Ingelheim International GmbH, Novo Nordisk. S. Trenkamp: None. V. Burkart: None. J.M. Szendroedi: Consultant; Boehringer Ingelheim International GmbH. D. Ziegler: None. M. Roden: Advisory Panel; Eli Lilly and Company. Research Support; Boehringer Ingelheim International GmbH, Nutricia. Speaker's Bureau; Novo Nordisk. C. Herder: Research Support; Sanofi. Funding DZD (FKZ82DZD02D2G)
    Type of Medium: Online Resource
    ISSN: 0012-1797
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2022
    detail.hit.zdb_id: 1501252-9
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  • 6
    In: Diabetes, American Diabetes Association, Vol. 68, No. Supplement_1 ( 2019-06-01)
    Abstract: Hepatic insulin metabolism in patients with newly diagnosed diabetes is not yet understood. Insulin clearance seems to be decreased in patients with obesity, visceral adiposity and type 2 diabetes (T2D), but data compared to glucose tolerant humans have been inconclusive. To this end, persons with type 1 diabetes (T1D; n=124) or type 2 diabetes (T2D; n=401) and glucose-tolerant humans (CON; n=245) underwent hyperinsulinemic-euglycemic clamps to assess insulin sensitivity (IS) and whole-body insulin clearance (ICWBIC, ml x kg-1 x min-1). Hepatic insulin clearance was also calculated from the ratio of the areas under the curve of plasma C-peptide and insulin (0-60 min) during intravenous glucose-tolerance test (IVGTT, 0-60 min) and mixed meal tolerance test (MMTT, 0-180 min). Hepatocellular lipid content (HCL) was measured by 1H-magnetic resonance spectroscopy. Analyses were adjusted for age, sex and BMI. In T1D, ICIVGTT (1.71±1.1 vs. 2.3±0.3 and 3.2±0.3, all p & lt;0.05) as well as ICMMT (1.6±0.7 vs. 2.0±0.4 and 2.1±0.3, all p & lt;0.05) were lowest compared to T2D and CON respectively and correlated negatively with HbA1c (r=-0.242 and r=-0.279, both p & lt;0.05). In T2D, ICIVGTT was positively correlated with HbA1c (r=0.178, p & lt;0.05) as well as with IS (r=0.242, p & lt;0.05). T2D patients with hepatic steatosis (n=73) had lower ICIVGTT, ICWBIC as well as ICMMT (2.2±0.31 vs. 2.4±0.31, 1.4±0.4 vs. 1.5±0.4 and 1.9 ±0.3 vs. 2.1±0.2 respectively, (i.e., differences of 8%, 9% and 7%, all p & lt;0.05) compared to T2D without steatosis (n=53). CON with steatosis also had lower ICIVGTT (n=103, 2.1±0.2 vs. 2.3±0.35, p & lt;0.05). ICMMT positively correlated with IS (r=0.338 and r=0.187, both p & lt;0.05) in T1D and T2D, but not in CON. In conclusion, glycemic control likely impairs insulin clearance particularly in T1D patients, whereas steatosis affects insulin clearance in T2D and in glucose tolerant humans. Disclosure S. Antoniou: None. O.P. Zaharia: None. K. Strassburger: None. Y. Karusheva: None. K. Bodis: None. Y. Kupriyanova: None. V. Burkart: None. K. Muessig: None. A. Gastaldelli: Consultant; Self; A. Menarini Diagnostics, Eli Lilly and Company, Genentech, Inc., Gilead Sciences, Inc., Inventiva Pharma. M. Roden: Advisory Panel; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Poxel SA, Servier. Board Member; Self; Eli Lilly and Company. Research Support; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Sanofi. Speaker's Bureau; Self; Novo Nordisk Inc. J. Szendroedi: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
    detail.hit.zdb_id: 1501252-9
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  • 7
    In: Diabetes, American Diabetes Association, Vol. 68, No. Supplement_1 ( 2019-06-01)
    Abstract: Cluster analysis using age, BMI, glycemia and homeostasis model estimates (HOMA-IR, -B) revealed distinct risk profiles for progression of diabetic nephropathy in large cohorts, but its relevance for other diabetes-related comorbidities remains unclear. We aimed to (i) examine whether intensified phenotyping would confirm the results of this cluster analysis and (ii) test the hypothesis that liver fat content (HCL), as marker of nonalcoholic fatty liver disease (NAFLD), differs among clusters at diabetes diagnosis and during follow-up. Thus, this cluster analysis was applied to recent-onset patients with non-autoimmune diabetes of the German Diabetes Study. This identified 286 mild age-related (MARD, 44%), 268 mild obesity-related (MOD, 42%), 66 severe insulin-resistant (SIRD, 10%) and 27 severe insulin-deficient (SIDD, 4%) diabetes patients. Furthermore, whole-body insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamps, HCL by magnetic resonance spectroscopy and hepatic fibrosis by a noninvasive score (NAFLD-FS). Congruently, whole-body insulin sensitivity was lowest in SIRD compared to MOD, SIDD and MARD (4.3±2.0 vs. 5.6±2.4, 6.5±2.6, 7.6±2.8 mg*kg-¹*min-¹, all p & lt;0.05). In SIRD, HCL (14±4%) was higher than in SIDD (5±2%), MOD (9±1%) and MARD (7±1%) (all p & lt;0.05). In SIRD, HCL negatively correlated with whole-body insulin sensitivity (r=-0.27, p & lt;0.05). NAFLD-FS was highest in SIRD (0.4) compared to SIDD (-2.9), MOD (-0.8) and MARD (-0.8) (all p & lt;0.05). At the 5-year follow-up (n=159), whole-body insulin sensitivity remained lowest in SIRD (p & lt;0.05 vs. all clusters) with no difference in changes between clusters. Also, significant fibrosis (NAFLD-FS & gt;0.6) was highest in SIRD (21%) compared to SIDD (0%), MOD (16%) and MARD (11%). In conclusion, patients of the SIRD cluster exhibit higher prevalence of steatosis at diagnosis and increased risk of NAFLD progression over 5 years. Disclosure O.P. Zaharia: None. K. Strassburger: None. Y. Kupriyanova: None. Y. Karusheva: None. S. Antoniou: None. K. Bodis: None. O. Asplund: Research Support; Self; Eli Lilly and Company. V. Burkart: None. K. Muessig: None. J. Hwang: None. O. Kuss: None. L. Groop: None. E. Ahlqvist: None. J. Szendroedi: None. M. Roden: Advisory Panel; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Poxel SA, Servier. Board Member; Self; Eli Lilly and Company. Research Support; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Sanofi. Speaker's Bureau; Self; Novo Nordisk Inc. Funding German Ministry of Culture and Science of the State of North Rhine-Westphalia; German Federal Ministry of Health; German Federal Ministry of Education and Research
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
    detail.hit.zdb_id: 1501252-9
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  • 8
    In: Diabetes, American Diabetes Association, Vol. 67, No. Supplement_1 ( 2018-07-01)
    Abstract: Mutations in the gene encoding glucokinase (GCK) cause maturity-onset diabetes of the young (MODY) 2, characterized by impaired prandial insulin secretion and hepatic glycogen storage. Recently diagnosed patients with type 1 diabetes (T1D) exhibit impairment of both beta cell function and hepatic energy metabolism. Thus, this study aimed at examining the effect of MODY 2 on hepatic insulin sensitivity and energy metabolism. Carriers of one recently described GCK mutation (D124N; c.370, GAC & gt;AAC in exon 4) were compared to controls (CON) with similar sex, age and body mass index (BMI) (female/male: 1/2 vs. 3/6; 36±4 vs. 35±2 years; 20.1±1.6 vs. 25.7±1.5 kg/m2) from the German Diabetes Study (Registration_Clinicaltrials.gov NCT01409330). Whole body and hepatic insulin sensitivity (IS) were assessed by Botnia-clamp tests with [6,6-2H2]glucose. Beta cell function was determined from incremental AUC(C-peptide)0-60min/δAUC(glucose)0-60min during intravenous glucose tolerance test. H epatocellular lipid content (HCL), γATP and inorganic phosphate (Pi) were measured with by 1H/31P magnetic resonance spectroscopy. MODY 2 patients had higher hemoglobin A1c (6.1±0.1 vs. 5.2±0.1%, p & lt;0.001) along with approximately 62% lower glucose-stimulated C-peptide secretion than CON (p & lt;0.05). They also had lower hepatic IS (1.8±0.1 vs. 2.3±0.1 mg/(kg*min), p & lt;0.05), but similar whole body IS (12.6±1.9 vs. 13.1±1.5 mg/(kg*min), p=0.87) compared to CON. However, HCL (1.0±0.9 vs. 0.5±0.2%, p=0.46), γATP (3.5±0.3 vs. 3.5±0.6 mmol/l, p=0.99) and Pi (1.9±0.5 vs. 2.9±0.7 mmol/l, p=0.45) in the liver were comparable between both groups. In conclusion, these data show that lower hepatic IS, but not abnormal hepatic energy metabolism, underlies the previously reported reduction in prandial hepatic glycogen synthesis. Moreover, impairment of hepatic IS is not necessarily associated with hepatic mitochondrial function. Disclosure K. Bódis: None. O.P. Zaharia: None. Y. Karusheva: None. P. Bobrov: None. D.F. Markgraf: None. B. Knebel: None. Y. Kupriyanova: None. J. Hwang: None. V. Burkart: None. K. Müssig: None. M. Roden: Speaker's Bureau; Self; Boehringer Ingelheim GmbH. Research Support; Self; Boehringer Ingelheim GmbH. Consultant; Self; Poxel SA. Research Support; Self; Danone Nutricia Early Life Nutrition, GlaxoSmithKline plc., Nutricia Advanced Medical Nutrition, Sanofi. J. Szendroedi: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
    detail.hit.zdb_id: 1501252-9
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  • 9
    In: Diabetes, American Diabetes Association, Vol. 69, No. Supplement_1 ( 2020-06-01)
    Abstract: The G-allele in the single-nucleotide polymorphism (SNP) rs738409 in the patatin-like phospholipase domain containing 3 (PNPLA3) gene associates with increased risk of nonalcoholic fatty liver disease (NAFLD) and its progression. As the recently-described severe insulin resistant diabetes (SIRD) cluster specifically relates to NAFLD, the present study examined whether this SNP differently associates with insulin sensitivity and hepatic lipid content (HCL) in clusters of new-onset diabetes patients. Participants (n=917) of the prospective German Diabetes Study underwent genotyping, hyperinsulinemic-euglycemic clamps and magnetic resonance spectroscopy. SIRD had the lowest whole-body insulin sensitivity compared to severe insulin deficient (SIDD), moderate obesity-related (MOD), moderate age-related (MARD) and severe autoimmune diabetes clusters (SAID; all p & lt;0.001). Interestingly, SIRD presented with higher prevalence of the G-allele compared to other clusters and the glucose tolerant controls (p & lt;0.05). Also, HCL was higher in SIRD [13.6 (5.8;19.1)%] compared to MOD [6.4 (2.1;12.4)%] , MARD [3.0 (1.0;7.9)%], SAID [0.4 (0.0;1.5)%] and the glucose tolerant group [0.9 (0.4;4.9)%] (all p & lt;0.05). Although the PNPLA3 polymorphism did not directly associate with whole-body insulin sensitivity or HCL in SIRD, G-allele carriers of this cluster had higher free fatty acids and greater adipose-tissue insulin resistance than non-carriers. In conclusion, SIRD patients are more frequently carriers of the G-allele which is associated with adipose-tissue insulin resistance and lipolysis. Together, these alterations may mutually accelerate NAFLD and progression of SIRD. Disclosure O.P. Zaharia: None. K. Strassburger: None. B. Knebel: None. Y. Kupriyanova: None. Y. Karusheva: None. K. Bodis: None. M. Wolkersdorfer: None. D.F. Markgraf: None. V. Burkart: None. J. Hwang: None. J. Kotzka: None. H. Al-Hasani: Consultant; Self; Bayer AG. J. Szendroedi: None. M. Roden: Advisory Panel; Self; Servier. Board Member; Self; Poxel SA. Consultant; Self; Eli Lilly and Company, Gilead Sciences, Inc., ProSciento, TARGET PharmaSolutions. Research Support; Self; Boehringer Ingelheim International GmbH, Novartis Pharma K.K., Sanofi US. Speaker’s Bureau; Self; Novo Nordisk A/S. Funding German Federal Ministry of Health; Ministry of Culture and Science of North Rhine-Westphalia; German Federal Ministry of Education and Research; German Center for Diabetes Research
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2020
    detail.hit.zdb_id: 1501252-9
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  • 10
    In: Diabetes, American Diabetes Association, Vol. 71, No. Supplement_1 ( 2022-06-01)
    Abstract: Insulin resistance and nonalcoholic fatty liver disease (NAFLD) frequently associate with type 2 diabetes (T2D) and cardiovascular disease and worsen their prognosis. We hypothesized that people with recent myocardial infarction (MI) have lower left ventricular ejection fraction (EF) and higher degree of insulin resistance (IR) , hepatocellular lipid content (HCL) and risk of hepatic fibrosis than matched people without MI. Thus, participants of the “DIabetes and ST-Elevation MI (DISTEMI) Study” were examined 6-12 weeks after MI (MI+; n=53, 28% T2D) and compared to age-, sex-, BMI-matched people without MI (MI-; n=48, 31% T2D) . Insulin sensitivity was assessed during fasting (Homeostasis Model Assessment (HOMA) 2-IR) and hyperinsulinemic-euglycemic clamps (M-value) . EF, HCL and liver stiffness, associated with fibrosis stages, were quantified by 1H-magnetic resonance imaging, spectroscopy and elastography, respectively. MI+ had a lower EF (47±2 vs. 58±1 %, p & lt;0.0001) and M-value (7.3±0.4 vs. 8.2±0.4 mg*kg-1*min-1, p & lt;0.05) compared to MI-, which was mainly due to a difference between the T2D groups (EF: 39±6 vs. 52±2 %, p & lt;0.001; M-value: 4.2±0.5 vs. 6.1±0.6 mg*kg-1*min-1, p & lt;0.05) . HCL (3.4±0.8 vs. 5.8±0.9 %) and liver stiffness (2.2±0.1 vs. 2.3±0.1 kPa) were comparable between MI+ and MI-. HCL correlated negatively with M-value (r=-0.95, p & lt;0.05) and positively with systolic blood pressure (r=0.91, p & lt;0.05) in MI+ with T2D. In MI+ without T2D, HCL correlated positively with HOMA2-IR (r=0.58, p & lt;0.01) and BMI (r=0.53, p & lt;0.01) . In conclusion, recent myocardial infarction in people with type 2 diabetes associates with decreased ejection fraction and increased insulin resistance. The correlation between insulin resistance and liver fat content suggests that HCL can serve as a non-invasive cardiovascular marker and may identify persons with a worse outcome after myocardial infarction. Disclosure C.Möser: None. M.Roden: Advisory Panel; Eli Lilly and Company, Research Support; Boehringer Ingelheim International GmbH, Nutricia, Speaker's Bureau; Novo Nordisk. O.P.Zaharia: n/a. F.C.Michlotti: None. Y.Kupriyanova: None. V.Schrauwen-hinderling: None. P.Bobrov: None. V.Burkart: None. M.Kelm: Board Member; DGIM-Deutsche Geselleschaft für Innere Medizin, DGK-Deutsche Gesellschaft für Kardiologie, DSHF-Deutsche Stiftung für Herzforschung, ESC- European Society of Cardiology, Other Relationship; Abiomed , Bayer AG, diaplan, Kel Con GmbH, Research Support; Abiomed Europe GmbH, B.Braun, Edwards Lifesciences Corporation, European Union, IPP Med GmbH - Institut für Pharmakologie u. präventive Medizin GmbH, Mars Scientific Advisory Council (MSAC) , Medicure Inc., Microvision Medical. J.M.Szendroedi: Consultant; Boehringer Ingelheim International GmbH. Funding Research Network SFB 1116 of the German Research Foundation
    Type of Medium: Online Resource
    ISSN: 0012-1797
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2022
    detail.hit.zdb_id: 1501252-9
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