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  • 1
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    Adipokine Protein Expression Pattern in Growth Hormone Deficiency Predisposes to the Increased Fat Cell Size and the Whole Body Metabolic Derangements
    The Endocrine Society ; 2008
    In:  The Journal of Clinical Endocrinology & Metabolism Vol. 93, No. 6 ( 2008-06-01), p. 2255-2262
    Details
    In: The Journal of Clinical Endocrinology & Metabolism, The Endocrine Society, Vol. 93, No. 6 ( 2008-06-01), p. 2255-2262
    Kurzfassung: Context: GH deficiency (GHD) in adults is associated with central adiposity, dyslipidemia, and insulin resistance. Objective: The objective of the study was to test the hypothesis that GHD might change the spectrum of adipokines and thus influence the adipose tissue and the whole-body metabolic and inflammatory status leading to development of insulin resistance. Design: This was a single-center observational study with a cross-sectional design. Participants and Methods: Protein arrays were used to characterize adipokines expressed in the sc adipose tissue obtained from young GHD adults and compared with age-, gender-, and body mass index (BMI)-matched group of healthy individuals. All subjects underwent an oral glucose tolerance test, euglycemic hyperinsulinemic clamp, and magnetic resonance imaging examination. Results: Presence of abdominal obesity, enlarged adipocytes, increased circulating high-sensitivity C-reactive protein, impaired glucose tolerance, and decreased insulin action were found in GHD. Changes in adipokine protein expression due to GHD were highly dependent on the obesity phenotype. Lean GHD individuals (BMI ∼23 kg/m2) had decreased protein levels for stem cell factor and epithelial growth factor, indicating a possible defect in adipocyte differentiation and proliferation. Decrease of vascular endothelial growth factor, stromal cell-derived factor, angiopoietin-2, and brain-derived neurotrophic factor advocated for attenuated angiogenesis and neurogenesis. Presence of obesity (BMI ∼31 kg/m2) eliminated these inhibitory effects. However, adipose tissue expansion in GHD individuals was paralleled by an elevation of adipose tissue proinflammatory cytokines (IL-1β, interferon-γ) and chemoattractants (interferon-inducible T cell α-chemoattractant, monocyte chemotactic protein-2, monocyte chemotactic protein-3, eotaxin). Conclusion: Our data demonstrate that GHD modulates adipokine and cytokine protein expression pattern, which might influence the adipose tissue growth and differentiation and predispose to tissue hypoxia, inflammation, and a defect in the whole-body insulin action.
    Materialart: Online-Ressource
    ISSN: 0021-972X , 1945-7197
    URL: Article
    DOI: 10.1210/jc.2007-2188
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The Endocrine Society
    Publikationsdatum: 2008
    ZDB Id: 2026217-6
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
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    The association of plasma cystatin C proteoforms with diabetic chronic kidney disease
    Springer Science and Business Media LLC ; 2016
    In:  Proteome Science Vol. 14, No. 1 ( 2016-12)
    Details
    In: Proteome Science, Springer Science and Business Media LLC, Vol. 14, No. 1 ( 2016-12)
    Materialart: Online-Ressource
    ISSN: 1477-5956
    URL: Article
    DOI: 10.1186/s12953-016-0096-7
    Sprache: Englisch
    Verlag: Springer Science and Business Media LLC
    Publikationsdatum: 2016
    ZDB Id: 2141087-2
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
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    187-OR: Advanced Glycation End Products Predict Loss of Renal Function and High-Risk Chronic Kidney Disease in Type 2 Diabetes in the ACCORD Trial
    American Diabetes Association ; 2021
    In:  Diabetes Vol. 70, No. Supplement_1 ( 2021-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 70, No. Supplement_1 ( 2021-06-01)
    Kurzfassung: Individual advanced glycation end products (AGEs) have been implicated in the development of chronic kidney disease (CKD). We evaluated the prognostic utility of a comprehensive multicomponent AGE panel in predicting long-term renal function loss and CKD when added to routine clinical measures in persons with type 2 diabetes (T2D) followed for 12.5 years (including risk factor intervention and observation phases). The five key AGEs (carboxymethyl and carboxyethyl lysine, and methylglyoxal, 3-deoxyglucosone and glyoxal hydroimidazolone) were measured via LC-MS/MS in baseline serum from 1,151 the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial participants. A composite AGE score was calculated as the mean of individual AGE z-scores. Outcomes were (1) renal function loss (≥40% decline in estimated glomerular filtration rate [eGFR]), (2) macroalbuminuria (MAU), and (3) high-risk CKD (hrCKD, KDIGO classification). Higher AGE score predicted greater risks of renal function loss (n=260 events, hazard ratio 1.49 [95%CI 1.24-1.79] , p & lt;0.0001), MAU (n=96, 1.45 [1.06-1.98], p=0.005) and hrCKD (n=128, 1.95 [1.47-2.57] , p & lt;0.0001), independent of baseline eGFR, urine albumin:creatinine, randomization arms, other standard risk factors and hemoglobin A1c. Higher AGE score predicted renal function loss even in those with normal renal function (1.40 [1.06-1.84], p=0.02). When added to routine risk factors, AGE score improved net-reclassification and integrated discrimination for renal function loss (by 19% and 17%, p=0.002) and hrCKD (by 34% and 4.9%; p=0.02), but not MAU (0.8% and 1.3%, p=0.6). There is a strong independent association between AGE burden and progression of CKD in T2D. Adding AGE measures to standard clinical parameters improves the prediction of multiple kidney outcomes, indicating its potential as prognostic biomarker of diabetes nephropathy. Disclosure J. Koska: None. H. C. Gerstein: Advisory Panel; Self; Novo Nordisk Inc., Pfizer Inc., Sanofi, Consultant; Self; Abbott, Covance Inc., Eli Lilly and Company, Kowa Company, Ltd., Sanofi, Other Relationship; Self; Boehringer Ingelheim (Canada) Ltd., DKSH, Eli Lilly and Company, Sanofi, Zuellig, Research Support; Self; AstraZeneca, Eli Lilly and Company, Merck & Co., Inc., Novo Nordisk Inc., Sanofi. P. J. Beisswenger: Stock/Shareholder; Self; PreventAGE Healthcare LLC. P. Reaven: Research Support; Self; AstraZeneca, Dexcom, Inc. Funding National Institutes of Health (R21HL150268)
    Materialart: Online-Ressource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db21-187-OR
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 2021
    ZDB Id: 1501252-9
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
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    Pancreatic Polypeptide Is Involved in the Regulation of Body Weight in Pima Indian Male Subjects
    American Diabetes Association ; 2004
    In:  Diabetes Vol. 53, No. 12 ( 2004-12-01), p. 3091-3096
    Details
    In: Diabetes, American Diabetes Association, Vol. 53, No. 12 ( 2004-12-01), p. 3091-3096
    Kurzfassung: Pancreatic polypeptide (PP) is released from the pancreas in response to a meal. In humans, low-circulating PP levels have been observed in obesity, and administration of pharmacological doses of PP has been shown to decrease food intake. The aim of the present study was to investigate whether low circulating PP is associated with weight gain in Pima Indians. Plasma PP concentrations were measured after an overnight fast and 30 min after a standardized mixed meal in 33 nondiabetic male subjects who had a follow-up visit 4.9 ± 2.5 years later. Cross-sectionally, fasting and postprandial PP levels were negatively associated with body size and adiposity. Prospectively, the change in PP response to the meal was negatively associated with the change in body weight (r = −0.53, P = 0.002). In contrast, a high fasting PP level was positively associated with change in body weight (r = 0.45, P = 0.009). In conclusion, our results provide evidence that, even within the physiological range, PP contributes to the regulation of energy balance in humans. However this contribution appears to be more complex than anticipated because of the opposite effect of fasting and postprandial PP on the risk of future weight gain.
    Materialart: Online-Ressource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diabetes.53.12.3091
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 2004
    ZDB Id: 1501252-9
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
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    Blood Pressure Variability and Risk of Heart Failure in ACCORD and the VADT
    American Diabetes Association ; 2020
    In:  Diabetes Care Vol. 43, No. 7 ( 2020-07-01), p. 1471-1478
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 43, No. 7 ( 2020-07-01), p. 1471-1478
    Kurzfassung: Although blood pressure variability is increasingly appreciated as a risk factor for cardiovascular disease, its relationship with heart failure (HF) is less clear. We examined the relationship between blood pressure variability and risk of HF in two cohorts of type 2 diabetes participating in trials of glucose and/or other risk factor management. RESEARCH DESIGN AND METHODS Data were drawn from the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial and the Veterans Affairs Diabetes Trial (VADT). Coefficient of variation (CV) and average real variability (ARV) were calculated for systolic (SBP) and diastolic blood pressure (DBP) along with maximum and cumulative mean SBP and DBP during both trials. RESULTS In ACCORD, CV and ARV of SBP and DBP were associated with increased risk of HF, even after adjusting for other risk factors and mean blood pressure (e.g., CV-SBP: hazard ratio [HR] 1.15, P = 0.01; CV-DBP: HR 1.18, P = 0.003). In the VADT, DBP variability was associated with increased risk of HF (ARV-DBP: HR 1.16, P = 0.001; CV-DBP: HR 1.09, P = 0.04). Further, in ACCORD, those with progressively lower baseline blood pressure demonstrated a stepwise increase in risk of HF with higher CV-SBP, ARV-SBP, and CV-DBP. Effects of blood pressure variability were related to dips, not elevations, in blood pressure. CONCLUSIONS Blood pressure variability is associated with HF risk in individuals with type 2 diabetes, possibly a consequence of periods of ischemia during diastole. These results may have implications for optimizing blood pressure treatment strategies in those with type 2 diabetes.
    Materialart: Online-Ressource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc19-2540
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 2020
    ZDB Id: 1490520-6
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
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    208-OR: Posttranslational Truncation of Apolipoproteins C1 and C2 and Plasma Lipids in Multiethnic Study of Atherosclerosis (MESA)
    American Diabetes Association ; 2022
    In:  Diabetes Vol. 71, No. Supplement_1 ( 2022-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 71, No. Supplement_1 ( 2022-06-01)
    Kurzfassung: Apolipoproteins (apo) C1 and C2 are small interchangeable molecules that regulate lipoprotein metabolism. ApoC1 inhibits lipoprotein lipase (LPL) and stimulates reverse cholesterol transport while apoC2 activates LPL. Both exist as full-size native and minor truncated proteoforms; however, whether distribution of these apoC1 and C2 proteoforms may influence plasma lipids is largely unknown. Baseline plasma from 5,791 MESA participants was tested for truncated to native apoC1 and apoC2 ratios (apoC1’/C1; apoC2’/C2) . Total apoC1 and C2 concentrations were measured in a subset of 3,851 participants. Plasma lipids were measured for up to 6 times over 15 years. In adjusted models (Table) , higher apoC1’/C1 was associated with lower triglycerides (TG) and higher total (TC) and LDL cholesterol both at baseline and follow-up, and higher HDL at follow-up. Higher apoC2’/C2 was associated with lower TG and higher LDL at baseline, and higher baseline and follow-up TC and HDL. In contrast, the associations of total apoC1 and apoC2 concentrations with TG and HDL were largely in opposite directions of their proteoform ratios. For example, plasma TG were inversely associated with apoC1 and apoC2 truncation but positively associated with total apoC1 and apoC2 concentrations. Our data indicate a possible role of posttranslational apoC1 and apoC2 modification in regulating lipid metabolism. Disclosure J.Koska: None. J.Furtado: Research Support; Eli Lilly and Company, Pfizer Inc. S.Sinari: None. R.Mcclelland: None. D.Billheimer: None. P.Reaven: Research Support; AstraZeneca, Dexcom, Inc. Funding National Institutes of Health (R01-HL138969
    Materialart: Online-Ressource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db22-208-OR
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 2022
    ZDB Id: 1501252-9
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
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    989-P: Influence of Baseline Blood Pressure on Associations of Visit-to-Visit Blood Pressure Variability and Cardiovascular Risk: Results from the ACCORD Trial
    American Diabetes Association ; 2021
    In:  Diabetes Vol. 70, No. Supplement_1 ( 2021-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 70, No. Supplement_1 ( 2021-06-01)
    Materialart: Online-Ressource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db21-989-P
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 2021
    ZDB Id: 1501252-9
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
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    1240-P: Triglyceride Variability and Risk of Adverse Cardiovascular Outcomes—Results from the ACCORD Trial
    American Diabetes Association ; 2023
    In:  Diabetes Vol. 72, No. Supplement_1 ( 2023-06-20)
    Details
    In: Diabetes, American Diabetes Association, Vol. 72, No. Supplement_1 ( 2023-06-20)
    Kurzfassung: The potential role of visit-to-visit variability of lipid parameters in risk of adverse cardiovascular events is not well established. We used data from the Action to Control Cardiovascular Risk in Diabetes (ACCORD) Trial to examine the relationship between visit-to-visit variability in triglycerides and risk of both heart failure (HF) events and the primary CVD outcome. Variability of triglycerides was computed as coefficient of variation (CV-Trig). In both age-adjusted models and models adjusting for covariates that differed between those who did and did not develop HF, CV-Trig was associated with risk of HF (Model 2, HR = 1.13, p = 0.03) (Table). This association was somewhat attenuated when accounting for mean triglyceride level (Table). Conversely, we did not observe any relationship between CV-Trig and the primary CVD outcome in ACCORD (Model 1: HR = 1.04, p = 0.21) (Table). LDL variability was not linked to risk of HF in ACCORD. Our results suggest that variability in triglycerides may play a more important role in HF than in other cardiovascular outcomes. Studies to elucidate mechanisms which may underlie these risk patterns are warranted. Disclosure D.S.Nuyujukian: None. J.Zhou: None. J.Koska: None. P.Reaven: Research Support; Dexcom, Inc. Funding National Heart, Lung, and Blood Institute (F32HL156626, R21HL150374, R21HL150268, R01HL138969)
    Materialart: Online-Ressource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db23-1240-P
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 2023
    ZDB Id: 1501252-9
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
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    The Effect of Intensive Glucose Lowering on Lipoprotein Particle Profiles and Inflammatory Markers in the Veterans Affairs Diabetes Trial (VADT)
    American Diabetes Association ; 2013
    In:  Diabetes Care Vol. 36, No. 8 ( 2013-08-01), p. 2408-2414
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 36, No. 8 ( 2013-08-01), p. 2408-2414
    Kurzfassung: Intensive glucose-lowering therapy (INT) did not reduce macrovascular events in the recent randomized trials, possibly because it did not improve or worsen other traditional or novel cardiovascular risk factors. RESEARCH DESIGN AND METHODS Standard plasma lipids, cholesterol content of lipoprotein subfractions, and plasma inflammatory and prothrombotic markers were determined in a subgroup of the Veterans Affairs Diabetes Trial (VADT) participants (n = 266) at baseline and after 9 months of INT or standard therapy. RESULTS INT lowered glycated hemoglobin (by a median of 2% vs. a median of 0.7% by standard treatment; P & lt; 0.0001); increased BMI (4 vs. 1%; P & lt; 0.001), total HDL (9 vs. 4%; P & lt; 0.05), HDL2 (14 vs. 0%; P = 0.009), LDL2 (36 vs. 1%; P & lt; 0.0001), and plasma adiponectin (130 vs. 80%; P & lt; 0.01); and reduced triglycerides (−13 vs. −4%; P = 0.02) and small, dense LDL4 (−39 vs. −13%; P & lt; 0.001), but had no effect on levels of plasma apolipoproteins B-100 and B-48, C-reactive protein, interleukin-6, lipoprotein-associated phospholipase A2, myeloperoxidase, fibrinogen, and plasminogen activator inhibitor 1. Incident macrovascular events were associated with baseline interleukin-6 (hazard ratio per each quartile increase 1.33 [95% CI 1.06–1.66]), total LDL (1.25 [1.01–1.55] ), apolipoprotein B-100 (1.29 [1.01–1.65]), and fibrinogen (1.26 [1.01–1.57] ) but not changes in any cardiovascular risk factors at 9 months. CONCLUSIONS INT was associated with improved adiponectin, lipid levels, and a favorable shift in LDL and HDL subfractions after 9 months. These data suggest that the failure of INT to lower cardiovascular outcomes occurred despite generally favorable changes in standard and novel risk factors early in the study.
    Materialart: Online-Ressource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc12-2082
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 2013
    ZDB Id: 1490520-6
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
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    The Effect of Exenatide Once Weekly on Carotid Atherosclerosis in Individuals With Type 2 Diabetes: An 18-Month Randomized Placebo-Controlled Study
    American Diabetes Association ; 2021
    In:  Diabetes Care Vol. 44, No. 6 ( 2021-06-01), p. 1385-1392
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 44, No. 6 ( 2021-06-01), p. 1385-1392
    Kurzfassung: Glucagon-like peptide 1 receptor agonists (GLP-1RAs) improved multiple proatherogenic risk factors and reduced cardiovascular events in recent clinical trials, suggesting that they may slow progression of atherosclerosis. We tested whether exenatide once weekly reduces carotid plaque progression in individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS In a double-blind, pragmatic trial, 163 participants were randomized (2:1) to exenatide (n = 109) or placebo (n = 54). Changes in carotid plaque volume and composition were measured at 9 and 18 months by multicontrast 3 Tesla MRI. Fasting and post–high-fat meal plasma glucose and lipids, and endothelial function responses, were measured at 3, 9, and 18 months. RESULTS Exenatide reduced hemoglobin A1c (HbA1c) (estimated difference vs. placebo 0.55%, P = 0.0007) and fasting and postmeal plasma glucose (19 mg/dL, P = 0.0002, and 25 mg/dL, P & lt; 0.0001, respectively). Mean (SD) change in plaque volume in the exenatide group (0.3% [2%]) was not different from that in the placebo group (−2.2% [8%] ) (P = 0.4). The change in plaque volume in the exenatide group was associated with changes in HbA1c (r = 0.38, P = 0.0004), body weight, and overall plasma glucose (r = 0.29, P = 0.007 both). There were no differences in changes in plaque composition, body weight, blood pressure, fasting and postmeal plasma triglycerides, and endothelial function between the groups. CONCLUSIONS Exenatide once weekly for up to 18 months improved fasting and postprandial glycemic control but did not modify change in carotid plaque volume or composition. This study raises the possibility that short-term antiatherosclerotic effects may not play a central role in the cardiovascular benefits of GLP-1RAs.
    Materialart: Online-Ressource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc20-2014
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 2021
    ZDB Id: 1490520-6
    Standort Signatur Einschränkungen Verfügbarkeit
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