دورية أكاديمية
أعرض في EDS

Ventricular assist device implantation improves skeletal muscle function, oxidative capacity, and growth hormone/insulin-like growth factor-1 axis signaling in patients with advanced heart failure.

التفاصيل البيبلوغرافية
العنوان: Ventricular assist device implantation improves skeletal muscle function, oxidative capacity, and growth hormone/insulin-like growth factor-1 axis signaling in patients with advanced heart failure.
المؤلفون: Khawaja T; Center for Advanced Cardiac Care, Department of Medicine, Division of Cardiology, Columbia University Medical Center, 622 West 168th Street, PH 10, Room 203, New York, NY, 10032, USA., Chokshi A, Ji R, Kato TS, Xu K, Zizola C, Wu C, Forman DE, Ota T, Kennel P, Takayama H, Naka Y, George I, Mancini D, Schulze CP
المصدر: Journal of cachexia, sarcopenia and muscle [J Cachexia Sarcopenia Muscle] 2014 Dec; Vol. 5 (4), pp. 297-305. Date of Electronic Publication: 2014 Aug 07.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders Country of Publication: Germany NLM ID: 101552883 Publication Model: Print-Electronic Cited Medium: Print ISSN: 2190-5991 (Print) Linking ISSN: 21905991 NLM ISO Abbreviation: J Cachexia Sarcopenia Muscle Subsets: PubMed not MEDLINE
أسماء مطبوعة: Publication: 2015- : Berlin : John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders
Original Publication: Heidelburg : Springer-Verlag
مستخلص: Background: Skeletal muscle dysfunction in patients with heart failure (HF) has been linked to impaired growth hormone (GH)/insulin-like growth factor (IGF)-1 signaling. We hypothesized that ventricular assist device (VAD) implantation reverses GH/IGF-1 axis dysfunction and improves muscle metabolism in HF.
Methods: Blood and rectus abdominis muscle samples were collected during VAD implantation and explantation from patients with HF and controls. Clinical data were obtained from medical records, biomarkers measured by enzyme-linked immunosorbent assay (ELISA), and gene expression analyzed by reverse transcription and real-time polymerase chain reaction (RT-PCR). Grip strength was assessed by dynamometry. Oxidative capacity was measured using oleate oxidation rates. Muscle fiber type and size were assessed by histology.
Results: Elevated GH (0.27 ± 0.27 versus 3.6 ± 7.7 ng/ml in HF; p = 0.0002) and lower IGF-1 and insulin-like growth factor binding protein (IGFBP)-3 were found in HF (IGF-1, 144 ± 41 versus 74 ± 45 ng/ml in HF, p < 0.05; and IGFBP-3, 3,880 ± 934 versus 1,935 ± 862 ng/ml in HF, p = 0.05). The GH/IGF-1 ratio, a marker of GH resistance, was elevated in HF (0.002 ± 0.002 versus 0.048 ± 0.1 pre-VAD; p < 0.0039). After VAD support, skeletal muscle expression of IGF-1 and IGFBP-3 increased (10-fold and 5-fold, respectively; p < 0.05) accompanied by enhanced oxidative gene expression (CD36, CPT1, and PGC1α) and increased oxidation rates (+1.37-fold; p < 0.05). Further, VAD implantation increased the oxidative muscle fiber proportion (38 versus 54 %, p = 0.031), fiber cross-sectional area (CSA) (1,005 ± 668 versus 1,240 ± 670 μm(2), p < 0.001), and Akt phosphorylation state in skeletal muscle. Finally, hand grip strength increased 26.5 ± 27.5 % at 180 days on-VAD (p < 0.05 versus baseline).
Conclusion: Our data demonstrate that VAD implantation corrects GH/IGF-1 signaling, improves muscle structure and function, and enhances oxidative muscle metabolism in patients with advanced HF.
التعليقات: Erratum in: J Cachexia Sarcopenia Muscle. 2014 Dec;5(4):349. (PMID: 25209627)
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معلومات مُعتمدة: K23 HL095742 United States HL NHLBI NIH HHS; P30 HL101272 United States HL NHLBI NIH HHS; R01 HL045095 United States HL NHLBI NIH HHS; UL1 RR024156 United States RR NCRR NIH HHS; R37 HL045095 United States HL NHLBI NIH HHS; R01 HL073029 United States HL NHLBI NIH HHS
تواريخ الأحداث: Date Created: 20140808 Date Completed: 20141126 Latest Revision: 20211021
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC4248410
DOI: 10.1007/s13539-014-0155-9
PMID: 25100356
قاعدة البيانات: MEDLINE
الوصف
تدمد:2190-5991
DOI:10.1007/s13539-014-0155-9