دورية أكاديمية
أعرض في EDS

Effect of LKB1 deficiency on mitochondrial content, fibre type and muscle performance in the mouse diaphragm.

التفاصيل البيبلوغرافية
العنوان: Effect of LKB1 deficiency on mitochondrial content, fibre type and muscle performance in the mouse diaphragm.
المؤلفون: Brown JD; Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT, USA., Hancock CR, Mongillo AD, Benjamin Barton J, DiGiovanni RA, Parcell AC, Winder WW, Thomson DM
المصدر: Acta physiologica (Oxford, England) [Acta Physiol (Oxf)] 2011 Apr; Vol. 201 (4), pp. 457-66. Date of Electronic Publication: 2011 Jan 19.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Wiley-Blackwell Country of Publication: England NLM ID: 101262545 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1748-1716 (Electronic) Linking ISSN: 17481708 NLM ISO Abbreviation: Acta Physiol (Oxf) Subsets: MEDLINE
أسماء مطبوعة: Publication: Oxford : Wiley-Blackwell
Original Publication: Oxford : Blackwell Pub., c2006-4
مواضيع طبية MeSH: Diaphragm/*anatomy & histology , Diaphragm/*physiology , Mitochondria/*metabolism , Muscle Fibers, Skeletal/*cytology , Muscle Fibers, Skeletal/*physiology , Protein Serine-Threonine Kinases/*deficiency, AMP-Activated Protein Kinases/metabolism ; Aminoimidazole Carboxamide/analogs & derivatives ; Aminoimidazole Carboxamide/pharmacology ; Animals ; Diaphragm/drug effects ; Electric Stimulation ; Enzyme Activation ; Male ; Mice ; Mice, Knockout ; Protein Serine-Threonine Kinases/genetics ; Ribonucleotides/pharmacology ; Signal Transduction/physiology
مستخلص: Aim: The liver kinase B1 (LKB1)/AMP-activated protein kinase (AMPK) signalling pathway is a major regulator of skeletal muscle metabolic processes. During exercise, LKB1-mediated phosphorylation of AMPK leads to its activation, promoting mitochondrial biogenesis and glucose transport, among other effects. The roles of LKB1 and AMPK have not been fully characterized in the diaphragm.
Methods: Two methods of AMPK activation were used to characterize LKB1/AMPK signalling in diaphragms from muscle-specific LKB1 knockout (KO) and littermate control mice: (1) acute injection of 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) and (2) 5-min direct electrical stimulation of the diaphragm. Diaphragms were excised 60 min post-AICAR injection and immediately after electrical stimulation.
Results: AMPK phosphorylation increased with AICAR and electrical stimulation in control but not KO mice. Acetyl CoA carboxylase phosphorylation increased with AICAR in control but not KO mice, but increased in both genotypes with electrical stimulation. While the majority of mitochondrial protein levels were lower in KO diaphragms, uncoupling protein 3, complex I and cytochrome oxidase IV protein levels were not different between genotypes. KO diaphragms have a lower percentage of IIx fibres and an elevated percentage of IIb fibres when compared with control diaphragms. While in vitro peak force generation was similar between genotypes, KO diaphragms fatigued more quickly and had an impaired ability to recover.
Conclusion: LKB1 regulates AMPK phosphorylation, mitochondrial protein expression, fibre type distribution, as well as recovery of the diaphragm from fatigue.
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معلومات مُعتمدة: R01 AR051928 United States AR NIAMS NIH HHS; R01 AR051928-04 United States AR NIAMS NIH HHS; AR-051928 United States AR NIAMS NIH HHS
المشرفين على المادة: 0 (Ribonucleotides)
360-97-4 (Aminoimidazole Carboxamide)
EC 2.7.11.1 (Protein Serine-Threonine Kinases)
EC 2.7.11.1 (Stk11 protein, mouse)
EC 2.7.11.31 (AMP-Activated Protein Kinases)
F0X88YW0YK (AICA ribonucleotide)
تواريخ الأحداث: Date Created: 20101116 Date Completed: 20110617 Latest Revision: 20211203
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC3053411
DOI: 10.1111/j.1748-1716.2010.02226.x
PMID: 21073663
قاعدة البيانات: MEDLINE
الوصف
تدمد:1748-1716
DOI:10.1111/j.1748-1716.2010.02226.x