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  • 1.
    Bondia-Pons, Isabel
    et al.
    VTT Technical Research Centre of Finland, Espoo, Finland; Department of Food Science and Physiology, University of Navarra, Pamplona, Spain.
    Maukonen, Johanna
    VTT Technical Research Centre of Finland, Espoo, Finland.
    Mattila, Ismo
    VTT Technical Research Centre of Finland, Espoo, Finland.
    Rissanen, Aila
    Obesity Research Unit, Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland; Department of Psychiatry, Helsinki University Central Hospital, Helsinki, Finland.
    Saarela, Maria
    VTT Technical Research Centre of Finland, Espoo, Finland.
    Kaprio, Jaakko
    Department of Public Health, Hjelt Institute, University of Helsinki, Helsinki, Finland; Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland; National Institute for Health and Welfare, Helsinki, Finland.
    Hakkarainen, Antti
    Department of Medicine, Division of Endocrinology, Helsinki University Central Hospital, Helsinki, Finland.
    Lundbom, Jesper
    Department of Radiology, Hospital District of Helsinki and Uusimaa (HUS) Medical Imaging Center, Helsinki University Central Hospital, Helsinki, Finland.
    Lundbom, Nina
    Department of Radiology, Hospital District of Helsinki and Uusimaa (HUS) Medical Imaging Center, Helsinki University Central Hospital, Helsinki, Finland.
    Hyötyläinen, Tuulia
    Örebro universitet, Institutionen för naturvetenskap och teknik. VTT Technical Research Centre of Finland, Espoo, Finland; Steno Diabetes Center, Gentofte, Denmark.
    Pietiläinen, Kirsi H.
    Obesity Research Unit, Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland; Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland; Department of Medicine, Division of Endocrinology, Helsinki University Central Hospital, Helsinki, Finland.
    Oresic, Matej
    Örebro universitet, Institutionen för medicinska vetenskaper. VTT Technical Research Centre of Finland, Espoo, Finland; Steno Diabetes Center, Gentofte, Denmark.
    Metabolome and fecal microbiota in monozygotic twin pairs discordant for weight: a Big Mac challenge2014Ingår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 28, nr 9, s. 4169-4179Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Postprandial responses to food are complex, involving both genetic and environmental factors. We studied postprandial responses to a Big Mac meal challenge in monozygotic co-twins highly discordant for body weight. This unique design allows assessment of the contribution of obesity, independent of genetic liability. Comprehensive metabolic profiling using 3 analytical platforms was applied to fasting and postprandial serum samples from 16 healthy monozygotic twin pairs discordant for weight (body mass index difference >3 kg/m(2)). Nine concordant monozygotic pairs were examined as control pairs. Fecal samples were analyzed to assess diversity of the major bacterial groups by using 5 different validated bacterial group specific denaturing gradient gel electrophoresis methods. No differences in fecal bacterial diversity were detected when comparing co-twins discordant for weight (ANOVA, P<0.05). We found that within-pair similarity is a dominant factor in the metabolic postprandial response, independent of acquired obesity. Branched chain amino acids were increased in heavier as compared with leaner co-twins in the fasting state, but their levels converged postprandially (paired t tests, FDR q<0.05). We also found that specific bacterial groups were associated with postprandial changes of specific metabolites. Our findings underline important roles of genetic and early life factors in the regulation of postprandial metabolite levels.

  • 2.
    Chaillou, Thomas
    et al.
    Université Grenoble Alpes, Grenoble, France .
    Koulmann, N.
    Simler, N.
    Meunier, A.
    Grégoire, C.
    Serrurier, B.
    Beaudry, M.
    Bigard, X.
    Ambient hypoxia enhances the muscle-mass loss after extensive injury2011Ingår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 25, nr 1 Suppl.Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The aim of this study was to examine the effect of ambient hypoxia on the main intracellular pathways involved in muscle regeneration. Left soleus muscles of female rats were degenerated by notexin injection before exposure to either normoxia (N) or ambient hypoxia (H) (10% O2) during 3, 7, 14 and 28 days (d). The expected muscle-mass loss of injured muscles was higher in H than in N rats at d3 and d7, whereas the recovery of muscle mass was similar in H and N rats at d28. The mammalian target of rapamycin (mTOR) activity, assessed from both eIF-4E binding protein (4E-BP1) and P70S6K phosphorylation, was markedly increased during the early period of regeneration, but remained two-fold lower in H than in N groups at d3. The hypoxia-induced alteration of mTOR activity, independently of Akt, was associated with an activation of AMP-activated kinase (AMPK) at d3. In contrast, REDD1, another negative regulator of mTOR, was markedly activated by H at d14 and d28 in intact muscles, but was blunted during the first days of regeneration (d3–7), independently of H. Taken together, we show for the first time, that hypoxia enhances the muscle-mass loss after extensive injury. This could be due to a specific impairment of mTOR activation during muscle regeneration, independently of Akt, at least partly related to AMPK activation, without detectable effect of REDD1.

  • 3.
    Chaillou, Thomas
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Lanner, Johanna T.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Regulation of myogenesis and skeletal muscle regeneration: effects of oxygen levels on satellite cell activity2016Ingår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 30, nr 12, s. 3929-3941Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Reduced oxygen (O2) levels (hypoxia) are present during embryogenesis and exposure to altitude and in pathologic conditions. During embryogenesis, myogenic progenitor cells reside in a hypoxic microenvironment, which may regulate their activity. Satellite cells are myogenic progenitor cells localized in a local environment, suggesting that the O2 level could affect their activity during muscle regeneration. In this review, we present the idea that O2 levels regulate myogenesis and muscle regeneration, we elucidate the molecular mechanisms underlying myogenesis and muscle regeneration in hypoxia and depict therapeutic strategies using changes in O2 levels to promote muscle regeneration. Severe hypoxia (≤1% O2) appears detrimental for myogenic differentiation in vitro, whereas a 3-6% O2 level could promote myogenesis. Hypoxia impairs the regenerative capacity of injured muscles. Although it remains to be explored, hypoxia may contribute to the muscle damage observed in patients with pathologies associated with hypoxia (chronic obstructive pulmonary disease, and peripheral arterial disease). Hypoxia affects satellite cell activity and myogenesis through mechanisms dependent and independent of hypoxia-inducible factor-1α. Finally, hyperbaric oxygen therapy and transplantation of hypoxia-conditioned myoblasts are beneficial procedures to enhance muscle regeneration in animals. These therapies may be clinically relevant to treatment of patients with severe muscle damage.-Chaillou, T. Lanner, J. T. Regulation of myogenesis and skeletal muscle regeneration: effects of oxygen levels on satellite cell activity.

  • 4.
    Kononenko, Olga
    et al.
    Uppsala University, Uppsala, Sweden; Bogomoletz Institute of Physiology, Kiev, Ukraine.
    Galatenko, Vladimir
    Moscow State University, Moscow, Russia.
    Andersson, Malin
    Uppsala University, Uppsala, Sweden.
    Bazov, Igor
    Uppsala University, Uppsala, Sweden.
    Watanabe, Hiroyuki
    Uppsala University, Uppsala, Sweden.
    Zhou, Xing Wu
    Uppsala University, Uppsala, Sweden.
    Iatsyshyna, Anna
    Uppsala University, Uppsala, Sweden; Institute of Molecular Biology and Genetics, Kiev, Ukraine.
    Mityakina, Irina
    Moscow State University, Moscow, Russia.
    Yakovleva, Tatiana
    Uppsala University, Uppsala, Sweden.
    Sarkisyan, Daniil
    Uppsala University, Uppsala, Sweden.
    Ponomarev, Igor
    The University of Texas, Austin, Texas, USA.
    Krishtal, Oleg
    Bogomoletz Institute of Physiology, Kiev, Ukraine.
    Marklund, Niklas
    Uppsala University Hospital, Uppsala, Sweden.
    Tonevitsky, Alex
    Moscow State University, Moscow, Russia.
    Adkins, DeAnna L.
    Medical University of South Carolina, Charleston, USA.
    Bakalkin, Georgy
    Uppsala University, Uppsala, Sweden.
    Intra- and interregional coregulation of opioid genes: broken symmetry in spinal circuits2017Ingår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 31, nr 5, s. 1953-1963Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Regulation of the formation and rewiring of neural circuits by neuropeptides may require coordinated production of these signaling molecules and their receptors that may be established at the transcriptional level. Here, we address this hypothesis by comparing absolute expression levels of opioid peptides with their receptors, the largest neuropeptide family, and by characterizing coexpression (transcriptionally coordinated) patterns of these genes. We demonstrated that expression patterns of opioid genes highly correlate within and across functionally and anatomically different areas. Opioid peptide genes, compared with their receptor genes, are transcribed at much greater absolute levels, which suggests formation of a neuropeptide cloud that covers the receptor-expressed circuits. Surprisingly, we found that both expression levels and the proportion of opioid receptors are strongly lateralized in the spinal cord, interregional coexpression patterns are side specific, and intraregional coexpression profiles are affected differently by left- and right-side unilateral body injury. We propose that opioid genes are regulated as interconnected components of the same molecular system distributed between distinct anatomic regions. The striking feature of this system is its asymmetric coexpression patterns, which suggest side-specific regulation of selective neural circuits by opioid neurohormones.-Kononenko, O., Galatenko, V., Andersson, M., Bazov, I., Watanabe, H., Zhou, X. W., Iatsyshyna, A., Mityakina, I., Yakovleva, T., Sarkisyan, D., Ponomarev, I., Krishtal, O., Marklund, N., Tonevitsky, A., Adkins, D. L., Bakalkin, G. Intra- and interregional coregulation of opioid genes: broken symmetry in spinal circuits.

  • 5.
    Liu, Zhengye
    et al.
    Department of Physiology and Pharmacology, Molecular Muscle Physiology and Pathophysiology, Karolinska Institutet, Stockholm, Sweden.
    Chaillou, Thomas
    Örebro universitet, Institutionen för hälsovetenskaper. Department of Physiology and Pharmacology, Molecular Muscle Physiology and Pathophysiology, Karolinska Institutet, Stockholm, Sweden.
    Santos Alves, Estela
    Department of Physiology and Pharmacology, Molecular Muscle Physiology and Pathophysiology, Karolinska Institutet, Stockholm, Sweden.
    Mader, Theresa
    Department of Physiology and Pharmacology, Molecular Muscle Physiology and Pathophysiology, Karolinska Institutet, Stockholm, Sweden.
    Jude, Baptiste
    Department of Physiology and Pharmacology, Molecular Muscle Physiology and Pathophysiology, Karolinska Institutet, Stockholm, Sweden.
    Ferreira, Duarte M. S.
    Department of Physiology and Pharmacology, Molecular and Cellular Exercise Physiology, Karolinska Institutet, Stockholm, Sweden.
    Hynynen, Heidi
    Department of Physiology and Pharmacology, Molecular and Cellular Exercise Physiology, Karolinska Institutet, Stockholm, Sweden.
    Cheng, Arthur J.
    Department of Physiology and Pharmacology, Molecular Muscle Physiology and Pathophysiology, Karolinska Institutet, Stockholm, Sweden.
    Jonsson, William O.
    Department of Physiology and Pharmacology, Molecular Muscle Physiology and Pathophysiology, Karolinska Institutet, Stockholm, Sweden.
    Pironti, Gianluigi
    Department of Physiology and Pharmacology, Medical Cardiac and Skeletal Muscle Research, Karolinska Institutet, Stockholm, Sweden.
    Andersson, Daniel C.
    Department of Physiology and Pharmacology, Medical Cardiac and Skeletal Muscle Research, Karolinska Institutet, Stockholm, Sweden; Heart, Vascular and Neurology Theme, Cardiology Unit, Karolinska University Hospital, Stockholm, Sweden.
    Kenne, Ellinor
    Department of Physiology and Pharmacology, Molecular Muscle Physiology and Pathophysiology, Karolinska Institutet, Stockholm, Sweden.
    Ruas, Jorge L.
    Department of Physiology and Pharmacology, Molecular and Cellular Exercise Physiology, Karolinska Institutet, Stockholm, Sweden.
    Tavi, Pasi
    A.I. Virtanen Institute, University of Eastern Finland, Kuopio, Finland.
    Lanner, Johanna T.
    Department of Physiology and Pharmacology, Molecular Muscle Physiology and Pathophysiology, Karolinska Institutet, Stockholm, Sweden.
    Mitochondrial NDUFA4L2 is a novel regulator of skeletal muscle mass and force2021Ingår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 35, nr 12, artikel-id e22010Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The hypoxia-inducible nuclear-encoded mitochondrial protein NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 4-like 2 (NDUFA4L2) has been demonstrated to decrease oxidative phosphorylation and production of reactive oxygen species in neonatal cardiomyocytes, brain tissue and hypoxic domains of cancer cells. Prolonged local hypoxia can negatively affect skeletal muscle size and tissue oxidative capacity. Although skeletal muscle is a mitochondrial rich, oxygen sensitive tissue, the role of NDUFA4L2 in skeletal muscle has not previously been investigated. Here we ectopically expressed NDUFA4L2 in mouse skeletal muscles using adenovirus-mediated expression and in vivo electroporation. Moreover, femoral artery ligation (FAL) was used as a model of peripheral vascular disease to induce hind limb ischemia and muscle damage. Ectopic NDUFA4L2 expression resulted in reduced mitochondrial respiration and reactive oxygen species followed by lowered AMP, ADP, ATP, and NAD(+) levels without affecting the overall protein content of the mitochondrial electron transport chain. Furthermore, ec-topically expressed NDUFA4L2 caused a similar to 20% reduction in muscle mass that resulted in weaker muscles. The loss of muscle mass was associated with increased gene expression of atrogenes MurF1 and Mul1, and apoptotic genes caspase 3 and Bax. Finally, we showed that NDUFA4L2 was induced by FAL and that the Ndufa4l2 mRNA expression correlated with the reduced capacity of the muscle to generate force after the ischemic insult. These results show, for the first time, that mitochondrial NDUFA4L2 is a novel regulator of skeletal muscle mass and force. Specifically, induced NDUFA4L2 reduces mitochondrial activity leading to lower levels of important intramuscular metabolites, including adenine nucleotides and NAD(+), which are hallmarks of mitochondrial dysfunction and hence shows that dysfunctional mitochondrial activity may drive muscle wasting.

  • 6.
    Mackey, Abigail L.
    et al.
    Institute of Sports Medicine Copenhagen, Department of Orthopaedic Surgery M, Bispebjerg Hospital, Copenhagen, Denmark; Department of Biomedical Sciences, Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
    Rasmussen, Lotte K.
    Institute of Sports Medicine Copenhagen, Department of Orthopaedic Surgery M, Bispebjerg Hospital, Copenhagen, Denmark.
    Kadi, Fawzi
    Örebro universitet, Institutionen för hälsovetenskaper.
    Schjerling, Peter
    Institute of Sports Medicine Copenhagen, Department of Orthopaedic Surgery M, Bispebjerg Hospital, Copenhagen, Denmark.
    Helmark, Ida C.
    Institute of Sports Medicine Copenhagen, Department of Orthopaedic Surgery M, Bispebjerg Hospital, Copenhagen, Denmark.
    Ponsot, Elodie
    Örebro universitet, Institutionen för hälsovetenskaper.
    Aagaard, Per
    Department of Sports Science and Clinical Biomechanics, Muscle Research Cluster, University of Southern Denmark, Odense, Denmark.
    Durigan, João Luiz Q.
    Physical Therapy Division, University of Brasília, Brasília, Brazil.
    Kjaer, Michael
    Institute of Sports Medicine Copenhagen, Department of Orthopaedic Surgery M, Bispebjerg Hospital, Copenhagen, Denmark; Department of Biomedical Sciences, Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
    Activation of satellite cells and the regeneration of human skeletal muscle are expedited by ingestion of nonsteroidal anti-inflammatory medication2016Ingår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 30, nr 6, s. 2266-2281Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    With this study we investigated the role of nonsteroidal anti-inflammatory drugs (NSAIDs) in human skeletal muscle regeneration. Young men ingested NSAID [1200 mg/d ibuprofen (IBU)] or placebo (PLA) daily for 2 wk before and 4 wk after an electrical stimulation-induced injury to the leg extensor muscles of one leg. Muscle biopsies were collected from the vastus lateralis muscles before and after stimulation (2.5 h and 2, 7, and 30 d) and were assessed for satellite cells and regeneration by immunohistochemistry and real-time RT-PCR, and we also measured telomere length. After injury, and compared with PLA, IBU was found to augment the proportion of ActiveNotch1(+) satellite cells at 2 d [IBU, 29 ± 3% vs. PLA, 19 ± 2% (means ± sem)], satellite cell content at 7 d [IBU, 0.16 ± 0.01 vs. PLA, 0.12 ± 0.01 (Pax7(+) cells/fiber)], and to expedite muscle repair at 30 d. The PLA group displayed a greater proportion of embryonic myosin(+) fibers and a residual ∼2-fold increase in mRNA levels of matrix proteins (all P < 0.05). Endomysial collagen was also elevated with PLA at 30 d. Minimum telomere length shortening was not observed. In conclusion, ingestion of NSAID has a potentiating effect on Notch activation of satellite cells and muscle remodeling during large-scale regeneration of injured human skeletal muscle.-Mackey, A. L., Rasmussen, L. K., Kadi, F., Schjerling, P., Helmark, I. C., Ponsot, E., Aagaard, P., Durigan, J. L. Q., Kjaer, M. Activation of satellite cells and the regeneration of human skeletal muscle are expedited by ingestion of nonsteroidal anti-inflammatory medication.

  • 7.
    Nilsson, Torbjörn K.
    et al.
    Department of Medical Biosciences/Clinical Chemistry, Umeå University, Umeå, Sweden.
    Hurtig-Wennlöf, Anita
    Örebro universitet, Institutionen för hälsovetenskaper.
    Sjöström, Michael
    Department of Biosciences and Nutrition, Karolinska Institute, Stockholm, Sweden.
    Herrmann, Wolfgang
    Department of Clinical Chemistry and Laboratory Medicine, Saarland University Hospital, Homburg, Germany.
    Obeid, Rima
    Department of Clinical Chemistry and Laboratory Medicine, Saarland University Hospital, Homburg, Germany.
    Owen, Jennifer R.
    Nutrition Research Institute, University of North Carolina, Chapel Hill, USA.
    Zeisel, Steven
    Nutrition Research Institute, University of North Carolina, Chapel Hill, USA; Department of Nutrition, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, North Carolina, USA.
    Plasma 1-carbon metabolites and academic achievement in 15-yr-old adolescents2016Ingår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 30, nr 4, s. 1683-1688Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Academic achievement in adolescents is correlated with 1-carbon metabolism (1-CM), as folate intake is positively related and total plasma homocysteine (tHcy) negatively related to academic success. Because another 1-CM nutrient, choline is essential for fetal neurocognitive development, we hypothesized that choline and betaine could also be positively related to academic achievement in adolescents. In a sample of 15-yr-old children (n = 324), we measured plasma concentrations of homocysteine, choline, and betaine and genotyped them for 2 polymorphisms with effects on 1-CM, methylenetetrahydrofolate reductase (MTHFR) 677C>T, rs1801133, and phosphatidylethanolamine N-methyltransferase (PEMT), rs12325817 (G>C). The sum of school grades in 17 major subjects was used as an outcome measure for academic achievement. Lifestyle and family socioeconomic status (SES) data were obtained from questionnaires. Plasma choline was significantly and positively associated with academic achievement independent of SES factors (paternal education and income, maternal education and income, smoking, school) and of folate intake (P = 0.009, R-2 = 0.285). With the addition of the PEMT rs12325817 polymorphism, the association value was only marginally changed. Plasma betaine concentration, tHcy, and the MTHFR 677C>T polymorphism did not affect academic achievement in any tested model involving choline. Dietary intake of choline is marginal in many adolescents and may be a public health concern.

  • 8.
    Rodriguez-Cuenca, Sergio
    et al.
    Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, UK.
    Lelliot, Christopher J.
    Discovery Sciences, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.
    Campbell, Mark
    Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, UK.
    Peddinti, Gopal
    VTT, Technical Research Center of Finland, Espoo, Finland.
    Martinez-Uña, Maite
    Department of Physiology, University of the Basque Country UPV/EHU, Bilbao, Spain.
    Ingvorsen, Camilla
    Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, UK.
    Dias, Ana Rita
    Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, UK.
    Relat, Joana
    Department of Nutrition, Food Science and Gastronomy, School of Pharmacy and Food Science, Food and Nutrition Torribera Campus, University of Barcelona (UB), Santa Coloma de Gramenet, Spain; INSA-UB, Nutrition and Food Safety Research Institute, University of Barcelona, Barcelona, Spain.
    Mora, Silvia
    Department of Cellular and Molecular Physiology, Institute of Translational Medicine, The University of Liverpool, Liverpool, UK.
    Hyötyläinen, Tuulia
    Örebro universitet, Institutionen för naturvetenskap och teknik.
    Zorzano, Antonio
    Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Barcelona, Spain; Dept. Biochemistry and Molecular Biomedicine, University of Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salud Carlos III, Madrid, Spain.
    Oresic, Matej
    Örebro universitet, Institutionen för medicinska vetenskaper. Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.
    Bjursell, Mikael
    Discovery Sciences, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.
    Bohlooly-Y, Mohammad
    Discovery Sciences, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.
    Lindén, Daniel
    Research and Early Development Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden; Division of Endocrinology, Department of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Vidal-Puig, Antonio
    Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, UK; Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK.
    Allostatic hypermetabolic response in PGC1α/β heterozygote mouse despite mitochondrial defects2021Ingår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 35, nr 9, artikel-id e21752Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Aging, obesity, and insulin resistance are associated with low levels of PGC1α and PGC1β coactivators and defective mitochondrial function. We studied mice deficient for PGC1α and PGC1β [double heterozygous (DH)] to investigate their combined pathogenic contribution. Contrary to our hypothesis, DH mice were leaner, had increased energy dissipation, a pro-thermogenic profile in BAT and WAT, and improved carbohydrate metabolism compared to wild types. WAT showed upregulation of mitochondriogenesis/oxphos machinery upon allelic compensation of PGC1α4 from the remaining allele. However, DH mice had decreased mitochondrial OXPHOS and biogenesis transcriptomes in mitochondria-rich organs. Despite being metabolically healthy, mitochondrial defects in DH mice impaired muscle fiber remodeling and caused qualitative changes in the hepatic lipidome. Our data evidence first the existence of organ-specific compensatory allostatic mechanisms are robust enough to drive an unexpected phenotype. Second, optimization of adipose tissue bioenergetics is sufficient to maintain a healthy metabolic phenotype despite a broad severe mitochondrial dysfunction in other relevant metabolic organs. Third, the decrease in PGC1s in adipose tissue of obese and diabetic patients is in contrast with the robustness of the compensatory upregulation in the adipose of the DH mice.

  • 9.
    Svärd, Anna
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Division of Surgery, Orthopedics and Oncology, Department of Biomedical and Clinical Sciences, Faculty of Health Science, Linköping University, Linköping, Sweden; Cardiovascular Research Centre (CVRC), School of Medical Sciences, Örebro University, Örebro, Sweden; Division of Biophysics and Bioengineering, Department of Physics, Chemistry and Biology, Linköping University, Linköping, Sweden.
    Hammerman, Malin
    Department of Biomedical Engineering, Lund University, Lund, Sweden.
    Eliasson, Pernilla
    Division of Surgery, Orthopedics and Oncology, Department of Biomedical and Clinical Sciences, Faculty of Health Science, Linköping University, Linköping, Sweden.
    Elastin levels are higher in healing tendons than in intact tendons and influence tissue compliance2020Ingår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 34, nr 10, s. 13409-13418Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Elastic fibers containing elastin play an important role in tendon functionality, but the knowledge on presence and function of elastin during tendon healing is limited. The aim of this study was to investigate elastin content and distribution in intact and healing Achilles tendons and to understand how elastin influence the viscoelastic properties of tendons. The right Achilles tendon was completely transected in 81 Sprague-Dawley rats. Elastin content was quantified in intact and healing tendons (7, 14, and 28 days post-surgery) and elastin distribution was visualized by immunohistochemistry at 14 days post-surgery. Degradation of elastin by elastase incubation was used to study the role of elastin on viscoelastic properties. Mechanical testing was either performed as a cyclic test (20x 10 N) or as a creep test. We found significantly higher levels of elastin in healing tendons at all time-points compared to intact tendons (4% in healing tendons 28 days post-surgery vs 2% in intact tendons). The elastin was more widely distributed throughout the extracellular matrix in the healing tendons in contrast to the intact tendon where the distribution was not so pronounced. Elastase incubation reduced the elastin levels by approximately 30% and led to a 40%-50% reduction in creep. This reduction was seen in both intact and healing tendons. Our results show that healing tendons contain more elastin and is more compliable than intact tendons. The role of elastin in tendon healing and tissue compliance indicates a protective role of elastic fibers to prevent re-injuries during early tendon healing. Plain Language Summary Tendons transfer high loads from muscles to bones during locomotion. They are primarily made by the protein collagen, a protein that provide strength to the tissues. Besides collagen, tendons also contain other building blocks such as, for example, elastic fibers. Elastic fibers contain elastin and elastin is important for the extensibility of the tendon. When a tendon is injured and ruptured the tissue heals through scar formation. This scar tissue is different from a normal intact tendon and it is important to understand how the tendons heal. Little is known about the presence and function of elastin during healing of tendon injuries. We have shown, in animal experiments, that healing tendons have higher amounts of elastin compared to intact tendons. The elastin is also spread throughout the tissue. When we reduced the levels of this protein, we discovered altered mechanical properties of the tendon. The healing tendon can normally extend quite a lot, but after elastin removal this extensibility was less obvious. The ability of the healing tissue to extend is probably important to protect the tendon from re-injuries during the first months after rupture. We therefore propose that the tendons heal with a large amount of elastin to prevent re-ruptures during early locomotion.

  • 10.
    Vedin, I.
    et al.
    Huddinge University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Cederholm, T.
    Huddinge University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Liden, J.
    Huddinge University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Freund-Levi, Yvonne
    Huddinge University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Palmblad, J.
    Huddinge University Hospital, Karolinska Institutet, Stockholm, Sweden.
    OmegAD, Study Grp
    Inflammatory gene expression changes by omega-3 fatty acids in patients with Alzheimer's disease2004Ingår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 18, nr 4, s. A501-A501Artikel i tidskrift (Övrigt vetenskapligt)
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