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( # [[Mitochondrial marker enzymes|Marker enzymes]] for the mitochondrial )

Burtscher 2022 Antioxid Redox Signal + ('''''Significance:''''' Oxygen is indispen … '''''Significance:''''' Oxygen is indispensable for aerobic life, but its utilization exposes cells and tissues to oxidative stress; thus, tight regulation of cellular, tissue, and systemic oxygen concentrations is crucial. Here, we review the current understanding of how the human organism (mal-)adapts to low (hypoxia) and high (hyperoxia) oxygen levels and how these adaptations may be harnessed as therapeutic or performance enhancing strategies at the systemic level. '''''Recent Advances:''''' Hyperbaric oxygen therapy is already a cornerstone of modern medicine, and the application of mild hypoxia, that is, hypoxia conditioning (HC), to strengthen the resilience of organs or the whole body to severe hypoxic insults is an important preparation for high-altitude sojourns or to protect the cardiovascular system from hypoxic/ischemic damage. Many other applications of adaptations to hypo- and/or hyperoxia are only just emerging. HC-sometimes in combination with hyperoxic interventions-is gaining traction for the treatment of chronic diseases, including numerous neurological disorders, and for performance enhancement. '''''Critical Issues:''''' The dose- and intensity-dependent effects of varying oxygen concentrations render hypoxia- and/or hyperoxia-based interventions potentially highly beneficial, yet hazardous, although the risks versus benefits are as yet ill-defined. '''''Future Directions:''''' The field of low and high oxygen conditioning is expanding rapidly, and novel applications are increasingly recognized, for example, the modulation of aging processes, mood disorders, or metabolic diseases. To advance hypoxia/hyperoxia conditioning to clinical applications, more research on the effects of the intensity, duration, and frequency of altered oxygen concentrations, as well as on individual vulnerabilities to such interventions, is paramount.ities to such interventions, is paramount.)
MiP2017/MitoEAGLE Hradec Kralove CZ + ('''12th Conference … '''12th Conference on Mitochondrial Physiology and MitoEAGLE WG and MC Meeting, 2017, Hradec Kralove, Czech Republic.'''Co-organized with COST Action MitoEAGLE: [[COST_Action_MitoEAGLE#Grant_periods |Management Committee Meeting and Working Group Meetings]].[[COST_Action_MitoEAGLE#Grant_periods |Management Committee Meeting and Working Group Meetings]].)
MiP2018/MitoEAGLE Jurmala LV + ('''13th Conference on Mitochondrial Physiology and MitoEAGLE WG and MC Meeting, 2018, Jurmala, Latvia.''')
IOC13 + ('''13th Workshop on High-Resolution Respirometry.''' Innsbruck, Tyrol, Austria; 1997 May 09-16. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
ASMRM 2017 Xian CN + ('''14thConference of the Asian Society of Mitochondrial Research and Medicine'''. Xi'an, Shaanxi, China; 2017 September.)
IOC16 + ('''16th International Course on High-Resolution Respirometry.''' Innsbruck, Tyrol, Austria; 1998 December 10. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
EBEC2016 Riva del Garda IT + ('''19th European Bioenergetics Conference 2016, Riva del Garda, IT''')
MitoEAGLE MC Meeting 2016 Brussels BE + ('''1st MC Meeting, [[COST Action MitoEAGLE]], Brussels, BE''')
1st Workshop on Mitochondrial Functional Diagnostics Innsbruck AT + ('''1st Workshop on Mitochondrial Functional Diagnostics - PBMCs.''' Innsbruck, Austria, 2023)
MitoFit Science Camp 2016 Kuehtai AT + ('''2016 Jul 07-13, Kuehtai, AT.''' The pr … '''2016 Jul 07-13, Kuehtai, AT.''' The project [[K-Regio MitoFit |MitoFit]] aims at developing novel laboratory standards and diagnostic monitoring of a mitochondrial fitness score. With an international team of outstanding mitochondrial experts, the '''MitoFit Science Camp''' will provide a unique opportunity to receive first-hand introductions to state-of-the-art diagnostic monitoring of mitochondrial respiratory function combined with hands-on training on HRR (IOC112). Diverse areas are covered such as protective medicine, exercise physiology, mitochondrial pharmacology, aging, and comparative mitochondrial physiology (cell types, tissues, species). The common focus is on methodology, experimental details and quality control. The MitoFit Science Camp is a student- and research-oriented even, and may be considered as a sequence of workshops rather than a conference or school, addressing key topics of the COST Action [[MitoEAGLE]] project. This will provide a key opportunity to prepare the [[COST Action MitoEAGLE |1st Management Committee Meeting]].[[COST Action MitoEAGLE |1st Management Committee Meeting]].)
MiPschool Obergurgl 2017 + ('''2017 Jul 23-30, Obergurgl, AT.''')
MitoEAGLE Obergurgl 2017 + ('''2017 Jul 27-30, Obergurgl, AT.''')
Padua-Mit-Innsbruck2017 Padua IT + ('''2nd Padua-Mit-Innsbruck “Mitochondrial Conference”. Pauda, Italy; 2017 September.)
2nd Workshop on Mitochondrial Functional Diagnostics Innsbruck AT + ('''2nd Workshop on Mitochondrial Functional Diagnostics - Diagnostic database''' Innsbruck, Austria, 2023)
Mitochondira in Health and Disease 2017 NY US + ('''2nd symposium Mitochondria in Health and Disease'''. New York, US; 2017.)
MiPschool Cambridge UK 2012 + ('''5th MiP''school'' on Mitochondrial Physiology, 2012 Jul 09-13, Cambridge, UK.''')
MiP2007 Ambleside UK + ('''64th Harden Conference on: Mitochondrial Physiology, 2007, Ambleside , United Kingdom.''')
Harden Conference 2016 Innsbruck AT + ('''79th Harden Conference: Oxygen Evolution and Reduction - Common Principles, [https://www.biochemistry.org/Events/tabid/379/MeetingNo/79HDN/view/Conference/Default.aspx Harden Conference 2016], Innsbruck, AT''')
MiPNet18.08 MiP2013 + ('''>> [[MiP2013 Abstracts|MiP2013 Abstracts in the MiPMap]] - >> [[Laner 2013 Mitochondr Physiol Network MiP2013]]''')
Hey-Mogensen 2010 Diabetologia + ('''AIM/HYPOTHESIS''':Studies have suggeste … '''AIM/HYPOTHESIS''':Studies have suggested a link between insulin resistance and mitochondrial dysfunction in skeletal muscles. Our primary aim was to investigate the effect of aerobic training on mitochondrial respiration and mitochondrial reactive oxygen species (ROS) release in skeletal muscle of obese participants with and without type 2 diabetes.'''METHODS''': Type 2 diabetic men (''n'' = 13) and control (''n'' = 14) participants matched for age, BMI and physical activity completed 10 weeks of aerobic training. Pre- and post-training muscle biopsies were obtained before a euglycaemic-hyperinsulinaemic clamp and used for measurement of respiratory function and ROS release in isolated mitochondria.'''RESULTS''': Training significantly increased insulin sensitivity, maximal oxygen consumption and muscle mitochondrial respiration with no difference between groups. When expressed in relation to a marker of mitochondrial density (intrinsic mitochondrial respiration), training resulted in increased mitochondrial ADP-stimulated respiration (with NADH-generating substrates) and decreased respiration without ADP. Intrinsic mitochondrial respiration was not different between groups despite lower insulin sensitivity in type 2 diabetic participants. Mitochondrial ROS release tended to be higher in participants with type 2 diabetes.'''CONCLUSIONS/INTERPRETATION''': Aerobic training improves muscle respiration and intrinsic mitochondrial respiration in untrained obese participants with and without type 2 diabetes. These adaptations demonstrate an increased metabolic fitness, but do not seem to be directly related to training-induced changes in insulin sensitivity.ng-induced changes in insulin sensitivity.)
Phielix 2010 Diabetologia + ('''AIMS/HYPOTHESIS:''' We previously showe … '''AIMS/HYPOTHESIS:''' We previously showed that type 2 diabetic patients are characterised by compromised intrinsic mitochondrial function. Here, we examined if exercise training could increase intrinsic mitochondrial function in diabetic patients compared with control individuals.'''METHODS:''' Fifteen male type 2 diabetic patients and 14 male control individuals matched for age, BMI and VO(2max) enrolled in a 12 week exercise intervention programme. ''Ex vivo'' mitochondrial function was assessed by high-resolution respirometry in permeabilised muscle fibres from vastus lateralis muscle. Before and after training, insulin-stimulated glucose disposal was examined during a hyperinsulinaemic-euglycaemic clamp.'''RESULTS:''' Diabetic patients had intrinsically lower ADP-stimulated state 3 respiration and lower carbonyl cyanide 4-(trifluoro-methoxy)phenylhydrazone (FCCP)-induced maximal oxidative respiration, both on glutamate and on glutamate and succinate, and in the presence of palmitoyl-carnitine (''p'' < 0.05). After training, diabetic patients and control individuals showed increased state 3 respiration on the previously mentioned substrates (''p'' < 0.05); however, an increase in FCCP-induced maximal oxidative respiration was observed only in diabetic patients (''p'' < 0.05). The increase in mitochondrial respiration was accompanied by a 30% increase in mitochondrial content upon training (''p'' < 0.01). After adjustment for mitochondrial density, state 3 and FCCP-induced maximal oxidative respiration were similar between groups after training. Improvements in mitochondrial respiration were paralleled by improvements in insulin-stimulated glucose disposal in diabetic patients, with a tendency for this in control individuals.'''CONCLUSIONS/INTERPRETATION:''' We confirmed lower intrinsic mitochondrial function in diabetic patients compared with control individuals. Diabetic patients increased their mitochondrial content to the same extent as control individuals and had similar intrinsic mitochondrial function, which occurred parallel with improved insulin sensitivity.h occurred parallel with improved insulin sensitivity.)
APS Conference: Physiological Bioenergetics: Mitochondria from Bench to Bedside + ('''APS Conference: Physiological Bioenergetics: Mitochondria from Bench to Bedside, Bioenergetics17'''. San Diego CA, USA; 2017 August.)
Author IOC61 + ('''Abstract''': Add a short abstract here, … '''Abstract''': Add a short abstract here, including title, authors, affiliations, text (up to 250 words), and 2-6 references. You may edit your abstract any time. Information will be provided on a deadline for editing/submitting final abstracts (including a pdf file in final format).'''Title''': Not capitalized.'''Authors''': Presenting author with full name (first name spelled out), other authors with initials only. Numbers in parentheses after each author should indicate the affiliations.'''Addresses''': Numbers in parentheses are placed at the beginning of the address for indicating the affiliation. The e-mail address of the presenting author should be given at the end of all addresses.'''Main text''': Structured into paragraphs without headers. The standard structure of abstracts should be followed as appropriate (Introduction / Methods / Results / Conclusions / References). '''Figure''': You may submit one or two figures (jpg format), without caption if full explanation is given in the abstract.'''References''' in the text are given by numbers in brackets. Full references should be numbered and include all authors (family name and initials without punctuation), followed by the year of publication in parentheses, full title, journal name abbreviated with punctuation (italic), volume number followed by a colon, and first and last pages. See abstracts on the MiP website for style – MiP2005/Organisation/Abstracts. Tick on appropriate boxes blow in the list of 'Labels', and add additional keywords not covered in these labels.An extension is possible in the free text (not more than 2 pages). Further comments may be added in the discussion.r comments may be added in the discussion.)
MiPauthor MiP2011 + ('''Abstract''': Add a short abstract here, … '''Abstract''': Add a short abstract here, including title, authors, affiliations, text (up to 250 words), and 2-6 references. You may edit your abstract any time. Information will be provided on a deadline for editing/submitting final abstracts (including a pdf file in final format), and on acceptance of the abstract for presentation at MiP2011.'''Title''': Not capitalized.'''Authors''': Presenting author with full name (first name spelled out), other authors with initials only. Numbers in parentheses after each author should indicate the affiliations.'''Addresses''': Numbers in parentheses are placed at the beginning of the address for indicating the affiliation. The e-mail address of the presenting author should be given at the end of all addresses.'''Main text''': Structured into paragraphs without headers. The standard structure of abstracts should be followed as appropriate (Introduction / Methods / Results / Conclusions / References). '''Figure''': You may submit one or two figures (jpg format), without caption if full explanation is given in the abstract.'''References''' in the text are given by numbers in brackets. Full references should be numbered and include all authors (family name and initials without punctuation), followed by the year of publication in parentheses, full title, journal name abbreviated with punctuation (italic), volume number followed by a colon, and first and last pages. See abstracts on the MiP website for style – MiP2005/Organisation/Abstracts. Tick on appropriate boxes blow in the list of 'Labels', and add additional keywords not covered in these labels.An extension is possible in the free text (not more than 2 pages). Further comments may be added in the discussion.r comments may be added in the discussion.)
MiPschool Cape Town 2015 + ('''Abstracts are listed here in the frame of the [[MiPMap]] for the 7th MiP''school'' on Mitochondrial Physiology, 2015 Mar 24-28, Cape Town, ZA.''')
Hassing 2010 Dement Geriatr Cogn Disord + ('''Aim''' To examine if the body mass inde … '''Aim'''To examine if the body mass index (BMI) in midlife is related to cognitive function 30 years later in a dementia-free sample.'''Methods'''BMI was reported in 1963 at age 50–60 years, and cognitive abilities were examined 30 years later in a longitudinal design with 5 measurement occasions at 2-year intervals (n = 417). The cognitive abilities examined included tests of long-term memory, short-term memory, speed, verbal and spatial ability.'''Results'''Multilevel modeling adjusting for demographic and lifestyle factors, and relevant diseases showed that a higher BMI in midlife predicted lower test performance 30 years later. Significant associations between BMI and level of performance were found in all cognitive abilities; however, a higher midlife BMI was not associated with steeper cognitive decline.'''Conclusion'''Our results indicate that midlife overweight is related to lower overall cognitive function in old age. The fact that BMI-related effects were noted in mean-level cognitive performance, whereas only one ability showed differences in slopes, suggests that the negative effect of overweight has an onset before the entry into very old age. onset before the entry into very old age.)
Raboel 2010 Diabetes Obes Metab + ('''Aim''': Skeletal muscle insulin resista … '''Aim''': Skeletal muscle insulin resistance has been linked to mitochondrial dysfunction. We examined how improvements in muscular insulin sensitivity following rosiglitazone (ROSI) or pioglitazone (PIO) treatment would affect muscle mitochondrial function in patients with type 2 diabetes mellitus (T2DM).'''Methods''': Muscle biopsies were obtained from 21 patients with T2DM before and after 12 weeks on either ROSI (4 mg once daily) [n = 12; age, 59.2 +/- 2.2 years; body mass index (BMI), 29.6 +/- 0.7 kg/m(2)] or PIO (30 mg once daily) (n = 9; age, 56.3 +/- 2.4 years; BMI, 29.5 +/- 1.5 kg/m(2)). An age- and BMI-matched control group was also included (n = 8; age, 61.8 +/- 2.3 years; BMI, 28.4 +/- 0.6 kg/m(2)). Insulin sensitivity, citrate synthase- and beta-hydroxyacyl-CoA-dehydrogenase (HAD) activity, intramuscular triglyceride (IMTG) and protein content of complexes I-IV were measured, while mitochondrial respiration per milligram muscle was measured in saponin-treated skinned muscle fibres using high-resolution respirometry.'''Results''': Mitochondrial respiration per milligram muscle was lower in T2DM compared to controls at baseline and decreased during ROSI treatment but increased during PIO treatment. Citrate synthase activity and average protein content of complexes I-IV were unchanged in the ROSI group, but protein content of complexes II and III increased during PIO treatment. Insulin sensitivity improved in all patients, but IMTG levels were unchanged.'''Conclusions''': We show opposite effects of ROSI and PIO on mitochondrial respiration, and also show that insulin sensitivity can be improved independently of changes in mitochondrial respiration. We confirm that mitochondrial respiration is reduced in T2DM compared to age- and BMI-matched control subjects. to age- and BMI-matched control subjects.)
Lai 2018 Acta Physiol (Oxf) + ('''Aim''': The subsarcolemmal (SSM) and in … '''Aim''': The subsarcolemmal (SSM) and interfibrillar (IFM) mitochondria in skeletal muscle appear to have distinct biochemical properties affecting metabolism in health and disease. The isolation of mitochondrial subpopulations has been a long-time challenge while the presence of a continuous mitochondrial reticulum challenges the view of distinctive SSM and IFM bioenergetics. Here, a comprehensive approach is developed to identify the best conditions to separate mitochondrial fractions.'''Methods''': The main modifications to the protocol to isolate SSM and IFM from rat skeletal muscle were: (a) decreased dispase content and homogenization speed; (b) trypsin treatment of SSM fractions; (c) recentrifugation of mitochondrial fractions at low speed to remove subcellular components. To identify the conditions preserving mitochondrial function, integrity, and maximizing their recovery, microscopy (light and electron) were used to monitor effectiveness and efficiency in separating mitochondrial subpopulations while respiratory and enzyme activities were employed to evaluate function, recovery, and integrity.'''Results''': With the modifications described, the total mitochondrial yield increased with a recovery of 80% of mitochondria contained in the original skeletal muscle sample. The difference between SSM and IFM oxidative capacity (10%) with complex-I substrate was significant only with a saturated ADP concentration. The inner and outer membrane damage for both subpopulations was <1% and 8%, respectively, while the respiratory control ratio was 16.'''Conclusion''': Using a multidisciplinary approach, conditions were identified to maximize SSM and IFM recovery while preserving mitochondrial integrity, biochemistry, and morphology. High quality and recovery of mitochondrial subpopulations allow to study the relationship between these organelles and disease.ionship between these organelles and disease.)
Johansen 2011 Acta Physiol Scand + ('''Aim:''' To investigate mechanisms behin … '''Aim:''' To investigate mechanisms behind heptanol (Hp)-induced infarct size reduction and in particular if protection by pre-treatment with Hp is triggered through mitochondrial mechanisms.'''Methods:''' Langendorff perfused rat hearts, isolated mitochondria and isolated myocytes were used. Infarct size, mitochondrial respiration, time to mitochondrial permeability transition pore (MPTP) opening and AKT and glycogen synthase kinase 3 beta (GSK-3β) phosphorylation were examined.'''Results:''' Pre-treatment with Hp reduced infarct size from 29.7 ± 3.4% to 12.6 ± 2.1%. Mitochondrial potassium channel blockers 5-hydroxy decanoic acid (5HD) blocking mitoK(ATP) and paxilline (PAX) blocking mitoK(Ca) abolished cardioprotective effect of Hp (Hp + 5HD 36.7 ± 2.9% and Hp + PAX 40.2 ± 2.8%). Hp significantly reduced respiratory control ratio in both subsarcolemmal and interfibrillar mitochondria in a dose-dependent manner (0.5-5.0 mm). The ADP oxygen ratio was also significantly reduced by Hp (2 mm). Laser scanning confocal microscopy of tetramethylrhodamine-loaded isolated rat myocytes using line scan mode showed that Hp increased time to MPTP opening. Western blot analysis showed that pre-treatment with Hp increased phosphorylation of AKT and GSK-3β before ischaemia and after 30 min of global ischaemia.'''Conclusion''': Pre-treatment with Hp protects the heart against ischaemia-reperfusion injury. This protection is most likely mediated via mitochondrial mechanisms which initiate a signalling cascade that converges on inhibition of opening of MPTP.onverges on inhibition of opening of MPTP.)
Larsen 2011 Diabetologia + ('''Aims/Hypothesis''': Mitochondrial respi … '''Aims/Hypothesis''': Mitochondrial respiration has been linked to insulin resistance. We studied mitochondrial respiratory capacity and substrate sensitivity in patients with type 2 diabetes (patients), and obese and lean control participants.'''Methods''': Mitochondrial respiration was measured in permeabilised muscle fibres by respirometry. Protocols for respirometry included titration of substrates for [[Complex I]] (glutamate), [[Complex II]] (succinate) and both (octanoyl-carnitine). Myosin heavy chain (MHC) composition, antioxidant capacity (manganese superoxide dismutase [MnSOD]), [[citrate synthase]] activity and maximal oxygen uptake (VO2) were also determined. Insulin sensitivity was determined with the isoglycaemic-hyperinsulinaemic clamp technique.'''Results''': Insulin sensitivity was different (''P'' < 0.05) between the groups (patients<obese controls<lean controls). MnSOD was lower in patients than in lean controls. MHC I content was lowest in patients (37 ± 11% [mean ± SE] vs 53 ± 6% and 56 ± 4%) vs obese controls and lean controls, respectively. VO2 was highest in lean controls (40 ± 3 ml min(-1) kg(-1) [mean ± SE]) compared with patients (25 ± 2) and obese controls (27 ± 2). Mitochondrial content (citrate synthase) was higher (''P'' < 0.05) in lean controls than in patients and obese controls. When normalised for mitochondrial content by citrate synthase, mitochondrial respiratory capacity was similar in all groups. However, the half maximal substrate concentration (''C''50) for Complex I was significantly lower (''P'' = 0.03) in patients (1.1 ± 0.2 mmol/l [mean ± SE]) than in obese (2.0 ± 0.3) and lean (1.8 ± 0.3) controls. Likewise, ''C''50 for Complex II was lower (''P'' = 0.02) in patients (3.5 ± 0.2 mmol/l [mean ± SE]) than in obese controls (4.1 ± 0.2), but did not differ from that in lean controls (3.8 ± 0.4). Substrate sensitivity for octanoyl-carnitine did not differ between groups.'''Conclusions/interpretation''': Increased mitochondrial substrate sensitivity is seen in skeletal muscle from type 2 diabetic patients and is confined to non-lipid substrates. Respiratory capacity per mitochondrion is not decreasedwith insulin resistance.spiratory capacity per mitochondrion is not decreased with insulin resistance.)
AussieMit 2016 Sydney AU + ('''AussieMit 2016, Sydney, AU''')
Othonicar 2023 MiPschool Obergurgl + ('''Authors:''' [[Othonicar Murilo F]] … '''Authors:''' [[Othonicar Murilo F]], [[Garcia Geovana S]], [[Oliveira Marcos Tulio]] Oxidative phosphorylation (OXPHOS) dysfunction can lead to decreased ATP levels and excessive reactive oxygen species (ROS) formation. Alternative enzymes (AEs) have been successfully used in model organisms to bypass OXPHOS defects and prevent high ROS levels, despite vertebrates and insects having lost their coding genes throughout evolution [1,2,3]. To get a deeper insight into the possible differences between AE-bearing and -lacking animals, we compared the genes coding for subunits of the OXPHOS complexes in tunicates of the genus ''Ciona'' with orthologs in ''Drosophila'' and humans. We found that ''Ciona'' species lack subunits necessary for the formation of respiratory supercomplexes (SCs), which are supramolecular organizations of the invidual OXPHOS complexes able to streamline electron transfer and prevent excessive ROS formation[4]. This suggests that ''Ciona'' species do not form SCs, or do so differently. In agreement, we also found that the ''Ciona intestinalis'' AE alternative oxidase (AOX), when transgenically expressed in ''Drosophila melanogaster'', preferentially receives electrons from the mitochondrial glycerol-3-phosphate dehydrogenase, which is not known to be involved in SCs. Only when ''Drosophila'' SCs appear to be disrupted, AOX is able to receive all electrons from Complex I, a well known SC component. We are currently investigating SC formation in AOX-expressing flies and in ''C. intestinalis''. Our findings could offer valuable insights for optimizing AOX expression in possible future therapeutic settings, and shed light on the evolutionary and functional variations between animal OXPHOS systems. # Szibor M, Schenkl C, Barsottini MR, Young L, Moore AL (2022) Targeting the alternative oxidase (AOX) for human health and food security, a pharmaceutical and agrochemical target or a rescue mechanism?. Biochemical Journal, 479(12), 1337-1359. https://doi.org/10.1042/BCJ20180192 # Viscomi C, Moore AL, Zeviani M, Szibor M (2023) Xenotopic expression of alternative oxidase (AOX) to study mechanisms of mitochondrial disease. Biochimica et Biophysica Acta (BBA)-Bioenergetics, 1864(2), 148947. https://doi.org/10.1016/j.bbabio.2022.148947 # Saari S. et al. (2019) Alternative respiratory chain enzymes: Therapeutic potential and possible pitfalls. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1865(4), 854-866.. https://doi.org/10.1016/j.bbadis.2018.10.012# Baker N, Patel J, Khacho M (2019) Linking mitochondrial dynamics, cristae remodeling and supercomplex formation: How mitochondrial structure can regulate bioenergetics. Mitochondrion, 49, 259-268. https://doi.org/10.1016/j.mito.2019.06.003 49, 259-268. https://doi.org/10.1016/j.mito.2019.06.003 )
Pesta 2023 MiP2023 + ('''Authors:''' Buescher F-M, [[Schrage-Knoll Irmtrud]] … '''Authors:''' Buescher F-M, [[Schrage-Knoll Irmtrud]], [[Bohmeier Maria]], Kaiser-Stolz C, Kramme J, Rittweger J, [[Pesta Dominik]] '''Introduction:''' Skeletal muscle mitochondrial function is altered in insulin resistant states. Its assessment, however, requires invasive muscle biopsies to obtain viable tissue for functional mitochondrial analysis. Blood cell-based bioenergetics potentially reflects systemic mitochondrial function. Here, we characterized respiratory capacity of skeletal muscle mitochondria and peripheral blood mononuclear cells (PBMCs) from patients with type 2 diabetes and assessed whether the latter reflect muscle mitochondrial respirometric measures. '''Methods:''' For that purpose, 20 patients with type 2 diabetes (30 % female, 57±9 years, BMI 28±4 kg/m2) participated in this study. We obtained muscle biopsies from the M. vastus lateralis and venous blood samples to isolate PBMCs. High-resolution respirometry was performed in duplicate to assess mitochondrial respiration from permeabilized muscle fibers and PBMCs using an established SUIT-protocol. '''Results and Discussion:''' Combined NADH-linked (N) electron transfer and succinate-linked (S) OXPHOS capacity was 59.4±13.0 pmol/(s*mg) for muscle and 16.6±5.3 pmol/(s*106 cells) for PBMCs. NS-OXPHOS capacity was not different between females and males for muscle (66.5±9.5 vs 56.3±13.0 pmol/(s*mg), p=0.10) or PBMCs (19.5±5.3 vs 15.3±5.0 pmol/(s*106), p=0.10), respectively. While PBMC mitochondrial function was not correlated with skeletal muscle respiratory function across several respiratory states (all p>0.05), muscle NS-OXPHOS capacity correlated negatively with diabetes disease duration (r=-0.50, p=0.02). These results suggest that there are no sex-specific differences with regard to muscle and PBMC mitochondrial function in individuals with type 2 diabetes. While bioenergetic phenotypes in PBMCs do not reflect muscle mitochondrial function in this cohort, diabetes disease duration negatively associates with muscle mitochondrial function. hort, diabetes disease duration negatively associates with muscle mitochondrial function. )
Alan 2023 MiP2023 + ('''Authors:''' [[Alan Lukas]] … '''Authors:''' [[Alan Lukas]], [[Calvo E]], [[Enriquez Jose A]], [[Soriano ME]], [[Bean C]], [[Mracek Tomas]] and [[Scorrano Luca]] '''Introduction:''' Obesity is turning into a worldwide pandemic, with most patients also affected by other comorbidities such as type 2 diabetes, hypertension, or cardiovascular disease. With mitochondria being a major site for fatty acid oxidation, they represent an important target for obesity treatment. Mitochondria are dynamic organelles, and their morphology influences both the organization of membrane protein complexes as well as mitochondrial substrate preference1. '''Methods:''' By combining 2-dimension blue native gel electrophoresis with proteomics and bioinformatics in heart mitochondria undergoing membrane remodelling we identified a strong correlation between the key cristae biogenesis protein Opa1 and Vwa8, a putative AAA+ ATPase with a dynein conformation. In order to study the role of Vwa8 protein in mitochondrial physiology, we developed the HEK293 Vwa8 knock-out cell line and Vwa8 KO mice. '''Results and discussion:''' Vwa8 protein localized to the mitochondrial intermembrane space where it formed discrete spots. Deletion of Vwa8 led to an increase in mitochondrial respiration on fatty acids but not on glucose or glutamine. The Vwa8 KO mice showed decreased resting energy requirements as well as higher heat production, indicating a stronger preference for lipid oxidation. Moreover, the subcutaneous adipose tissue of Vwa8 KO mice showed increased markers of browning such as an increase in mitochondria content and lipid droplet multilocularity. The Vwa8 KO mice remained more insulin sensitive and with higher lean mass proportion upon a high-fat diet. In conclusion, Vwa8 affects mitochondrial substrate preference, induces browning of subcutaneous adipose tissue and represents a new target for obesity treatment. # Alan L, Scorrano L. (2022) Shaping fuel utilization by mitochondria. Curr Biol. 2022 Jun 20;32(12):R618-R623. doi: 10.1016/j.cub.2022.05.006.r Biol. 2022 Jun 20;32(12):R618-R623. doi: 10.1016/j.cub.2022.05.006. )
Hand 2023 MiP2023 + ('''Authors:''' [[Arabie D]] … '''Authors:''' [[Arabie D]], [[Hand Steven C]] '''Introduction:''' Invertebrate extremophiles experience metabolic transitions promoted by diapause, anoxia and extreme dehydration/rehydration [1-3]. For embryos of brine shrimp, ''Artemia franciscana'', these reversible shifts are dramatic with respiration depressed below 1% of active states. Recovery from metabolic disruption in mammals is accompanied by generation of reactive oxygen species (ROS) that cause tissue damage during ischemia-reperfusion [4]. Yet embryos of ''A. franciscana'' survive frequent shifts in metabolism, which implies their mitochondria are poised to tolerate such reactivations without accumulation of damaging ROS. '''Methods:''' Mitochondria were isolated [5] and subjected to anoxia for 30 min while controls received continuous normoxia [4]. Samples were pelleted and resuspended in oxygenated buffer containing fresh substrate, ADP and Amplex Red assay components [4]. Parallel samples included auranofin and dinitrochlorobenzene (DNCB) to inhibit thioredoxin reductase and glutathione peroxidase, respectively. Protein carbonyls, aconitase/citrate synthase activity ratios, and lipid hydroperoxides were quantified [4,6]. '''Results and Discussion:''' H2O2 accumulation did not increase significantly in mitochondria exposed to anoxia-reoxygenation compared to normoxic controls. By comparison, an 8-fold increase in H2O2 was reported for rat heart mitochondria given the same treatment [4]. As anticipated, inclusion of auranofin and DNCB statistically increased the H2O2 accumulation 2-3 fold in both control and experimental mitochondria. Consistent with the lack of elevated H2O2 after anoxia-reoxygenation, aconitase inactivation also was not detected compared to controls. Statistical increases were not observed in protein carbonyls or lipid hydroperoxides. Evidence suggests mitochondria from ''A. franciscana'' embryos are well protected against ROS accumulation and oxidative damage during severe metabolic transitions. # Hand SC, Denlinger DL, Podrabsky JE, Roy R (2016) Mechanisms of animal diapause: Recent developments from nematodes, crustaceans, insects and fish. https://doi.org/10.1152/ajpregu.00250.2015# Hand SC, Menze MA, Borcar A, Patil Y, Covi JA, Reynolds JA, Toner M (2011) Metabolic restructuring during energy-limited states: Insights from ''Artemia franciscana'' embryos and other animals. https://doi.org/10.1016/j.jinsphys.2011.02.010# Hand SC, Moore DS, Patil Y (2018) Challenges during diapause and anhydrobiosis: mitochondrial bioenergetics and desiccation tolerance. https://doi.org/10.1002/iub.1953# Chouchani et al. (2013) Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial Complex I. https://doi.org/10.1038/nm.3212# Kwast K, Hand SC (1993) Regulatory features of protein synthesis in isolated mitochondria from ''Artemia'' embryos. https://doi.org/10.1152/ajpregu.1993.265.6.R1238# Chouchani et al. (2016) Mitochondrial ROS regulate thermogenic energy expenditure and sulfenylation of UCP1. https://doi.org/10.1038/nature17399== Affiliation and acknowledgements ==::::Arabie D, Hand Steven C:::: Dept Biological Sciences, Louisiana State Univ, Baton Rouge, USA:::: Corresponding author: shand@lsu.edu.:::: '''Funding:''' NSF grant IOS-1457061/IOS-1456809Hand Steven C :::: Dept Biological Sciences, Louisiana State Univ, Baton Rouge, USA :::: Corresponding author: shand@lsu.edu. :::: '''Funding:''' NSF grant IOS-1457061/IOS-1456809)