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https://www.readbyqxmd.com/read/28822233/obese-fathers-lead-to-an-altered-metabolism-and-obesity-in-their-children-in-adulthood-review-of-experimental-and-human-studies
#1
REVIEW
Fernanda Ornellas, Priscila V Carapeto, Carlos A Mandarim-de-Lacerda, Marcia B Aguila
OBJECTIVE: To discuss the recent literature on paternal obesity, focusing on the possible mechanisms of transmission of the phenotypes from the father to the children. SOURCES: A non-systematic review in the PubMed database found few publications in which paternal obesity was implicated in the adverse transmission of characteristics to offspring. Specific articles on epigenetics were also evaluated. As the subject is recent and still controversial, all articles were considered regardless of year of publication...
August 16, 2017: Jornal de Pediatria
https://www.readbyqxmd.com/read/28822073/isorhynchophylline-attenuates-mpp-induced-apoptosis-through-endoplasmic-reticulum-stress-and-mitochondria-dependent-pathways-in-pc12-cells-involvement-of-antioxidant-activity
#2
Xiao-Ming Li, Xiao-Jie Zhang, Miao-Xian Dong
Endoplasmic reticulum stress (ERS) and mitochondrial dysfunctions are thought to be involved in the dopaminergic neuronal death in Parkinson's disease (PD). In this study, we found that isorhynchophylline (IRN) significantly attenuated 1-methyl-4-phenylpyridinium (MPP(+))-induced apoptotic cell death and oxidative stress in PC12 cells. IRN markedly reduced MPP(+)-induced-ERS responses, indicative of inositol-requiring enzyme 1 (IRE1) phosphorylation and caspase-12 activation. Furthermore, IRN inhibits MPP(+)-triggered apoptosis signal-regulating kinase 1 (ASK1)/c-Jun N-terminal Kinase (JNK) signaling-mediated mitochondria-dependent apoptosis pathway...
August 18, 2017: Neuromolecular Medicine
https://www.readbyqxmd.com/read/28821956/effects-of-ageing-on-pro-arrhythmic-ventricular-phenotypes-in-incrementally-paced-murine-pgc-1%C3%AE-hearts
#3
Shiraz Ahmad, Haseeb Valli, Charlotte E Edling, Andrew A Grace, Kamalan Jeevaratnam, Christopher L-H Huang
A range of chronic clinical conditions accompany cardiomyocyte energetic dysfunction and constitute independent risk factors for cardiac arrhythmia. We investigated pro-arrhythmic and arrhythmic phenotypes in energetically deficient C57BL mice with genetic ablation of the mitochondrial promoter peroxisome proliferator-activated receptor-γ coactivator-1β (Pgc-1β), a known model of ventricular arrhythmia. Pro-arrhythmic and cellular action potential (AP) characteristics were compared in intact Langendorff-perfused hearts from young (12-16 week) and aged (> 52 week), wild-type (WT) and Pgc-1β (-/-) mice...
August 18, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28821609/insulin-like-growth-factor-1-signalling-is-essential-for-mitochondrial-biogenesis-and-mitophagy-in-cancer-cells
#4
Amy Lyons, Michael Coleman, Sarah Riis, Cedric Favre, Ciara H O'Flanagan, Alexander V Zhdanov, Dmitri B Papkovsky, Stephen D Hursting, Rosemary O'Connor
Mitochondrial activity and metabolic reprogramming influence the phenotype of cancer cells and resistance to targeted therapy. We previously established that an Insulin-like Growth Factor 1 (IGF-1)-inducible mitochondrial UTP carrier (PNC1/SLC25A33) promotes cell growth. This prompted us to investigate whether IGF signaling is essential for mitochondrial maintenance in cancer cells, and whether this contributes to therapy resistance. Here, we show that IGF-1 stimulates mitochondrial biogenesis in a range of cell lines...
August 18, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28819865/melatonin-mitochondria-and-the-metabolic-syndrome
#5
REVIEW
Daniel P Cardinali, Daniel E Vigo
A number of risk factors for cardiovascular disease including hyperinsulinemia, glucose intolerance, dyslipidemia, obesity, and elevated blood pressure are collectively known as metabolic syndrome (MS). Since mitochondrial activity is modulated by the availability of energy in cells, the disruption of key regulators of metabolism in MS not only affects the activity of mitochondria but also their dynamics and turnover. Therefore, a link of MS with mitochondrial dysfunction has been suspected since long. As a chronobiotic/cytoprotective agent, melatonin has a special place in prevention and treatment of MS...
August 17, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28819639/antioxidant-treatment-in-male-mice-prevents-mitochondrial-and-synaptic-changes-in-an-nmda-receptor-dysfunction-model-of-schizophrenia
#6
Aarron Phensy, Christopher Driskill, Karen Lindquist, Lan Guo, Vivek Jeevakumar, Bryan Fowler, Heng Du, Sven Kroener
Glutamate theories of schizophrenia suggest that the disease is associated with a loss of NMDA receptors, specifically on GABAergic parvalbumin-expressing interneurons (PVIs), leading to changes in the excitation-inhibition balance in the prefrontal cortex (PFC). Oxidative stress contributes to the loss of PVI and the development of schizophrenia. Here, we investigated whether the glutathione precursor N-acetyl cysteine (NAC) can prevent changes in synaptic transmission at pyramidal cells and PVIs that result from developmental NMDAR blockade and how these changes are related to mitochondrial dysfunction in the PFCs of mice...
July 2017: ENeuro
https://www.readbyqxmd.com/read/28819266/amalaki-rasayana-a-traditional-indian-drug-enhances-cardiac-mitochondrial-and-contractile-functions-and-improves-cardiac-function-in-rats-with-hypertrophy
#7
Vikas Kumar, Kumar A Aneesh, K Kshemada, Kumar G S Ajith, Raj S S Binil, Neha Deora, G Sanjay, A Jaleel, T S Muraleedharan, E M Anandan, R S Mony, M S Valiathan, Kumar T R Santhosh, C C Kartha
We evaluated the cardioprotective effect of Amalaki Rasayana (AR), a rejuvenating Ayurvedic drug prepared from Phyllanthus emblica fruits in the reversal of remodeling changes in pressure overload left ventricular cardiac hypertrophy (LVH) and age-associated cardiac dysfunction in male Wistar rats. Six groups (aging groups) of 3 months old animals were given either AR or ghee and honey (GH) orally; seventh group was untreated. Ascending aorta was constricted using titanium clips in 3 months old rats (N = 24; AC groups) and after 6 months, AR or GH was given for further 12 months to two groups; one group was untreated...
August 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28819074/-molecular-pathogenesis-of-polyglutamine-diseases
#8
Yuji Takahashi
Polyglutamine diseases result from gain-of-function mutations. The expanded polyglutamine tracts lead to conformational changes in proteins, resulting in their aggregation. The intermediates including monomers or oligomers, are more toxic than the aggregates to neurons. At the molecular level, protein misfolding, transcriptional dysregulation, deranged calcium homeostasis, impaired cytoskeleton/axonal transport, mitochondrial dysfunction, and RNA toxicity contribute to disease progression. Understanding the underlying pathogenesis facilitates development of therapy for polyglutamine diseases...
August 2017: Brain and Nerve, Shinkei Kenkyū No Shinpo
https://www.readbyqxmd.com/read/28819044/the-parkinson-s-disease-associated-protein-dj-1-plays-a-positive-nonmitochondrial-role-in-endocytosis-in-dictyostelium-cells
#9
Suwei Chen, Sarah J Annesley, Rasha A F Jasim, Vanessa J Musco, Oana Sanislav, Paul R Fisher
The loss of function of DJ-1 caused by mutations of DJ-1 causes a form of familial Parkinson's Disease (PD). However, the role of DJ-1 in healthy and in PD cells is poorly understood. Even its subcellular localization in mammalian cells is uncertain, both cytosolic and mitochondrial locations having been reported. We show here that DJ-1 is normally located in the cytoplasm in healthy Dictyostelium discoideum cells. With its unique life cycle, straightforward genotype-phenotype relationships, experimental accesibility and genetic tractability, Dictyostelium discoideum offers an attractive model to investigate the roles of PD-associated genes...
August 17, 2017: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/28819004/acute-oxygen-sensing-by-the-carotid-body-from-mitochondria-to-plasma-membrane
#10
Andy J Chang
Maintaining oxygen homeostasis is crucial to the survival of animals. Mammals respond acutely to changes in blood oxygen levels by modulating cardiopulmonary function. The major sensor of blood oxygen that regulates breathing is the carotid body (CB), a small chemosensory organ located at the carotid bifurcation. When arterial blood oxygen levels drop in hypoxia, neuroendocrine cells in the CB called glomus cells are activated to signal to afferent nerves that project to the brainstem. The mechanism by which hypoxia stimulates CB sensory activity has been the subject of many studies over the last 90 years...
August 17, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28818596/cardiometabolic-phenotypes-and-mitochondrial-dna-copy-number-in-two-cohorts-of-uk-women
#11
Anna L Guyatt, Kimberley Burrows, Philip A I Guthrie, Sue Ring, Wendy McArdle, Ian N M Day, Raimondo Ascione, Debbie A Lawlor, Tom R Gaunt, Santiago Rodriguez
The mitochondrial genome is present at variable copy number between individuals. Mitochondria are vulnerable to oxidative stress, and their dysfunction may be associated with cardiovascular disease. The association of mitochondrial DNA copy number with cardiometabolic risk factors (lipids, glycaemic traits, inflammatory markers, anthropometry and blood pressure) was assessed in two independent cohorts of European origin women, one in whom outcomes were measured at mean (SD) age 30 (4.3) years (N=2278) and the second at 69...
August 14, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28817209/huntington-s-disease-a-clinical-review
#12
Peter McColgan, Sarah J Tabrizi
Huntington's disease (HD) is a fully penetrant neurodegenerative disease caused by a dominantly inherited CAG trinucleotide repeat expansion in the huntingtin gene on chromosome 4. In Western populations HD has a prevalence of 10.6-13.7 individuals per 100,000. It is characterised by cognitive, motor and psychiatric disturbance. At the cellular level mutant huntingtin results in neuronal dysfunction and death through a number of mechanisms, including disruption of proteostasis, transcription and mitochondrial function and direct toxicity of the mutant protein...
August 17, 2017: European Journal of Neurology: the Official Journal of the European Federation of Neurological Societies
https://www.readbyqxmd.com/read/28817120/the-erythropoietin-derived-peptide-mk-x-and-erythropoietin-have-neuroprotective-effects-against-ischemic-brain-damage
#13
Seung-Jun Yoo, Bongki Cho, Deokho Lee, Gowoon Son, Yeong-Bae Lee, Hyung Soo Han, Eunjoo Kim, Chanil Moon, Cheil Moon
Erythropoietin (EPO) has been well known as a hematopoietic cytokine over the past decades. However, recent reports have demonstrated that EPO plays a neuroprotective role in the central nervous system, and EPO has been considered as a therapeutic target in neurodegenerative diseases such as ischemic stroke. Despite the neuroprotective effect of EPO, clinical trials have shown its unexpected side effects, including undesirable proliferative effects such as erythropoiesis and tumor growth. Therefore, the development of EPO analogs that would confer neuroprotection without adverse effects has been attempted...
August 17, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28816359/chrysin-attenuates-progression-of-ovarian-cancer-cells-by-regulating-signaling-cascades-and-mitochondrial-dysfunction
#14
Whasun Lim, Soomin Ryu, Fuller W Bazer, Sung-Man Kim, Gwonhwa Song
Chrysin is mainly found in passion flowers, honey, and propolis acts as a potential therapeutic and preventive agent to inhibit proliferation and invasion of various human cancer cells. Although chrysin has anti-carcinogenic effects in several cancers, little is known about its functional roles in ovarian cancer which shows poor prognosis and chemoresistance to traditional therapeutic agents. In the present study, we investigated functional roles of chrysin in progression of ovarian cancer cells using ES2 and OV90 (clear cell and serous carcinoma, respectively) cell lines...
August 17, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28816057/mitochondrial-complex-i-reversible-s-nitrosation-improves-bioenergetics-and-is-protective-in-parkinson-s-disease
#15
Chiara Milanese, Victor Tapias, Sylvia Gabriels, Silvia Cerri, Giovanna Levandis, Fabio Blandini, Maria Tresini, Sruti Shiva, J Timothy Greenamyre, Mark T Gladwin, Pier G Mastroberardino
AIMS: The present study was designed to explore the neuroprotective potential of inorganic nitrite as a new therapeutic avenue in Parkinson's disease (PD). RESULTS: Administration of inorganic nitrite ameliorates neuropathology in phylogenetically distinct animal models of PD. Beneficial effects are not confined to prophylactic treatment and occur also if nitrite is administered when the pathogenic cascade is already active. Mechanistically, the effect is mediated by both complex I S-nitrosation, which under nitrite administration is favored over formation of other forms of oxidation, and as well as down-stream activation of the antioxidant Nrf2 pathway...
August 17, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28815872/a-multimethod-computational-simulation-approach-for-investigating-mitochondrial-dynamics-and-dysfunction-in-degenerative-aging
#16
Timothy E Hoffman, Katherine J Barnett, Lyle Wallis, William H Hanneman
Research in biogerontology has largely focused on the complex relationship between mitochondrial dysfunction and biological aging. In particular, the mitochondrial free radical theory of aging (MFRTA) has been well accepted. However, this theory has been challenged by recent studies showing minimal increases in reactive oxygen species (ROS) as not entirely deleterious in nature, and even beneficial under the appropriate cellular circumstances. To assess these significant and nonintuitive observations in the context of a functional system, we have taken an in silico approach to expand the focus of the MFRTA by including other key mitochondrial stress response pathways, as they have been observed in the nematode Caenorhabditis elegans...
August 16, 2017: Aging Cell
https://www.readbyqxmd.com/read/28815530/role-of-endoplasmic-reticulum-mitochondria-communication-in-type-2-diabetes
#17
Jennifer Rieusset
Although mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and disrupted lipid and calcium (Ca(2+)) homeostasis are classically associated with both insulin resistance and β-cell dysfunction in type 2 diabetes mellitus (T2DM), the interplay between these metabolic stresses is less known. Both organelles interact through contact points known as mitochondria-associated membranes (MAM), in order to exchange both lipids and Ca(2+) and regulate cellular homeostasis. Recent evidences suggest that MAM could be an important hub for hormonal and nutrient signaling in the liver and that ER-mitochondria miscommunication could participate to hepatic insulin resistance, highlighting the importance of MAM in the control of glucose homeostasis...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28815529/mitochondrial-associated-membranes-in-parkinson-s-disease
#18
Nobutaka Hattori, Taku Arano, Taku Hatano, Akio Mori, Yuzuru Imai
Parkinson's disease (PD) is a common neurodegenerative disorder, with ageing being a major risk factor. Accordingly, estimates predict an increasing number of PD patients due to our expanding life span. Consequently, developing a true disease-modifying therapy is necessary. In this regard, monogenic PD offers a suitable means for determining pathogenesis. Among monogenic forms of PD, mitochondrial dysfunction may be a major cause and is also likely to be involved in sporadic PD. Thus, mitochondrial impairment may be a common pathway...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28814227/mitochondrial-aconitase-in-neurodegenerative-disorders-role-of-a-metabolism-related-molecule-in-neurodegeneration
#19
Fariba Khodagholi, Fatemeh Shaerzadeh, Fateme Montazeri
Mitochondrial aconitase (Aco2), a member of the family of iron-sulfur [4Fe-4S]-containing dehydratases, is involved in cellular metabolism through the tricarboxylic acid cycle. Aco2 is highly susceptible to oxidative damage in a way that exposure to the reactive species and free radicals lead to release of iron from the central [4Fe-4S] cluster resulting in the production of the inactive form of Aco2. There is increasing evidence supporting a direct association between impaired energy metabolism and the incidence and progression of neurodegenerative disorders in neuronal cells...
August 16, 2017: Current Drug Targets
https://www.readbyqxmd.com/read/28813700/regenerative-medicine-approaches-for-age-related-muscle-loss-and-sarcopenia-a-mini-review
#20
Juan Diego Naranjo, Jenna L Dziki, Stephen F Badylak
Sarcopenia is a complex and multifactorial disease that includes a decrease in the number, structure and physiology of muscle fibers, and age-related muscle mass loss, and is associated with loss of strength, increased frailty, and increased risk for fractures and falls. Treatment options are suboptimal and consist of exercise and nutrition as the cornerstone of therapy. Current treatment principles involve identification and modification of risk factors to prevent the disease, but these efforts are of limited value to the elderly individuals currently affected by sarcopenia...
August 17, 2017: Gerontology
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