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Mitochondrial diabetes

P Abreu, K F Vitzel, I C C R Monteiro, T I Lima, A N Queiroz, J H Leal-Cardoso, S M Hirabara, V M Ceccatto
The aim of this research was to investigate the effects of endurance training on reduction of plasma glucose during high intensity constant and incremental speed tests in Wistar rats. We hypothesized that plasma glucose might be decreased in the exercised group during heavy (more intense) exercise. Twenty-four 10-week-old male Wistar rats were randomly assigned to sedentary and exercised groups. The prescription of endurance exercise training intensity was determined as 60% of the maximum intensity reached at the incremental speed test...
October 24, 2016: Brazilian Journal of Medical and Biological Research, Revista Brasileira de Pesquisas Médicas e Biológicas
Devasena Ponnalagu, Harpreet Singh
Mitochondria are the "power house" of a cell continuously generating ATP to ensure its proper functioning. The constant production of ATP via oxidative phosphorylation demands a large electrochemical force that drives protons across the highly selective and low-permeable mitochondrial inner membrane. Besides the conventional role of generating ATP, mitochondria also play an active role in calcium signaling, generation of reactive oxygen species (ROS), stress responses, and regulation of cell-death pathways...
October 26, 2016: Handbook of Experimental Pharmacology
R E Frye, S Rose, J Chacko, R Wynne, S C Bennuri, J C Slattery, M Tippett, L Delhey, S Melnyk, S G Kahler, D F MacFabe
Propionic acid (PPA) is a ubiquitous short-chain fatty acid, which is a major fermentation product of the enteric microbiome. PPA is a normal intermediate of metabolism and is found in foods, either naturally or as a preservative. PPA and its derivatives have been implicated in both health and disease. Whereas PPA is an energy substrate and has many proposed beneficial effects, it is also associated with human disorders involving mitochondrial dysfunction, including propionic acidemia and autism spectrum disorders (ASDs)...
October 25, 2016: Translational Psychiatry
Elena V Galitsyna, Margarita A Sazonova, Tatiana P Shkurat, Natalya A Demakova, Alexsandra A Melnichenko, Vasily V Sinyov, Anastasia I Ryzhkova, Konstantin Y Mitrofanov, Andrey V Zhelankin, Igor A Sobenin, Alexander N Orekhov
The present article considers chronic diseases of non-inflammatory genesis, the reasons of which may be mitochondrial dysfunctions. Among them are: coronary heart disease (CHD), hypertension, cardiomyopathy, cerebrovascular accidents and type 2 diabetes mellitus (T2D). Very often, in the long course of the disease, complications may occur, leading to myocardial infarction or ischemic stroke and as a result, death. The main cause of mitochondrial dysfunction are point mitochondrial genome mutations. During the analysis of the literature, data showing the association of the mitochondrial genome mutations with the above diseases were revealed...
October 18, 2016: Current Pharmaceutical Design
Xiaocui Jiao, Ying Li, Tao Zhang, Maodong Liu, Yanqing Chi
The apoptosis of renal tubular epithelial cells contributes to the pathogenesis of diabetic nephropathy. High glucose-induced mitochondrial oxidative stress is considered to be an important mediator for renal tubular cell apoptosis. Sirtuin3(Sirt3), a kind of mitochondria-localized nicotinamide adenine dinucleotide(NAD(+))-dependent protein deacetylase, has been reported to regulate the generation of ROS in mitochondria through regulating acetylation level and activity of several key mitochondrial enzymes. In this study, we investigated the role of Sirt3 on high glucose-induced apoptosis in HK-2 cells...
October 20, 2016: Biochemical and Biophysical Research Communications
Akos A Gerencser, Shona A Mookerjee, Martin Jastroch, Martin D Brand
Analysis of the cellular mechanisms of metabolic disorders, including type 2 diabetes mellitus, is complicated by the large number of reactions and interactions in metabolic networks. Metabolic control analysis with appropriate modularization is a powerful method for simplifying and analyzing these networks. To analyze control of cellular energy metabolism in adherent cell cultures of the INS-1832/13 pancreatic β-cell model we adapted our microscopy assay of absolute mitochondrial membrane potential (ΔψM) to a fluorescence microplate reader format, and applied it in conjunction with cell respirometry...
October 20, 2016: Biochimica et Biophysica Acta
Stepana Boukalova, Jan Stursa, Lukas Werner, Zuzana Ezrova, Jiri Cerny, Ayenachew Bezawork-Geleta, Alena Pecinova, Lanfeng Dong, Zdenek Drahota, Jiri Neuzil
Pancreatic cancer is one of the hardest-to-treat types of neoplastic diseases. Metformin, a widely prescribed drug against type 2 diabetes mellitus, is being trialed as an agent against pancreatic cancer, although its efficacy is low. With the idea of delivering metformin to its molecular target, the mitochondrial complex I (CI), we tagged the agent with the mitochondrial vector, triphenylphosphonium group. Mitochondrially targeted metformin (MitoMet) was found to kill a panel of pancreatic cancer cells 3-4 orders of magnitude more efficiently than found for the parental compound...
October 7, 2016: Molecular Cancer Therapeutics
Jianyin Long, Shawn S Badal, Zengchun Ye, Yin Wang, Bernard A Ayanga, Daniel L Galvan, Nathanael H Green, Benny H Chang, Paul A Overbeek, Farhad R Danesh
The regulatory roles of long noncoding RNAs (lncRNAs) in transcriptional coactivators are still largely unknown. Here, we have shown that the peroxisome proliferator-activated receptor γ (PPARγ) coactivator α (PGC-1α, encoded by Ppargc1a) is functionally regulated by the lncRNA taurine-upregulated gene 1 (Tug1). Further, we have described a role for Tug1 in the regulation of mitochondrial function in podocytes. Using a murine model of diabetic nephropathy (DN), we performed an unbiased RNA-sequencing (RNA-seq) analysis of kidney glomeruli and identified Tug1 as a differentially expressed lncRNA in the diabetic milieu...
October 17, 2016: Journal of Clinical Investigation
Szu Yuan Li, Katalin Susztak
An increasing amount of evidence suggests that metabolic alterations play a key role in chronic kidney disease (CKD) pathogenesis. In this issue of the JCI, Long et al. report that the long noncoding RNA (lncRNA) taurine-upregulated 1 (Tug1) contributes to CKD development. The authors show that Tug1 regulates mitochondrial function in podocytes by epigenetic targeting of expression of the transcription factor PPARγ coactivator 1α (PGC-1α, encoded by Ppargc1a). Transgenic overexpression of Tug1 specifically in podocytes ameliorated diabetes-induced CKD in mice...
October 17, 2016: Journal of Clinical Investigation
Eun Hee Koh, Yong Chen, David A Bader, Mark P Hamilton, Bin He, Brian York, Shingo Kajimura, Sean E McGuire, Sean M Hartig
The acquisition of beige adipocyte features by white fat cells corresponds to protection against obesity-induced metabolic diseases in humans and animal models of type 2 diabetes. In adipose tissue, expression of the E2-SUMO ligase Ubiquitin Carrier Protein 9 (Ubc9) is positively correlated with markers of insulin resistance and corresponds with impaired browning of human white adipocytes. However, the molecular regulation of Ubc9 expression in adipocytes and other cells remains unclear. In this study, we demonstrated the mRNA and protein expression of Ubc9 are regulated by the microRNA miRNA-30a (miR-30a) in human subcutaneous adipocytes...
October 10, 2016: Journal of Biological Chemistry
Mohammad Massumi, Farzaneh Pourasgari, Amarnadh Nalla, Battsetseg Batchuluun, Kristina Nagy, Eric Neely, Rida Gull, Andras Nagy, Michael B Wheeler
The ability to yield glucose-responsive pancreatic beta-cells from human pluripotent stem cells in vitro will facilitate the development of the cell replacement therapies for the treatment of Type 1 Diabetes. Here, through the sequential in vitro targeting of selected signaling pathways, we have developed an abbreviated five-stage protocol (25-30 days) to generate human Embryonic Stem Cell-Derived Beta-like Cells (ES-DBCs). We showed that Geltrex, as an extracellular matrix, could support the generation of ES-DBCs more efficiently than that of the previously described culture systems...
2016: PloS One
Antonius Baartscheer, Cees A Schumacher, Rob C I Wüst, Jan W T Fiolet, Ger J M Stienen, Ruben Coronel, Coert J Zuurbier
AIMS/HYPOTHESIS: Empagliflozin (EMPA), an inhibitor of the renal sodium-glucose cotransporter (SGLT) 2, reduces the risk of cardiovascular death in patients with type 2 diabetes. The underlying mechanism of this effect is unknown. Elevated cardiac cytoplasmic Na(+) ([Na(+)]c) and Ca(2+) ([Ca(2+)]c) concentrations and decreased mitochondrial Ca(2+) concentration ([Ca(2+)]m) are drivers of heart failure and cardiac death. We therefore hypothesised that EMPA would directly modify [Na(+)]c, [Ca(2+)]c and [Ca(2+)]m in cardiomyocytes...
October 17, 2016: Diabetologia
Albert R Jones Iv, Tova Meshulam, Marcus F Oliveira, Nathan Burritt, Barbara E Corkey
BACKGROUND: Many tissues play an important role in metabolic homeostasis and the development of diabetes and obesity. We hypothesized that the circulating redox metabolome is a master metabolic regulatory system that impacts all organs and modulates reactive oxygen species (ROS) production, lipid peroxidation, energy production and changes in lipid turnover in many cells including adipocytes. METHODS: Differentiated human preadipocytes were exposed to the redox couples, lactate (L) and pyruvate (P), β-hydroxybutyrate (βOHB) and acetoacetate (Acoc), and the thiol-disulfides cysteine/ cystine (Cys/CySS) and GSH/GSSG for 1...
2016: PloS One
E M Ribe, S Lovestone
As populations across the world both age and become more obese, the numbers of individuals with Alzheimer's disease and diabetes are increasing; posing enormous challenges for society and consequently becoming priorities for governments and global organizations. These issues, an ageing population at risk of neurodegenerative diseases such as Alzheimer's disease and an increasingly obese population at risk of metabolic alterations such as type 2 diabetes, are usually considered as independent conditions, but increasing evidence from both epidemiological and molecular studies link these disorders...
October 14, 2016: Journal of Internal Medicine
E D Rosen
Insulin resistance is one of the defining features of type 2 diabetes and the metabolic syndrome and accompanies many other clinical conditions, ranging from obesity to lipodystrophy to glucocorticoid excess. Extraordinary efforts have gone into defining the mechanisms that underlie insulin resistance, with most attention focused on altered signalling as well as mitochondrial and endoplasmic reticulum stress. Here, nuclear mechanisms of insulin resistance, including transcriptional and epigenomic effects, will be discussed...
October 14, 2016: Journal of Internal Medicine
Elisa Fabbri, Chee W Chia, Richard G Spencer, Kenneth W Fishbein, David A Reiter, Donnie Cameron, Ariel C Zane, Zenobia A Moore, Marta Gonzalez-Freire, Marco Zoli, Stephanie A Studenski, Rita R Kalyani, Josephine M Egan, Luigi Ferrucci
Whether individuals with insulin resistance but without criteria for diabetes exhibit reduced mitochondrial oxidative capacity is unclear; addressing this question could guide research for new therapeutics. We investigated 248 non-diabetic participants from the Baltimore Longitudinal Study of Aging (BLSA) to determine whether impaired mitochondrial capacity is associated with prediabetes, insulin resistance, duration and severity of hyperglycemia exposure. Mitochondrial capacity was assessed as post-exercise phosphocreatine recovery time constant (τPCr) by (31)P-magnetic resonance spectroscopy, with higher τPCr reflecting reduced capacity...
October 13, 2016: Diabetes
Qilong Wang, Miao Zhang, Gloria Torres, Shengnan Wu, Changhan Ouyang, Zhonglin Xie, Ming-Hui Zou
Metformin is a widely used anti-diabetic drug that exerts cardiovascular protective effects in patients with diabetes. How metformin protects diabetes-related cardiovascular diseases remains poorly understood. Here, we show that metformin abated the progression of diabetes-accelerated atherosclerosis by inhibiting mitochondrial fission in endothelial cells.Metformin treatments markedly reduced mitochondrial fragmentation, mitigated mitochondrial-derived superoxide release, improved endothelial-dependent vasodilation, inhibited vascular inflammation, and suppressed atherosclerotic lesions in streptozotocin (STZ)-induced diabetic ApoE(-/-) mice...
October 13, 2016: Diabetes
Vishal R Mali, Guodong Pan, Mandar Deshpande, Rajarajan A Thandavarayan, Jiang Xu, Xiao-Ping Yang, Suresh S Palaniyandi
Aldehyde dehydrogenase (ALDH) 2 is a mitochondrial isozyme of the heart involved in the metabolism of toxic aldehydes produced from oxidative stress. We hypothesized that hyperglycemia-mediated decrease in ALDH2 activity may impair mitochondrial respiration and ultimately result in cardiac damage. A single dose (65 mg/kg; i.p.) streptozotocin injection to rats resulted in hyperglycemia with blood glucose levels of 443 ± 9 mg/dl versus 121 ± 7 mg/dl in control animals, p<0.0001, N = 7-11. After 6 months of diabetes mellitus (DM) induction, the rats were sacrificed after recording the functionality of their hearts...
2016: PloS One
Tanes I Lima, Hygor N Araujo, Eveline S Menezes, Carlos H Sponton, Michel B Araújo, Lucas H M Bomfim, André L Queiroz, Madla A Passos, Thais Amaral E Sousa, Sandro M Hirabara, Amanda R Martins, Helena C L B Sampaio, Alice Rodrigues, Rui Curi, Everardo M Carneiro, Antônio C Boschero, Leonardo R Silveira
Mitochondria play a critical role in several cellular processes and cellular homeostasis. Mitochondrion dysfunction has been correlated with numerous metabolic diseases such as obesity and type 2 diabetes. MicroRNAs are non-coding RNAs that have emerged as key regulators of cell metabolism. The microRNAs act as central regulators of metabolic gene networks by leading to the degradation of their target messenger RNA or repression of protein translation. In addition, vesicular and non-vesicular circulating miRNAs exhibit a potential role as mediators of the cross-talk between the skeletal muscle and other tissues/organs...
October 13, 2016: Journal of Cellular Physiology
Chao-Wei Huang, Yi-Shan Chien, Yu-Jen Chen, Kolapo M Ajuwon, Harry M Mersmann, Shih-Torng Ding
The incidence of obesity and its comorbidities, such as insulin resistance and type II diabetes, are increasing dramatically, perhaps caused by the change in the fatty acid composition of common human diets. Adipose tissue plays a role as the major energy reservoir in the body. An excess of adipose mass accumulation caused by chronic positive energy balance results in obesity. The n-3 polyunsaturated fatty acids (n-3 PUFA), DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) exert numerous beneficial effects to maintain physiological homeostasis...
October 9, 2016: International Journal of Molecular Sciences
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