Oxidative stress and metabolic disorders: Pathogenesis and therapeutic strategies

Rani, Vibha; Deep, Gagan; Singh, Rakesh K.; Palle, Komaraiah; Yadav, Umesh C. S.

doi:10.1016/j.lfs.2016.02.002

Cited by 869 publications

(645 citation statements)

References 140 publications

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“…However, other studies suggest that obesity per se can induce systemic oxidative stress through multiple biochemical mechanisms, such as the generation of superoxide, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, oxidative phosphorylation, glyceraldehyde autoxidation, activation of protein kinase (PK)-C and pathways of hexosamine and polyol. On the other hand, studies suggest that obesity may be caused by oxidative stress through the proliferation of preadipocytes and increased size of differentiated adipocytes [63][64][65]. Obesity is an important risk factor for the development of metabolic syndrome (MetS), diabetes mellitus, dyslipidemia, atherosclerosis, hypertension, insulin resistance, hepatic steatosis, non-alcoholic liver disease, and high morbidity and mortality [66] (Figure 5).…”

Section: Oxidative Stress and Obesitymentioning

confidence: 99%

“…Among these signaling roles are transcriptional control and cell cycle regulation. Oxidative stress occurs when free radical species such as ROS and reactive nitrogen species exceed the capacity of cells to eliminate them through their antioxidant defense mechanisms, which have multiple nocuous effects on the cellular metabolism [65,72]. It has long been accepted that ROS becomes harmful to cells even at low physiological levels.…”

Section: Oxidative Stress and Obesitymentioning

confidence: 99%

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Adipose Tissue and Inflammation

Muñoz‐Carrillo¹,

Campo²,

Coronado³

et al. 2018

Adipose Tissue

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Adipose tissue is composed mainly by adipocytes and stromal-vascular fraction, which are composed by different cell types including macrophages. There are three types of adipose tissue: brown (BrAT), white (WAT), and beige (BeAT). BrAT is less abundant and is implicated in lipid oxidation and energy balance; BeAT has the pathway of adaptive thermogenesis, and WAT is endocrine in nature and lipid storage site and is implicated as an endocrine organ that secretes hormones and different molecules. These molecules are pro-inflammatory and anti-inflammatory factors, including the adipokines leptin, adiponectin, resistin, and visfatin, as well as cytokines and chemokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, leptin, adiponectin, and others, are involved with the development of adipose tissue inflammation and obesity. This pathological condition, together with other factors such as oxidative stress, may develop insulin resistance and the pathogenesis of type 2 diabetes mellitus (T2DM).

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Section: Oxidative Stress and Obesitymentioning

confidence: 99%

Section: Oxidative Stress and Obesitymentioning

confidence: 99%

Adipose Tissue and Inflammation

Muñoz‐Carrillo¹,

Campo²,

Coronado³

et al. 2018

Adipose Tissue

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“…Az utóbbi években többen vizsgálták a krónikus gyulladásos folyamatok összefüggéseit az elhízással és az inzulinrezisztenciával [14,25]. Magasabb IL-1b-, IL-6-és TNF-α-szintek mérhetők T2DM-betegeknél, és össze-függés mutatható ki e gyulladásos markerek és a DN incidenciája között [14,26].…”

Section: A Gyulladás Szerepeunclassified

“…A glutation antioxidáns szerepe régóta ismert, tiolcsoportja révén reverzibilisen oxidálódhat és így segíti a fehérjék kéntartalmú oldalláncainak redukált állapotban tartását, elősegíti a reaktív gyökök eliminálását, koenzimként szolgál számos enzimreakcióban, ezért a sejtszintű redoxiegyensúly felborulásával kapcsolatos biomarkerként szolgálhat [25]. A glutation-peroxidáz enzim a glutation oxidálásával neutralizálja a hidrogén-peroxidot, az oxidált glutation redukcióját a glutationreduktáz végzi.…”

Section: Az Oxidatív Stresszt Jellemző Biomarkerek Diabeteses Neuropaunclassified

Az oxidatív stressz szerepe a diabeteses neuropathia kialakulásában

2016

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A diabeteses neuropathia egyik leggyakoribb és súlyos szövődmény lehet diabetes mellitusban. Az oxidatív stressz fontos szerepet játszik a cukorbetegség microvascularis komplikációinak progressziójában. A fokozott oxidatív stressz elősegíti bizonyos kóros metabolikus útvonalak, mint a poliol-és hexózamin-útvonal, az előrehaladott glikációs vég-termékek, a poli-ADP-ribóz polimeráz és a proteinkináz-C aktivációját. Jelen összefoglalóban a szerzők áttekintik az oxidatív stressz és a cukorbetegség kapcsolatának legfrissebb ismereteit és összegzik a fokozott oxidatív stressz patofiziológiai hatásait a diabeteses neuropathia kialakulásában. A diabeteses neuropathia kezelésében alkalmazott modern gyógyszerek vizsgálatában még intenzív, hosszú távú összehasonlító vizsgálatokra van szükség a közeljövőben. Orv. Hetil., 2016Hetil., , 157(49), 1939Hetil., -1946. Kulcsszavak: diabeteses neuropathia, oxidatív stressz, gyulladás, endothelialis diszfunkció, microvascularis szövőd-ményekThe role of oxidative stress in the development of diabetic neuropathy Diabetic neuropathy may be one of the most common and severe complications of diabetes mellitus. Oxidative stress plays a pivotal role in the development of microvascular complications of diabetes. The majority of related pathways like polyol and hexosamine, advanced glycation end products, poly-ADP-ribose polymerase, and protein kinase-C all originated from initial oxidative stress. In this review, the authors present the current oxidative stress hypothesis in diabetes mellitus and summarize the pathophysiological mechanisms of diabetic neuropathy associated with increased oxidative stress. The development of modern medicines to treat diabetic neuropathy needs intensive long-term comparative trials in the future. , F., M. Molnár, Á., Balogh, Z. [The role of oxidative stress in the development of diabetic neuropathy]. Orv. Hetil., 2016, 157(49), 1939-1946. (Beérkezett: 2016 elfogadva: 2016. október Rövidítések ADMA = aszimmetrikus dimetil-arginin; AGE-k = előrehala-dott glikációs végtermékek; DN = diabeteses neuropathia; GAPDH = glicerinaldehid-3-foszfát-dehidrogenáz; IL-1b/-6 = interleukin-1b/-6; MDA = malondialdehid; NFκB = nuclear factor kappa-light-chain-enhancer of activated B cells; NGF = idegi növekedési faktor; NO = nitrogén-monoxid; PAI-1 = 1-es típusú plazminogénaktivátor-inhibitor; PARP = poli(ADPribóz)-polimeráz; PKC = proteinkináz-C; RAGE = előrehala-dott glikációs végtermékek receptora; ROS = reaktív oxigén-gyökök; T2DM = 2-es típusú cukorbetegség; TBARS = tiobarbitursav-reaktív anyagok; TGF-β = transzformáló növe-kedési faktor-béta; TNF-α = tumornekrózis-faktor-alfa; VEGF = vascularis endothelialis növekedési faktor A polyneuropathiák gyűjtőfogalma alatt a perifériás és autonóm idegek degeneratív károsodását értjük, amely legtöbbször valamilyen anyagcsere-betegség vagy toxikus ártalom következtében alakul ki, leggyakoribb endo-ÖSSZEFOGLALÓ KÖZLEMÉNY Keywords: diabetic neuropathy, oxidative stress, inflammation, endothelial dysfunction, microvascular comp...

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“…Several studies have shown that DNA damage, from reactive metabolites [(17); (18); (19); (20)], play an important role in the development of late diabetic complications [(21); (22); (17); (18); (23); (24)]. Increased damage to the DNA would result in an increased demand on repair processes, in particularly the purine building blocks required for the DNA structure.…”

mentioning

confidence: 99%

High-glucose toxicity is mediated by AICAR-transformylase/IMP cyclohydrolase and mitigated by AMP-activated protein kinase in Caenorhabditis elegans

Riedinger

Mendler

Schlotterer

et al. 2018

Journal of Biological Chemistry

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The enzyme AICAR-transformylase/IMP cyclohydrolase (ATIC) catalyzes the last two steps of purine de-novo synthesis. It metabolizes AICAR, which is an AMP analogue, leading to activation of AMPK. It was investigated whether the AICAR-ATIC pathway plays a role in the high glucose (HG) mediated DNA damage response and AICAR mediated AMPK activation, explaining the detrimental effects of glucose on neuronal damages and shortening of lifespan. HG upregulated the expression and activity of Caenorhabditis elegans homologue of ATIC, C55F2.1 (atic-1), as well as increased the levels of reactive oxygen species (ROS) and methylglyoxalderived advanced glycation endproducts (MGAGEs). Overexpression of atic-1 decreased lifespan and head motility and increased neuronal damage under both standard (S) and high glucose (HG) conditions. Inhibition of atic-1 expression, by RNAi, under HG was associated with increased lifespan and head motility and reduced neuronal damage, ROS and MG-AGE accumulation. This effect was independent of an effect on DNA damage or antioxidant defense pathways, such as superoxide dismutase (sod-3) or glyoxalase-1 (glod-4), but was dependent upon AMPK and an accumulation of AICAR. Through AMPK, AICAR treatment also reduced the negative effects of HG. The Protective Effect of AICAR under High Glucose 2 mitochondrial inhibitor rotenone abolished the AICAR/AMPK-induced amelioration of HG effects, pointing to mitochondria as a prime target of the glucotoxic effects in C. elegans. We conclude that atic-1 is involved in glucotoxic effects under HG conditions, either by blocked atic-1 expression or via AICAR and AMPK induction.The enzyme AICAR-transformylase/IMP cyclohydrolase (ATIC) catalyzes the last two steps of purine de-novo synthesis. ATIC metabolites 5-Aminoimidazole-4-carboxamide-riboside (AICAR) to N-formyl-5-aminoimidazol-4-carboxamide-ribonucleotide (FAICAR) and then to inosine monophosphate (IMP), analog of adenosine monophosphate (AMP). IMP can then be phosphorylated by adenosine kinase to become ZMP, which can bind to the cystathionine-betasynthase (CBS) domains of the -subunit of AMPactivated protein kinase (AMPK), leading to an allosteric change [(1)]. This change makes AMPK a better substrate for its upstream kinases to phosphorylate it at Thr172 and inhibits dephosphorylation at this site by the protein phosphatases, PP2A and PP2C [(2); (3)]. This combined effect significantly increases the activity of AMPK ex vivo [(4)].Treatment with AICAR has been shown to prevent and/or reverse metabolic syndrome in animal models. In ob/ob mice, fa/fa rats, as well as rats fed on a high-fat diet, AICAR treatment has been shown to improve glucose tolerance, whole-body glucose disposal, as well as reduce hepatic glucose output and plasma triglycerides and free fatty acids levels [(5); (6); (7); (8)]. In streptozotocin (STZ)-induced diabetic mice, treatment with AICAR increased AMPK activity within the kidney and was linked with reduction in glomerular matrix and albuminuria [(9)]. Exogenous AICAR can...

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Oxidative stress and metabolic disorders: Pathogenesis and therapeutic strategies

Cited by 869 publications

References 140 publications

Adipose Tissue and Inflammation

Adipose Tissue and Inflammation

Az oxidatív stressz szerepe a diabeteses neuropathia kialakulásában

High-glucose toxicity is mediated by AICAR-transformylase/IMP cyclohydrolase and mitigated by AMP-activated protein kinase in Caenorhabditis elegans

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