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Le diabète mellitus est une maladie de plus en plus présente au sein de l’espèce féline. En effet, on estime qu’environ un chat sur deux cents est atteint de cette maladie. Les chats développent majoritairement un diabète de type2. Celui-ci se caractérise par une résistance et une diminution de la sécrétion d’insuline. Son développement est influencé par un grand nombre de facteurs prédisposants qui rend cette pathologie complexe. Actuellement, le traitement du diabète chez le chat se résume à trois axes dont les deux principaux sont la mise en place d’une insulinothérapie et d’un régime alimentaire pauvre en glucides. Certains vétérinaires mettent également en place des hypoglycémiants oraux mais ceux-ci sont pour la plupart peu efficaces. Récemment, une nouvelle classe de molécule a suscité l’intérêt du monde scientifique : les inhibiteurs du co-transporteurs sodium/glucose 2. Plusieurs études ont été menés afin de déterminer si ces inhibiteurs étaient efficaces pour traiter le diabète chez le chat et dans quelle mesure, ils présentaient des effets secondaires. Il en ressort une diminution significative du glucose et de la fructosamine sanguine ainsi qu’une amélioration voire une disparition des signes cliniques. Cette classe de molécules, à l’inverse de l’insuline, n’a pas induit d’hypoglycémie. Quant aux effets secondaires, ils sont principalement mineurs et se présentaient majoritairement sous la forme de vomissements, de diarrhée, de léthargie, de déshydratation ou d’anorexie. Cependant, d’autres effets secondaires plus graves sont survenus dont le développement d’un diabète céto-acidosique. Cette découverte souligne la nécessité d’une surveillance accrue lors de la mise en place du traitement. Un point négatif mais non négligeable était la présence importante de conflits d’intérêt au sein des différentes études liées à l’influence potentiel des firmes pharmaceutiques ce qui nécessiterait donc la réalisation d’études indépendantes pour confirmer ces résultats.
diabète --- chat --- SGLT2 --- hypoglycémiant --- traitement --- Sciences du vivant > Médecine vétérinaire & santé animale
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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact
Science: general issues --- Physiology --- diabetes --- Heart Failure --- diastolic dysfunction --- arrhythmia --- SGLT2 (sodium-glucose cotransporter 2) inhibitor --- GLP-1 - glucagon-like peptide-1 --- diabetes --- Heart Failure --- diastolic dysfunction --- arrhythmia --- SGLT2 (sodium-glucose cotransporter 2) inhibitor --- GLP-1 - glucagon-like peptide-1
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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact
diabetes --- Heart Failure --- diastolic dysfunction --- arrhythmia --- SGLT2 (sodium-glucose cotransporter 2) inhibitor --- GLP-1 - glucagon-like peptide-1
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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact
Science: general issues --- Physiology --- diabetes --- Heart Failure --- diastolic dysfunction --- arrhythmia --- SGLT2 (sodium-glucose cotransporter 2) inhibitor --- GLP-1 - glucagon-like peptide-1
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The kidney performs important functions in the human body and can inflict either acute kidney injury (AKI) or chronic kidney disease (CKD). AKI can be induced by kidney ischemia, drugs such as cisplatin, and heavy metals such as cadmium and arsenic. CKD can be induced by drugs, heavy metals, hypertension, and diabetes, as well as cancer. Importantly, nearly all kidney disorders have been shown to involve redox imbalance, reductive stress, oxidative stress, and mitochondrial abnormalities such as impaired mitochondrial homeostasis, including disrupted mitophagy and deranged mitochondrial unfolded protein responses. Understanding how these redox-related dysregulated pathways operate may give us new insights into how to design novel approaches to fighting kidney disease. This Special Issue of Biomolecules entitled “Redox imbalance and mitochondrial abnormalities in kidney disease” covers a variety of topics focusing on oxidative stress, mitochondrial dysfunction, and antioxidation enhancement implicated in kidney disease or kidney transplantation.
Medicine --- Pharmacology --- diabetic kidney disease --- caloric restriction --- NADH/NAD+ --- redox imbalance --- mitochondrial homeostasis --- mitophagy --- oxidative stress --- kidney allograft --- kidney rejection --- ischemia --- acute kidney injury (AKI) --- chronic kidney disease (CKD) --- tricarboxylic acid (TCA) cycle --- mitochondrial metabolism --- mitochondrial redox signaling --- mitochondrial proteins --- oxidative phosphorylation (OXPHOS) --- fatty acid (FA) β-oxidation --- mitochondrial dynamics --- biogenesis --- diabetes --- kidney --- mitochondria --- Oryza sativa --- rice husk --- TCA cycle metabolites --- kidney diseases --- renalase --- chronic kidney disease --- major adverse cardiovascular outcomes --- cadmium --- kidney injury --- renal toxicity --- oxidative damage --- proximal tubule --- controlled oxygenated rewarming --- mitochondrial uncoupling --- rewarming injury --- temperature paradox --- redox --- mitochondrial dysfunction --- SGLT2 --- mitochondrial reactive oxygen species --- Warburg effect --- podocytopathies --- mitochondrial oxidative stress --- reactive oxygen species (ROS) --- antioxidant defense --- cell death --- n/a
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The kidney performs important functions in the human body and can inflict either acute kidney injury (AKI) or chronic kidney disease (CKD). AKI can be induced by kidney ischemia, drugs such as cisplatin, and heavy metals such as cadmium and arsenic. CKD can be induced by drugs, heavy metals, hypertension, and diabetes, as well as cancer. Importantly, nearly all kidney disorders have been shown to involve redox imbalance, reductive stress, oxidative stress, and mitochondrial abnormalities such as impaired mitochondrial homeostasis, including disrupted mitophagy and deranged mitochondrial unfolded protein responses. Understanding how these redox-related dysregulated pathways operate may give us new insights into how to design novel approaches to fighting kidney disease. This Special Issue of Biomolecules entitled “Redox imbalance and mitochondrial abnormalities in kidney disease” covers a variety of topics focusing on oxidative stress, mitochondrial dysfunction, and antioxidation enhancement implicated in kidney disease or kidney transplantation.
diabetic kidney disease --- caloric restriction --- NADH/NAD+ --- redox imbalance --- mitochondrial homeostasis --- mitophagy --- oxidative stress --- kidney allograft --- kidney rejection --- ischemia --- acute kidney injury (AKI) --- chronic kidney disease (CKD) --- tricarboxylic acid (TCA) cycle --- mitochondrial metabolism --- mitochondrial redox signaling --- mitochondrial proteins --- oxidative phosphorylation (OXPHOS) --- fatty acid (FA) β-oxidation --- mitochondrial dynamics --- biogenesis --- diabetes --- kidney --- mitochondria --- Oryza sativa --- rice husk --- TCA cycle metabolites --- kidney diseases --- renalase --- chronic kidney disease --- major adverse cardiovascular outcomes --- cadmium --- kidney injury --- renal toxicity --- oxidative damage --- proximal tubule --- controlled oxygenated rewarming --- mitochondrial uncoupling --- rewarming injury --- temperature paradox --- redox --- mitochondrial dysfunction --- SGLT2 --- mitochondrial reactive oxygen species --- Warburg effect --- podocytopathies --- mitochondrial oxidative stress --- reactive oxygen species (ROS) --- antioxidant defense --- cell death --- n/a
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The kidney performs important functions in the human body and can inflict either acute kidney injury (AKI) or chronic kidney disease (CKD). AKI can be induced by kidney ischemia, drugs such as cisplatin, and heavy metals such as cadmium and arsenic. CKD can be induced by drugs, heavy metals, hypertension, and diabetes, as well as cancer. Importantly, nearly all kidney disorders have been shown to involve redox imbalance, reductive stress, oxidative stress, and mitochondrial abnormalities such as impaired mitochondrial homeostasis, including disrupted mitophagy and deranged mitochondrial unfolded protein responses. Understanding how these redox-related dysregulated pathways operate may give us new insights into how to design novel approaches to fighting kidney disease. This Special Issue of Biomolecules entitled “Redox imbalance and mitochondrial abnormalities in kidney disease” covers a variety of topics focusing on oxidative stress, mitochondrial dysfunction, and antioxidation enhancement implicated in kidney disease or kidney transplantation.
Medicine --- Pharmacology --- diabetic kidney disease --- caloric restriction --- NADH/NAD+ --- redox imbalance --- mitochondrial homeostasis --- mitophagy --- oxidative stress --- kidney allograft --- kidney rejection --- ischemia --- acute kidney injury (AKI) --- chronic kidney disease (CKD) --- tricarboxylic acid (TCA) cycle --- mitochondrial metabolism --- mitochondrial redox signaling --- mitochondrial proteins --- oxidative phosphorylation (OXPHOS) --- fatty acid (FA) β-oxidation --- mitochondrial dynamics --- biogenesis --- diabetes --- kidney --- mitochondria --- Oryza sativa --- rice husk --- TCA cycle metabolites --- kidney diseases --- renalase --- chronic kidney disease --- major adverse cardiovascular outcomes --- cadmium --- kidney injury --- renal toxicity --- oxidative damage --- proximal tubule --- controlled oxygenated rewarming --- mitochondrial uncoupling --- rewarming injury --- temperature paradox --- redox --- mitochondrial dysfunction --- SGLT2 --- mitochondrial reactive oxygen species --- Warburg effect --- podocytopathies --- mitochondrial oxidative stress --- reactive oxygen species (ROS) --- antioxidant defense --- cell death --- diabetic kidney disease --- caloric restriction --- NADH/NAD+ --- redox imbalance --- mitochondrial homeostasis --- mitophagy --- oxidative stress --- kidney allograft --- kidney rejection --- ischemia --- acute kidney injury (AKI) --- chronic kidney disease (CKD) --- tricarboxylic acid (TCA) cycle --- mitochondrial metabolism --- mitochondrial redox signaling --- mitochondrial proteins --- oxidative phosphorylation (OXPHOS) --- fatty acid (FA) β-oxidation --- mitochondrial dynamics --- biogenesis --- diabetes --- kidney --- mitochondria --- Oryza sativa --- rice husk --- TCA cycle metabolites --- kidney diseases --- renalase --- chronic kidney disease --- major adverse cardiovascular outcomes --- cadmium --- kidney injury --- renal toxicity --- oxidative damage --- proximal tubule --- controlled oxygenated rewarming --- mitochondrial uncoupling --- rewarming injury --- temperature paradox --- redox --- mitochondrial dysfunction --- SGLT2 --- mitochondrial reactive oxygen species --- Warburg effect --- podocytopathies --- mitochondrial oxidative stress --- reactive oxygen species (ROS) --- antioxidant defense --- cell death
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This book serves to highlight the pharmacokinetics/drug–drug interactions and mechanistic understanding in relation to the drug-metabolizing enzymes and drug transporters.This book presents a series of drug metabolism and transport mechanisms that govern the pharmacokinetic features of therapeutic drugs as well as natural herbal medicines. It also covers the pharmacokinetic interactions caused by inhibiting or inducing the metabolic or transport activities under disease states or the coadministration of potential inhibitors. It also deals with microenvironmental pharmacokinetic profiles as well as population pharmacokinetics, which gives new insights regarding the pharmacokinetic features with regard to drug metabolism and transporters.
Medicine --- Pharmaceutical industries --- tofacitinib --- dose-dependent pharmacokinetics --- hepatic and intestinal first-pass effect --- rats --- catalposide --- in vitro human metabolism --- UDP-glucuronosyltransferase --- sulfotransferase --- carboxylesterase --- celecoxib --- drug–drug interaction --- fluorescence --- HPLC --- metabolism --- repaglinide --- HSG4112 --- anti-obesity agent --- stereoselectivity --- pharmacokinetics --- compound K --- protopanaxadiol (PPD) --- biliary excretion --- intestinal metabolism --- Carthamus tinctorius extract --- notoginseng total saponins --- comparative pharmacokinetic study --- large volume direct injection --- compatibility mechanism --- mertansine --- human hepatocytes --- cytochrome P450 --- UDP-glucuronosyltransferases --- sodium-glucose cotransporter 2 (SGLT2) inhibitors --- DWP16001 --- kidney distribution --- inhibition mode --- diabetes --- transporter-enzyme interplay --- influx transporter --- efflux transporter --- physiologically based pharmacokinetic model --- cytochrome P450 enzymes --- tiropramide --- healthy Korean subjects --- modeling --- population pharmacokinetic --- quercetin --- breast cancer resistance protein --- inhibitor --- prazosin --- sulfasalazine --- kinetic analysis --- food–drug interactions --- Caco-2 --- EpiIntestinal --- first-pass --- P-gp --- BCRP --- drug transporter --- CYP3A4 --- oral availability --- automatization --- drug absorption --- drug dosing --- head-and-neck cancer --- real-time measurements --- taxanes --- tissue engineering --- UHPLC-MS/MS --- metformin --- verapamil --- drug interaction --- organic cation transporter 2 --- renal excretion --- acute renal failure --- gentamicin --- cisplatin --- hepatic CYP3A1(23) --- creatinine clearance --- renal clearance --- nonrenal clearance --- tofacitinib --- dose-dependent pharmacokinetics --- hepatic and intestinal first-pass effect --- rats --- catalposide --- in vitro human metabolism --- UDP-glucuronosyltransferase --- sulfotransferase --- carboxylesterase --- celecoxib --- drug–drug interaction --- fluorescence --- HPLC --- metabolism --- repaglinide --- HSG4112 --- anti-obesity agent --- stereoselectivity --- pharmacokinetics --- compound K --- protopanaxadiol (PPD) --- biliary excretion --- intestinal metabolism --- Carthamus tinctorius extract --- notoginseng total saponins --- comparative pharmacokinetic study --- large volume direct injection --- compatibility mechanism --- mertansine --- human hepatocytes --- cytochrome P450 --- UDP-glucuronosyltransferases --- sodium-glucose cotransporter 2 (SGLT2) inhibitors --- DWP16001 --- kidney distribution --- inhibition mode --- diabetes --- transporter-enzyme interplay --- influx transporter --- efflux transporter --- physiologically based pharmacokinetic model --- cytochrome P450 enzymes --- tiropramide --- healthy Korean subjects --- modeling --- population pharmacokinetic --- quercetin --- breast cancer resistance protein --- inhibitor --- prazosin --- sulfasalazine --- kinetic analysis --- food–drug interactions --- Caco-2 --- EpiIntestinal --- first-pass --- P-gp --- BCRP --- drug transporter --- CYP3A4 --- oral availability --- automatization --- drug absorption --- drug dosing --- head-and-neck cancer --- real-time measurements --- taxanes --- tissue engineering --- UHPLC-MS/MS --- metformin --- verapamil --- drug interaction --- organic cation transporter 2 --- renal excretion --- acute renal failure --- gentamicin --- cisplatin --- hepatic CYP3A1(23) --- creatinine clearance --- renal clearance --- nonrenal clearance
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This book serves to highlight the pharmacokinetics/drug–drug interactions and mechanistic understanding in relation to the drug-metabolizing enzymes and drug transporters.This book presents a series of drug metabolism and transport mechanisms that govern the pharmacokinetic features of therapeutic drugs as well as natural herbal medicines. It also covers the pharmacokinetic interactions caused by inhibiting or inducing the metabolic or transport activities under disease states or the coadministration of potential inhibitors. It also deals with microenvironmental pharmacokinetic profiles as well as population pharmacokinetics, which gives new insights regarding the pharmacokinetic features with regard to drug metabolism and transporters.
tofacitinib --- dose-dependent pharmacokinetics --- hepatic and intestinal first-pass effect --- rats --- catalposide --- in vitro human metabolism --- UDP-glucuronosyltransferase --- sulfotransferase --- carboxylesterase --- celecoxib --- drug–drug interaction --- fluorescence --- HPLC --- metabolism --- repaglinide --- HSG4112 --- anti-obesity agent --- stereoselectivity --- pharmacokinetics --- compound K --- protopanaxadiol (PPD) --- biliary excretion --- intestinal metabolism --- Carthamus tinctorius extract --- notoginseng total saponins --- comparative pharmacokinetic study --- large volume direct injection --- compatibility mechanism --- mertansine --- human hepatocytes --- cytochrome P450 --- UDP-glucuronosyltransferases --- sodium-glucose cotransporter 2 (SGLT2) inhibitors --- DWP16001 --- kidney distribution --- inhibition mode --- diabetes --- transporter-enzyme interplay --- influx transporter --- efflux transporter --- physiologically based pharmacokinetic model --- cytochrome P450 enzymes --- tiropramide --- healthy Korean subjects --- modeling --- population pharmacokinetic --- quercetin --- breast cancer resistance protein --- inhibitor --- prazosin --- sulfasalazine --- kinetic analysis --- food–drug interactions --- Caco-2 --- EpiIntestinal --- first-pass --- P-gp --- BCRP --- drug transporter --- CYP3A4 --- oral availability --- automatization --- drug absorption --- drug dosing --- head-and-neck cancer --- real-time measurements --- taxanes --- tissue engineering --- UHPLC-MS/MS --- metformin --- verapamil --- drug interaction --- organic cation transporter 2 --- renal excretion --- acute renal failure --- gentamicin --- cisplatin --- hepatic CYP3A1(23) --- creatinine clearance --- renal clearance --- nonrenal clearance
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Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of subsequent chronic kidney disease. Although the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function is urgently needed. The Special Issue covers research articles that investigated the molecular mechanisms of inflammation and injury during different renal pathologies, renal regeneration, diagnostics using new biomarkers, and the effects of different stimuli like medication or bacterial components on isolated renal cells or in vivo models. The Special Issue contains important reviews that consider the current knowledge of cell death and regeneration, inflammation, and the molecular mechanisms of kidney diseases. In addition, the potential of cell-based therapy approaches that use mesenchymal stromal/stem cells or their derivates is summarized. This edition is complemented by reviews that deal with the current data situation on other specific topics like diabetes and diabetic nephropathy or new therapeutic targets.
microRNAs --- n/a --- transcription --- ischemia/reperfusion injury --- DSS-colitis --- kidney inflammation --- therapeutics targets --- CXCL13 --- glomerulus --- interleukin-6 --- rhabdomyolysis --- IgA nephropathy --- CREB Regulated Transcriptional Coactivators (CRTC) --- slit diaphragm --- injury --- xanthine oxidase --- Salt Inducible Kinase (SIK) --- acute and chronic kidney disease --- therapeutic target --- KIT-IgA score --- G-protein-coupled bile acid receptor (TGR5) --- lysophosphatidic acid --- glomerular injury --- IL-18 --- mesenchymal stem cells --- Taiwan --- acute kidney injury --- renal ischemia-reperfusion --- long non-coding RNA --- fibrosis --- acute kidney failure --- diabetic kidney diseases --- chronic kidney disease --- lncRNA --- LPS-binding protein --- endotoxemia-induced oliguric kidney injury --- dapagliflozin --- cPLA2 and COX-2 --- NLRP3 inflammasome --- CmklR1 --- haem --- chronic kidney injury --- omega-3 fatty acid --- noninvasive --- inflammation --- regulated necrosis --- GLP-1 receptor agonists --- miRNA --- AKI --- SGLT2 inhibitors --- diabetic kidney disease --- extracellular vesicles --- podocin --- type IV collagen --- epithelial cells --- nephrin --- 2-kidney-1-clip --- renal fibrosis --- papilla --- diagnostics --- necrosis --- non-coding RNAs --- podocyte --- Thy1.1 nephritis --- KIT assay --- oxidative stress --- conditioned medium --- C-reactive protein --- pericyte --- myofibroblast --- Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-?B) --- endotoxemia --- modifier gene --- polymorphism --- renal stem cells --- kidney --- polyploidization --- Class IIa Histone Deacetylases (HDAC) --- 2k1c --- molecular signaling --- proximal tubule --- arachidonic acid --- empagliflozin --- tubular injury --- signaling cascade --- signal transduction --- inflammatory maker --- niches --- biomarkers --- renal progenitors --- type V collagen --- cyclooxygenase --- focal segmental glomerulosclerosis --- inflammatory bowel disease (IBD) --- chronic kidney disease (CKD) --- allograft rejection --- renovascular hypertension --- genotype --- molecular mechanisms --- ROS --- prediction --- glomerular filtration barrier (GFB) --- alport syndrome --- scattered tubular cells --- long non-coding RNAs --- renal inflammation --- lysophosphatidic acid receptor --- cAMP Regulatory Element Binding Protein (CREB) --- Farnesiferol B --- differentiation --- mesenchymal stromal cells --- modified-MSCs --- kidney transplantation --- polyunsaturated fatty acids --- apoptosis --- type I collagen --- diabetes mellitus --- natural products --- lipoxygenase --- stem cell --- T cell-mediated rejection --- exosomes --- renal injury --- obese kidney fibrosis --- kidney injury --- cytotoxicity --- mesenchymal stem cell --- pigment nephropathy --- mesodermal stem cell --- ischemia-reperfusion --- cytochrome P450 --- renal cell carcinoma --- hematuria --- B-cell attracting chemokine --- microRNA --- chemerin --- glomerular basement membrane --- glomerular damage --- renal tubular cells --- kidney proximal tubule --- exosome --- hypertension --- diabetic nephropathy
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