Mitochondrial dysfunction in patients with primary congenital insulin resistance.
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Treatment with the 3-ketoacyl-CoA thiolase inhibitor trimetazidine does not exacerbate whole-body insulin resistance in obese mice.What causes the insulin resistance underlying obesity?Skeletal muscle phosphodiester content relates to body mass and glycemic control.Metabolic syndrome and insulin resistance: underlying causes and modification by exercise training.Erythropoietin, a novel versatile player regulating energy metabolism beyond the erythroid systemMaternal insulin resistance causes oxidative stress and mitochondrial dysfunction in mouse oocytes.Targeting mitochondrial alterations to prevent type 2 diabetes--evidence from studies of dietary redox-active compounds.Defective mitochondrial function in vivo in skeletal muscle in adults with Down's syndrome: a 31P-MRS study.Low circulating levels of IGF-1 in healthy adults are associated with reduced β-cell function, increased intramyocellular lipid, and enhanced fat utilization during fasting.Severe insulin resistance alters metabolism in mesenchymal progenitor cells.Insulin Resistance Is Not Associated with an Impaired Mitochondrial Function in Contracting Gastrocnemius Muscle of Goto-Kakizaki Diabetic Rats In VivoInsulin resistance is associated with epigenetic and genetic regulation of mitochondrial DNA in obese humans.Mechanistic insights revealed by lipid profiling in monogenic insulin resistance syndromes.Mitochondrial oxidative phosphorylation is impaired in patients with congenital lipodystrophyWhat do magnetic resonance-based measurements of Pi→ATP flux tell us about skeletal muscle metabolism?³¹P-magnetization transfer magnetic resonance spectroscopy measurements of in vivo metabolism.Simple and effective exercise design for assessing in vivo mitochondrial function in clinical applications using (31)P magnetic resonance spectroscopy.Altered Skeletal Muscle Mitochondrial Proteome As the Basis of Disruption of Mitochondrial Function in Diabetic Mice.Insulin Resistance in Human iPS Cells Reduces Mitochondrial Size and Function.31P magnetization transfer measurements of Pi→ATP flux in exercising human muscle.Postexercise phosphocreatine recovery, an index of mitochondrial oxidative phosphorylation, is reduced in diabetic patients with lower extremity complicationsErythropoietin contributes to slow oxidative muscle fiber specification via PGC-1α and AMPK activation.Mitochondrial plasticity in obesity and diabetes mellitus.Mitochondrial Epigenetic Changes Link to Increased Diabetes Risk and Early-Stage Prediabetes Indicator.Central role and mechanisms of β-cell dysfunction and death in friedreich ataxia-associated diabetes.Syndromic insulin resistance: models for the therapeutic basis of the metabolic syndrome and other targets of insulin resistance.Increased Prevalence of Hypertension in Young Adults with High Heteroplasmy Levels of the MELAS m.3243A>G Mutation.Developmental programming by maternal insulin resistance: hyperinsulinemia, glucose intolerance, and dysregulated lipid metabolism in male offspring of insulin-resistant mice.Bezafibrate ameliorates diabetes via reduced steatosis and improved hepatic insulin sensitivity in diabetic TallyHo mice.Mechanistic insights into insulin resistance in the genetic era.Mitochondrial dysfunction in non-alcoholic fatty liver disease and insulin resistance: cause or consequence?Mitochondrial alteration in type 2 diabetes and obesity: an epigenetic link.Mechanisms linking obesity to altered metabolism in mice colon carcinogenesis.Complete failure of insulin-transmitted signaling, but not obesity-induced insulin resistance, impairs respiratory chain function in muscle.Drosophila melanogaster: An emerging model of transgenerational effects of maternal obesity.Impaired Insulin Signaling is Associated with Hepatic Mitochondrial Dysfunction in IR+/--IRS-1+/- Double Heterozygous (IR-IRS1dh) Mice.Mitochondrial DNA content and function, childhood obesity, and insulin resistance.A Patient with Congenital Generalized Lipodystrophy Due To a Novel Mutation in BSCL2: Indications for Secondary Mitochondrial Dysfunction.Ectopic lipid storage in non-alcoholic fatty liver disease is not mediated by impaired mitochondrial oxidative capacity in skeletal muscleCommon variation in oxidative phosphorylation genes is not a major cause of insulin resistance or type 2 diabetes
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P2860
Mitochondrial dysfunction in patients with primary congenital insulin resistance.
description
2011 nî lūn-bûn
@nan
2011 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年学术文章
@wuu
2011年学术文章
@zh-cn
2011年学术文章
@zh-hans
2011年学术文章
@zh-my
2011年学术文章
@zh-sg
2011年學術文章
@yue
name
Mitochondrial dysfunction in patients with primary congenital insulin resistance.
@ast
Mitochondrial dysfunction in patients with primary congenital insulin resistance.
@en
type
label
Mitochondrial dysfunction in patients with primary congenital insulin resistance.
@ast
Mitochondrial dysfunction in patients with primary congenital insulin resistance.
@en
prefLabel
Mitochondrial dysfunction in patients with primary congenital insulin resistance.
@ast
Mitochondrial dysfunction in patients with primary congenital insulin resistance.
@en
P2093
P2860
P50
P356
P1476
Mitochondrial dysfunction in patients with primary congenital insulin resistance.
@en
P2093
Alessandra Vottero
Catherine Mitchell
David Porter
Kerrie Thackray
Kevin M Brindle
Martin McIntyre
Peter R Murgatroyd
Philippa Raymond-Barker
T Adrian Carpenter
P2860
P304
P356
10.1172/JCI46405
P407
P50
P577
2011-05-09T00:00:00Z