mTOR inhibition by rapamycin prevents beta-cell adaptation to hyperglycemia and exacerbates the metabolic state in type 2 diabetes. - Wikidata - awgldk - TriplyDB

mTOR inhibition by rapamycin prevents beta-cell adaptation to hyperglycemia and exacerbates the metabolic state in type 2 diabetes.

mTOR inhibition by rapamycin prevents beta-cell adaptation to hyperglycemia and exacerbates the metabolic state in type 2 diabetes.

http://www.wikidata.org/entity/Q46823840

about

Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity mTOR signaling in growth control and disease Influence of Acute and Chronic Exercise on Glucose Uptake Novel nervous and multi-system regenerative therapeutic strategies for diabetes mellitus with mTOR The mTOR pathway in obesity driven gastrointestinal cancers: Potential targets and clinical trials The short-lived African turquoise killifish: an emerging experimental model for ageing The two faces of miR-29 Management of metabolic effects associated with anticancer agents targeting the PI3K-Akt-mTOR pathway Role of AKT/mTORC1 pathway in pancreatic β-cell proliferation Metabolic complications in liver transplant recipients mTOR activation is a biomarker and a central pathway to autoimmune disorders, cancer, obesity, and aging Management of the hospitalized transplant patient Mechanisms of activation of the transcription factor Nrf2 by redox stressors, nutrient cues, and energy status and the pathways through which it attenuates degenerative disease Stimulation of autophagy improves endoplasmic reticulum stress-induced diabetes Regulation of cardiac expression of the diabetic marker microRNA miR-29 Rap1 promotes multiple pancreatic islet cell functions and signals through mammalian target of rapamycin complex 1 to enhance proliferation Glucose amplifies fatty acid-induced endoplasmic reticulum stress in pancreatic beta-cells via activation of mTORC1.Protein restriction in the pregnant mouse modifies fetal growth and pulmonary development: role of fetal exposure to {beta}-hydroxybutyrate.Mammalian target of rapamycin inhibition abrogates insulin-mediated mammary tumor progression in type 2 diabetes.Late-life rapamycin treatment reverses age-related heart dysfunction.Amyloidogenic peptide oligomer accumulation in autophagy-deficient β cells induces diabetes.Chronic rapamycin treatment causes diabetes in male mice Acute mTOR inhibition induces insulin resistance and alters substrate utilization in vivo Metabolic syndrome as a risk factor for neurological disorders.DEP domain-containing mTOR-interacting protein in the rat brain: distribution of expression and potential implication.Rapamycin-induced metabolic defects are reversible in both lean and obese mice Rapamycin-mediated mTORC2 inhibition is determined by the relative expression of FK506-binding proteins.Jejunal proteins secreted by db/db mice or insulin-resistant humans impair the insulin signaling and determine insulin resistance Targeting β-catenin signaling for therapeutic intervention in MEN1-deficient pancreatic neuroendocrine tumours.Beneficial metabolic effects of rapamycin are associated with enhanced regulatory cells in diet-induced obese mice.Single rapamycin administration induces prolonged downward shift in defended body weight in rats Inhibition of autophagic turnover in β-cells by fatty acids and glucose leads to apoptotic cell death Exposure of mouse embryonic pancreas to metformin enhances the number of pancreatic progenitors Everolimus induces rapid plasma glucose normalization in insulinoma patients by effects on tumor as well as normal tissues.Insulin Resistance Is Not Associated with an Impaired Mitochondrial Function in Contracting Gastrocnemius Muscle of Goto-Kakizaki Diabetic Rats In Vivo The Prevalence and Impact of Hyperglycemia and Hyperlipidemia in Patients With Advanced Cancer Receiving Combination Treatment With the Mammalian Target of Rapamycin Inhibitor Temsirolimus and Insulin Growth Factor-Receptor Antibody Cixutumumab The cannabinoid CB1 receptor and mTORC1 signalling pathways interact to modulate glucose homeostasis in mice.Yin Yang 1 deficiency in skeletal muscle protects against rapamycin-induced diabetic-like symptoms through activation of insulin/IGF signaling.Rapamycin impairs HPD-induced beneficial effects on glucose homeostasis.Rapamycin induces glucose intolerance in mice by reducing islet mass, insulin content, and insulin sensitivity.

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P2860

mTOR inhibition by rapamycin prevents beta-cell adaptation to hyperglycemia and exacerbates the metabolic state in type 2 diabetes.

http://www.wikidata.org/entity/Q46823840

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

@zh-my

2008年学术文章

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2008年學術文章

@yue

2008年學術文章

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name

mTOR inhibition by rapamycin p ...... olic state in type 2 diabetes.

@en

mTOR inhibition by rapamycin p ...... olic state in type 2 diabetes.

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type

label

mTOR inhibition by rapamycin p ...... olic state in type 2 diabetes.

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mTOR inhibition by rapamycin p ...... olic state in type 2 diabetes.

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prefLabel

mTOR inhibition by rapamycin p ...... olic state in type 2 diabetes.

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mTOR inhibition by rapamycin p ...... olic state in type 2 diabetes.

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mTOR inhibition by rapamycin p ...... olic state in type 2 diabetes.

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Erol Cerasi

http://www.w3.org/2001/XMLSchema#string

Gil Leibowitz

http://www.w3.org/2001/XMLSchema#string

Julien Castel

http://www.w3.org/2001/XMLSchema#string

Mali Ketzinel-Gilad

http://www.w3.org/2001/XMLSchema#string

Marie-France Berthault

http://www.w3.org/2001/XMLSchema#string

Merav Fraenkel

http://www.w3.org/2001/XMLSchema#string

Nurit Kaiser

http://www.w3.org/2001/XMLSchema#string

Orit Pappo

http://www.w3.org/2001/XMLSchema#string

Yafa Ariav

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945-957

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scholarly article

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10.2337/DB07-0922

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4

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57

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Mali Ketzinel-Gilad

Christophe Magnan

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2008-01-03T00:00:00Z

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5674585

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type-2 diabetes

metabolic adaptation