mTOR Complex 1 Regulates Lipin 1 Localization to Control the SREBP Pathway

Cell, Journal Year: 2011, Volume and Issue: 146(3), P. 408 - 420

Published: Aug. 1, 2011

Language: Английский

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Increased De Novo Lipogenesis Is a Distinct Characteristic of Individuals With Nonalcoholic Fatty Liver Disease

Gastroenterology, Journal Year: 2013, Volume and Issue: 146(3), P. 726 - 735

Published: Dec. 5, 2013

Language: Английский

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Regulation of insulin sensitivity by serine/threonine phosphorylation of insulin receptor substrate proteins IRS1 and IRS2

Diabetologia, Journal Year: 2012, Volume and Issue: 55(10), P. 2565 - 2582

Published: Aug. 6, 2012

Language: Английский

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The integrative biology of type 2 diabetes

Nature, Journal Year: 2019, Volume and Issue: 576(7785), P. 51 - 60

Published: Dec. 4, 2019

Language: Английский

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SREBP-regulated lipid metabolism: convergent physiology — divergent pathophysiology

Nature Reviews Endocrinology, Journal Year: 2017, Volume and Issue: 13(12), P. 710 - 730

Published: Aug. 29, 2017

Language: Английский

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The interaction of hepatic lipid and glucose metabolism in liver diseases

Journal of Hepatology, Journal Year: 2011, Volume and Issue: 56(4), P. 952 - 964

Published: Dec. 13, 2011

It is widely known that the liver a central organ in lipogenesis, gluconeogenesis and cholesterol metabolism. However, over last decades, variety of pathological conditions highlighted importance metabolic functions within diseased liver. As observed Western societies, an increase prevalence obesity syndrome promotes pathophysiological changes cause non-alcoholic fatty disease (NAFLD). NAFLD increases susceptibility to acute injury may lead cirrhosis hepatocellular cancer. Alterations insulin response, β-oxidation, lipid storage transport, autophagy imbalance chemokines nuclear receptor signaling are held accountable for these changes. Furthermore, recent studies revealed role accumulation inflammation ER stress clinical context regeneration hepatic carcinogenesis. This review focuses on novel findings related - including vitamin D homolog 1 glucose uptake, metabolism NAFLD, regeneration,

Language: Английский

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Mechanisms of hepatic triglyceride accumulation in non-alcoholic fatty liver disease

Journal of Gastroenterology, Journal Year: 2013, Volume and Issue: 48(4), P. 434 - 441

Published: Feb. 9, 2013

Non-alcoholic fatty liver disease (NAFLD) is characterized by hepatic lipid accumulation in the absence of excess alcohol intake. NAFLD most common chronic disease, and ongoing research efforts are focused on understanding underlying pathobiology steatosis with anticipation that these will identify novel therapeutic targets. Under physiological conditions, low steady-state triglyceride concentrations attributable to a precise balance between acquisition uptake non-esterified acids from plasma de novo lipogenesis, versus disposal acid oxidation secretion triglyceride-rich lipoproteins. In patients, insulin resistance leads multiple mechanisms. Greater rates increased release an expanded mass adipose tissue as consequence diminished responsiveness. Hyperinsulinemia promotes transcriptional upregulation genes promote lipogenesis liver. Increased not offset or This review discusses molecular mechanisms which homeostasis achieved under normal well metabolic alterations occur setting contribute pathogenesis NAFLD.

Language: Английский

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Nonalcoholic fatty liver disease

Nature Reviews Disease Primers, Journal Year: 2015, Volume and Issue: 1(1)

Published: Dec. 16, 2015

Language: Английский

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Hepatic steatosis: a role for de novo lipogenesis and the transcription factor SREBP‐1c

Diabetes Obesity and Metabolism, Journal Year: 2010, Volume and Issue: 12(s2), P. 83 - 92

Published: Oct. 1, 2010

Steatosis is an accumulation of triglycerides in the liver. Although excessive availability plasma fatty acids important determinant steatosis, lipid synthesis from glucose (lipogenesis) now also considered as contributing factor. Lipogenesis insulin‐ and glucose‐dependent process that under control specific transcription factors, sterol regulatory element binding protein 1c (SREBP‐1c), activated by insulin carbohydrate response (ChREBP) glucose. Insulin induces maturation SREBP‐1c a proteolytic mechanism initiated endoplasmic reticulum (ER). turn activates glycolytic gene expression, allowing metabolism, lipogenic genes conjunction with ChREBP. activation liver obese markedly insulin‐resistant steatotic rodents then paradoxical. Recent data suggest thus lipogenesis secondary to ER stress. The stress cleavage independent insulin, explaining paradoxical stimulation Inhibition decreases improves hepatic steatosis sensitivity. new partner metabolic syndrome which worth considering potential therapeutic target.

Language: Английский

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Regulation of mTORC1 and its impact on gene expression at a glance

Journal of Cell Science, Journal Year: 2013, Volume and Issue: unknown

Published: Jan. 1, 2013

The mechanistic (or mammalian) target of rapamycin (mTOR) is a kinase that regulates key cellular functions linked to the promotion cell growth and metabolism. This kinase, which part two protein complexes termed mTOR complex 1 (mTORC1) 2 (mTORC2), has fundamental role in coordinating anabolic catabolic processes response factors nutrients. Of complexes, mTORC1 by far best characterized. When active, triggers proliferation promoting synthesis, lipid biogenesis, metabolism, reducing autophagy. fact deregulation associated with several human diseases, such as type diabetes, cancer, obesity neurodegeneration, highlights its importance maintenance homeostasis. Over last years, groups observed inhibition, addition deeply affects gene transcription. Here, we review connections between transcription focusing on impact regulating activation specific including STAT3, SREBPs, PPARγ, PPARα, HIF1α, YY1–PGC1α TFEB. We also discuss these mediating effects various physiological pathological contexts.

Language: Английский

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