AMPK/mTOR pathway significance in healthy liver and non‐alcoholic fatty liver disease and its progression

Obesity is related to several organs, but the liver is particularly affected. Adenosine monophosphate‐activated protein kinase (AMPK) is a cellular energy sensor and regulator of liver lipid dysfunction and glucose metabolism. The mechanistic target of rapamycin (mTOR) is a protein kinase regulating...

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Vydané v:Journal of gastroenterology and hepatology Ročník 38; číslo 11; s. 1868 - 1876
Hlavní autori: Marcondes‐de‐Castro, Ilitch Aquino, Reis‐Barbosa, Pedro Henrique, Marinho, Thatiany Souza, Aguila, Marcia Barbosa, Mandarim‐de‐Lacerda, Carlos Alberto
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Australia Wiley Subscription Services, Inc 01.11.2023
Predmet:
Adenosine kinase
Adipogenesis
AMP
AMPK/mTOR pathway
Autophagy
Cell survival
Cirrhosis
Fatty acids
Fatty liver
Forkhead protein
Glucose metabolism
Hepatocellular carcinoma
Insulin resistance
Kinases
Lipid metabolism
Lipogenesis
Liver diseases
Metabolism
non‐alcoholic fatty liver disease
Obesity
Phagosomes
Phosphorylation
Protein kinase
Protein turnover
Proteins
Rapamycin
TOR protein
autophagy
non-alcoholic fatty liver disease
AMPK/mTOR pathway
obesity
lipid metabolism
ISSN:0815-9319, 1440-1746, 1440-1746
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Abstract Obesity is related to several organs, but the liver is particularly affected. Adenosine monophosphate‐activated protein kinase (AMPK) is a cellular energy sensor and regulator of liver lipid dysfunction and glucose metabolism. The mechanistic target of rapamycin (mTOR) is a protein kinase regulating cell growth, survival, metabolism, and immunity. Together, these pathways are involved in obesity, insulin resistance, non‐alcoholic fatty liver disease (NAFLD) and its progression, and autophagy. During energy demand, liver kinase B (LKB) phosphorylation helps activate the AMPK/mTOR pathways. Likewise, the protein forkhead box O family (FOXO) negatively regulates adipogenesis by binding to the promoter sites of peroxisome proliferator‐activated receptor‐gamma coactivator 1‐alpha, initiating adipogenesis. In addition, acetyl‐CoA carboxylase, which regulates de novo lipogenesis, is linked to LKB and FOXO in developing NAFLD. The kinase complex, consisting of Unc‐51‐like autophagy‐activating kinase 1 or 2 (ULK1, ULK2) by stimulating autophagy, and eliminating fat droplets in NAFLD, is regulated by mTORC1 and negatively regulated by AMPK that suppresses liver lipogenesis and increases fatty acid oxidation. Also, ULK1 is essential for initiating phagophore formation, establishing macrophagy, and generating autophagosomes. The selective breakdown of lipid droplets through macroautophagy, or macrolipophagy, occurs on a cellular energy level using free fatty acids. In addition, mTORC1 promotes lipogenesis by activating sterol regulatory element‐binding protein. Finding new components and novel regulatory modes in signaling is significant for a better understanding of the AMPK/mTOR pathways, potentially facilitating the development of future diagnostic and therapeutic strategies for NAFLD and its progression to non‐alcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma. AMPK activation appears in a healthy liver during fasting in response to energy generation needs. AMPK enhances FA oxidation and autophagy, reducing lipid accumulation. mTORC1 activation occurs in high food intake in a diseased liver, leading to lipogenesis, reducing FA oxidation, lipolysis, and autophagy, leading to liver lipid accumulation and NAFLD. ACC2, acetyl‐Coa carboxylase 2; AKT, protein kinase B; AMPK, AMP‐activated protein kinase; CPT1, carnitine palmitoyl transferase I; DNL, de novo lipogenesis; FA, fatty acid; GTP, GTPase‐activating protein; HSL, hormone‐sensitive lipase; IR, insulin receptor; LKB, liver kinase B; mTOR, mechanistic target of rapamycin; NAFLD, non‐alcoholic fatty liver disease; PGC‐1α, peroxisome proliferator‐activated receptor‐gamma coactivator‐1 alpha; PI3K, phosphoinositide 3‐ kinase; PPARa, peroxisome proliferator‐activated receptors alpha; RHEB, Ras homolog enriched in the brain; TSC, tuberous sclerosis complex; ULK1, unc‐51‐like kinase 1.
AbstractList Obesity is related to several organs, but the liver is particularly affected. Adenosine monophosphate‐activated protein kinase (AMPK) is a cellular energy sensor and regulator of liver lipid dysfunction and glucose metabolism. The mechanistic target of rapamycin (mTOR) is a protein kinase regulating cell growth, survival, metabolism, and immunity. Together, these pathways are involved in obesity, insulin resistance, non‐alcoholic fatty liver disease (NAFLD) and its progression, and autophagy. During energy demand, liver kinase B (LKB) phosphorylation helps activate the AMPK/mTOR pathways. Likewise, the protein forkhead box O family (FOXO) negatively regulates adipogenesis by binding to the promoter sites of peroxisome proliferator‐activated receptor‐gamma coactivator 1‐alpha, initiating adipogenesis. In addition, acetyl‐CoA carboxylase, which regulates de novo lipogenesis, is linked to LKB and FOXO in developing NAFLD. The kinase complex, consisting of Unc‐51‐like autophagy‐activating kinase 1 or 2 (ULK1, ULK2) by stimulating autophagy, and eliminating fat droplets in NAFLD, is regulated by mTORC1 and negatively regulated by AMPK that suppresses liver lipogenesis and increases fatty acid oxidation. Also, ULK1 is essential for initiating phagophore formation, establishing macrophagy, and generating autophagosomes. The selective breakdown of lipid droplets through macroautophagy, or macrolipophagy, occurs on a cellular energy level using free fatty acids. In addition, mTORC1 promotes lipogenesis by activating sterol regulatory element‐binding protein. Finding new components and novel regulatory modes in signaling is significant for a better understanding of the AMPK/mTOR pathways, potentially facilitating the development of future diagnostic and therapeutic strategies for NAFLD and its progression to non‐alcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma.
Obesity is related to several organs, but the liver is particularly affected. Adenosine monophosphate-activated protein kinase (AMPK) is a cellular energy sensor and regulator of liver lipid dysfunction and glucose metabolism. The mechanistic target of rapamycin (mTOR) is a protein kinase regulating cell growth, survival, metabolism, and immunity. Together, these pathways are involved in obesity, insulin resistance, non-alcoholic fatty liver disease (NAFLD) and its progression, and autophagy. During energy demand, liver kinase B (LKB) phosphorylation helps activate the AMPK/mTOR pathways. Likewise, the protein forkhead box O family (FOXO) negatively regulates adipogenesis by binding to the promoter sites of peroxisome proliferator-activated receptor-gamma coactivator 1-alpha, initiating adipogenesis. In addition, acetyl-CoA carboxylase, which regulates de novo lipogenesis, is linked to LKB and FOXO in developing NAFLD. The kinase complex, consisting of Unc-51-like autophagy-activating kinase 1 or 2 (ULK1, ULK2) by stimulating autophagy, and eliminating fat droplets in NAFLD, is regulated by mTORC1 and negatively regulated by AMPK that suppresses liver lipogenesis and increases fatty acid oxidation. Also, ULK1 is essential for initiating phagophore formation, establishing macrophagy, and generating autophagosomes. The selective breakdown of lipid droplets through macroautophagy, or macrolipophagy, occurs on a cellular energy level using free fatty acids. In addition, mTORC1 promotes lipogenesis by activating sterol regulatory element-binding protein. Finding new components and novel regulatory modes in signaling is significant for a better understanding of the AMPK/mTOR pathways, potentially facilitating the development of future diagnostic and therapeutic strategies for NAFLD and its progression to non-alcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma.Obesity is related to several organs, but the liver is particularly affected. Adenosine monophosphate-activated protein kinase (AMPK) is a cellular energy sensor and regulator of liver lipid dysfunction and glucose metabolism. The mechanistic target of rapamycin (mTOR) is a protein kinase regulating cell growth, survival, metabolism, and immunity. Together, these pathways are involved in obesity, insulin resistance, non-alcoholic fatty liver disease (NAFLD) and its progression, and autophagy. During energy demand, liver kinase B (LKB) phosphorylation helps activate the AMPK/mTOR pathways. Likewise, the protein forkhead box O family (FOXO) negatively regulates adipogenesis by binding to the promoter sites of peroxisome proliferator-activated receptor-gamma coactivator 1-alpha, initiating adipogenesis. In addition, acetyl-CoA carboxylase, which regulates de novo lipogenesis, is linked to LKB and FOXO in developing NAFLD. The kinase complex, consisting of Unc-51-like autophagy-activating kinase 1 or 2 (ULK1, ULK2) by stimulating autophagy, and eliminating fat droplets in NAFLD, is regulated by mTORC1 and negatively regulated by AMPK that suppresses liver lipogenesis and increases fatty acid oxidation. Also, ULK1 is essential for initiating phagophore formation, establishing macrophagy, and generating autophagosomes. The selective breakdown of lipid droplets through macroautophagy, or macrolipophagy, occurs on a cellular energy level using free fatty acids. In addition, mTORC1 promotes lipogenesis by activating sterol regulatory element-binding protein. Finding new components and novel regulatory modes in signaling is significant for a better understanding of the AMPK/mTOR pathways, potentially facilitating the development of future diagnostic and therapeutic strategies for NAFLD and its progression to non-alcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma.
Obesity is related to several organs, but the liver is particularly affected. Adenosine monophosphate‐activated protein kinase (AMPK) is a cellular energy sensor and regulator of liver lipid dysfunction and glucose metabolism. The mechanistic target of rapamycin (mTOR) is a protein kinase regulating cell growth, survival, metabolism, and immunity. Together, these pathways are involved in obesity, insulin resistance, non‐alcoholic fatty liver disease (NAFLD) and its progression, and autophagy. During energy demand, liver kinase B (LKB) phosphorylation helps activate the AMPK/mTOR pathways. Likewise, the protein forkhead box O family (FOXO) negatively regulates adipogenesis by binding to the promoter sites of peroxisome proliferator‐activated receptor‐gamma coactivator 1‐alpha, initiating adipogenesis. In addition, acetyl‐CoA carboxylase, which regulates de novo lipogenesis, is linked to LKB and FOXO in developing NAFLD. The kinase complex, consisting of Unc‐51‐like autophagy‐activating kinase 1 or 2 (ULK1, ULK2) by stimulating autophagy, and eliminating fat droplets in NAFLD, is regulated by mTORC1 and negatively regulated by AMPK that suppresses liver lipogenesis and increases fatty acid oxidation. Also, ULK1 is essential for initiating phagophore formation, establishing macrophagy, and generating autophagosomes. The selective breakdown of lipid droplets through macroautophagy, or macrolipophagy, occurs on a cellular energy level using free fatty acids. In addition, mTORC1 promotes lipogenesis by activating sterol regulatory element‐binding protein. Finding new components and novel regulatory modes in signaling is significant for a better understanding of the AMPK/mTOR pathways, potentially facilitating the development of future diagnostic and therapeutic strategies for NAFLD and its progression to non‐alcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma. AMPK activation appears in a healthy liver during fasting in response to energy generation needs. AMPK enhances FA oxidation and autophagy, reducing lipid accumulation. mTORC1 activation occurs in high food intake in a diseased liver, leading to lipogenesis, reducing FA oxidation, lipolysis, and autophagy, leading to liver lipid accumulation and NAFLD. ACC2, acetyl‐Coa carboxylase 2; AKT, protein kinase B; AMPK, AMP‐activated protein kinase; CPT1, carnitine palmitoyl transferase I; DNL, de novo lipogenesis; FA, fatty acid; GTP, GTPase‐activating protein; HSL, hormone‐sensitive lipase; IR, insulin receptor; LKB, liver kinase B; mTOR, mechanistic target of rapamycin; NAFLD, non‐alcoholic fatty liver disease; PGC‐1α, peroxisome proliferator‐activated receptor‐gamma coactivator‐1 alpha; PI3K, phosphoinositide 3‐ kinase; PPARa, peroxisome proliferator‐activated receptors alpha; RHEB, Ras homolog enriched in the brain; TSC, tuberous sclerosis complex; ULK1, unc‐51‐like kinase 1.
Author Marinho, Thatiany Souza
Marcondes‐de‐Castro, Ilitch Aquino
Mandarim‐de‐Lacerda, Carlos Alberto
Reis‐Barbosa, Pedro Henrique
Aguila, Marcia Barbosa
Author_xml – sequence: 1
  givenname: Ilitch Aquino
  orcidid: 0000-0003-3104-4033
  surname: Marcondes‐de‐Castro
  fullname: Marcondes‐de‐Castro, Ilitch Aquino
  organization: Rio de Janeiro State University
– sequence: 2
  givenname: Pedro Henrique
  orcidid: 0000-0002-4731-7422
  surname: Reis‐Barbosa
  fullname: Reis‐Barbosa, Pedro Henrique
  organization: Rio de Janeiro State University
– sequence: 3
  givenname: Thatiany Souza
  orcidid: 0000-0001-9976-9466
  surname: Marinho
  fullname: Marinho, Thatiany Souza
  organization: Rio de Janeiro State University
– sequence: 4
  givenname: Marcia Barbosa
  orcidid: 0000-0003-3994-4589
  surname: Aguila
  fullname: Aguila, Marcia Barbosa
  organization: Rio de Janeiro State University
– sequence: 5
  givenname: Carlos Alberto
  orcidid: 0000-0003-4134-7978
  surname: Mandarim‐de‐Lacerda
  fullname: Mandarim‐de‐Lacerda, Carlos Alberto
  email: mandarim@uerj.br
  organization: Rio de Janeiro State University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/37438882$$D View this record in MEDLINE/PubMed
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Issue 11
Keywords autophagy
non-alcoholic fatty liver disease
AMPK/mTOR pathway
obesity
lipid metabolism
Language English
License 2023 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.
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PublicationTitle Journal of gastroenterology and hepatology
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Snippet Obesity is related to several organs, but the liver is particularly affected. Adenosine monophosphate‐activated protein kinase (AMPK) is a cellular energy...
Obesity is related to several organs, but the liver is particularly affected. Adenosine monophosphate-activated protein kinase (AMPK) is a cellular energy...
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SubjectTerms Adenosine kinase
Adipogenesis
AMP
AMPK/mTOR pathway
Autophagy
Cell survival
Cirrhosis
Fatty acids
Fatty liver
Forkhead protein
Glucose metabolism
Hepatocellular carcinoma
Insulin resistance
Kinases
Lipid metabolism
Lipogenesis
Liver diseases
Metabolism
non‐alcoholic fatty liver disease
Obesity
Phagosomes
Phosphorylation
Protein kinase
Protein turnover
Proteins
Rapamycin
TOR protein
Title AMPK/mTOR pathway significance in healthy liver and non‐alcoholic fatty liver disease and its progression
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjgh.16272
https://www.ncbi.nlm.nih.gov/pubmed/37438882
https://www.proquest.com/docview/2892833128
https://www.proquest.com/docview/2836877375
Volume 38
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