Coordinated Modulation of Energy Metabolism and Inflammation by Branched-Chain Amino Acids and Fatty Acids

As important metabolic substrates, branched-chain amino acids (BCAAs) and fatty acids (FAs) participate in many significant physiological processes, such as mitochondrial biogenesis, energy metabolism, and inflammation, along with intermediate metabolites generated in their catabolism. The increased...

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Published inFrontiers in endocrinology (Lausanne) Vol. 11; p. 617
Main Authors Ye, Zhenhong, Wang, Siyu, Zhang, Chunmei, Zhao, Yue
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 08.09.2020
Subjects
Amino Acids, Branched-Chain - metabolism
branched-amino acids
Endocrinology
energy metabolism
Energy Metabolism - physiology
fatty acids
Fatty Acids - metabolism
Humans
inflammation
Inflammation - metabolism
insulin resistance
Insulin Resistance - physiology
Lipid Metabolism - physiology
mitochondrial biogenesis
Organelle Biogenesis
Oxidative Phosphorylation
Signal Transduction - physiology
branched-amino acids
fatty acids
inflammation
insulin resistance
mitochondrial biogenesis
energy metabolism
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Abstract As important metabolic substrates, branched-chain amino acids (BCAAs) and fatty acids (FAs) participate in many significant physiological processes, such as mitochondrial biogenesis, energy metabolism, and inflammation, along with intermediate metabolites generated in their catabolism. The increased levels of BCAAs and fatty acids can lead to mitochondrial dysfunction by altering mitochondrial biogenesis and adenosine triphosphate (ATP) production and interfering with glycolysis, fatty acid oxidation, the tricarboxylic acid cycle (TCA) cycle, and oxidative phosphorylation. BCAAs can directly activate the mammalian target of rapamycin (mTOR) signaling pathway to induce insulin resistance, or function together with fatty acids. In addition, elevated levels of BCAAs and fatty acids can activate the canonical nuclear factor-κB (NF-κB) signaling pathway and inflammasome and regulate mitochondrial dysfunction and metabolic disorders through upregulated inflammatory signals. This review provides a comprehensive summary of the mechanisms through which BCAAs and fatty acids modulate energy metabolism, insulin sensitivity, and inflammation synergistically.
AbstractList As important metabolic substrates, branched-chain amino acids (BCAAs) and fatty acids (FAs) participate in many significant physiological processes, such as mitochondrial biogenesis, energy metabolism, and inflammation, along with intermediate metabolites generated in their catabolism. The increased levels of BCAAs and fatty acids can lead to mitochondrial dysfunction by altering mitochondrial biogenesis and adenosine triphosphate (ATP) production and interfering with glycolysis, fatty acid oxidation, the tricarboxylic acid cycle (TCA) cycle, and oxidative phosphorylation. BCAAs can directly activate the mammalian target of rapamycin (mTOR) signaling pathway to induce insulin resistance, or function together with fatty acids. In addition, elevated levels of BCAAs and fatty acids can activate the canonical nuclear factor-κB (NF-κB) signaling pathway and inflammasome and regulate mitochondrial dysfunction and metabolic disorders through upregulated inflammatory signals. This review provides a comprehensive summary of the mechanisms through which BCAAs and fatty acids modulate energy metabolism, insulin sensitivity, and inflammation synergistically.
As important metabolic substrates, branched-chain amino acids (BCAAs) and fatty acids (FAs) participate in many significant physiological processes, such as mitochondrial biogenesis, energy metabolism, and inflammation, along with intermediate metabolites generated in their catabolism. The increased levels of BCAAs and fatty acids can lead to mitochondrial dysfunction by altering mitochondrial biogenesis and adenosine triphosphate (ATP) production and interfering with glycolysis, fatty acid oxidation, the tricarboxylic acid cycle (TCA) cycle, and oxidative phosphorylation. BCAAs can directly activate the mammalian target of rapamycin (mTOR) signaling pathway to induce insulin resistance, or function together with fatty acids. In addition, elevated levels of BCAAs and fatty acids can activate the canonical nuclear factor-κB (NF-κB) signaling pathway and inflammasome and regulate mitochondrial dysfunction and metabolic disorders through upregulated inflammatory signals. This review provides a comprehensive summary of the mechanisms through which BCAAs and fatty acids modulate energy metabolism, insulin sensitivity, and inflammation synergistically.As important metabolic substrates, branched-chain amino acids (BCAAs) and fatty acids (FAs) participate in many significant physiological processes, such as mitochondrial biogenesis, energy metabolism, and inflammation, along with intermediate metabolites generated in their catabolism. The increased levels of BCAAs and fatty acids can lead to mitochondrial dysfunction by altering mitochondrial biogenesis and adenosine triphosphate (ATP) production and interfering with glycolysis, fatty acid oxidation, the tricarboxylic acid cycle (TCA) cycle, and oxidative phosphorylation. BCAAs can directly activate the mammalian target of rapamycin (mTOR) signaling pathway to induce insulin resistance, or function together with fatty acids. In addition, elevated levels of BCAAs and fatty acids can activate the canonical nuclear factor-κB (NF-κB) signaling pathway and inflammasome and regulate mitochondrial dysfunction and metabolic disorders through upregulated inflammatory signals. This review provides a comprehensive summary of the mechanisms through which BCAAs and fatty acids modulate energy metabolism, insulin sensitivity, and inflammation synergistically.
Author Zhang, Chunmei
Zhao, Yue
Ye, Zhenhong
Wang, Siyu
AuthorAffiliation 2 National Clinical Research Center for Obstetrics and Gynecology (Peking University Third Hospital) , Beijing , China
4 Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Peking University , Beijing , China
1 Department of Obstetrics and Gynecology, Center for Reproductive Medicine, Peking University Third Hospital , Beijing , China
3 Key Laboratory of Assisted Reproduction (Peking University), Ministry of Education , Beijing , China
5 Research Units of Comprehensive Diagnosis and Treatment of Oocyte Maturation Arrest, Chinese Academy of Medical Sciences , Beijing , China
AuthorAffiliation_xml – name: 5 Research Units of Comprehensive Diagnosis and Treatment of Oocyte Maturation Arrest, Chinese Academy of Medical Sciences , Beijing , China
– name: 2 National Clinical Research Center for Obstetrics and Gynecology (Peking University Third Hospital) , Beijing , China
– name: 3 Key Laboratory of Assisted Reproduction (Peking University), Ministry of Education , Beijing , China
– name: 1 Department of Obstetrics and Gynecology, Center for Reproductive Medicine, Peking University Third Hospital , Beijing , China
– name: 4 Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Peking University , Beijing , China
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Keywords branched-amino acids
fatty acids
inflammation
insulin resistance
mitochondrial biogenesis
energy metabolism
Language English
License Copyright © 2020 Ye, Wang, Zhang and Zhao.
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Reviewed by: Charles E. McCall, Wake Forest Baptist Medical Center, United States; Gary David Lopaschuk, University of Alberta, Canada; Rolf Kristian Berge, University of Bergen, Norway; Tie Fu Liu, Fudan University, China
Edited by: Maria Clara Franco, Oregon State University, United States
This article was submitted to Diabetes: Molecular Mechanisms, a section of the journal Frontiers in Endocrinology
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SubjectTerms Amino Acids, Branched-Chain - metabolism
branched-amino acids
Endocrinology
energy metabolism
Energy Metabolism - physiology
fatty acids
Fatty Acids - metabolism
Humans
inflammation
Inflammation - metabolism
insulin resistance
Insulin Resistance - physiology
Lipid Metabolism - physiology
mitochondrial biogenesis
Organelle Biogenesis
Oxidative Phosphorylation
Signal Transduction - physiology
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Title Coordinated Modulation of Energy Metabolism and Inflammation by Branched-Chain Amino Acids and Fatty Acids
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