Mitochondrial Phenotype as a Driver of the Racial Dichotomy in Obesity and Insulin Resistance

African Americans (AA) are disproportionately burdened by metabolic diseases. While largely unexplored between Caucasian (C) and AA, differences in mitochondrial bioenergetics may provide crucial insight to mechanisms for increased susceptibility to metabolic diseases. AA display lower total energy...

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Published inBiomedicines Vol. 10; no. 6; p. 1456
Main Authors Jevtovic, Filip, Krassovskaia, Polina M., Lopez, Christian A., Fisher-Wellman, Kelsey H., Cortright, Ronald N., Broskey, Nicholas T.
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 20.06.2022
MDPI
Subjects
Adaptation
African American
African Americans
Bioenergetics
Cytosol
Efficiency
Energy
Energy expenditure
Genotype & phenotype
Glucose
Glycolysis
Hispanic Americans
Hypotheses
Inequality
Insulin
Insulin resistance
Metabolic disorders
metabolic flexibility
Metabolic rate
Mitochondria
Mitochondrial DNA
Musculoskeletal system
Obesity
Overnutrition
Oxidation
Phenotypes
Race
Racial differences
Reactive oxygen species
Respiration
Review
Skeletal muscle
Socioeconomic factors
Substrate preferences
Online AccessGet full text
ISSN2227-9059
2227-9059
DOI10.3390/biomedicines10061456

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Abstract African Americans (AA) are disproportionately burdened by metabolic diseases. While largely unexplored between Caucasian (C) and AA, differences in mitochondrial bioenergetics may provide crucial insight to mechanisms for increased susceptibility to metabolic diseases. AA display lower total energy expenditure and resting metabolic rate compared to C, but paradoxically have a higher amount of skeletal muscle mass, suggestive of inherent energetic efficiency differences between these races. Such adaptations would increase the chances of overnutrition in AA; however, these disparities would not explain the racial difference in insulin resistance (IR) in healthy subjects. Hallmarks associated with insulin resistance (IR), such as reduced mitochondrial oxidative capacity and metabolic inflexibility are present even in healthy AA without a metabolic disease. These adaptations might be influential of mitochondrial “substrate preference” and could play a role in disproportionate IR rates among races. A higher glycolytic flux and provision of shuttles transferring electrons from cytosol to mitochondrial matrix could be a contributing factor in development of IR via heightened reactive oxygen species (ROS) production. This review highlights the above concepts and provides suggestions for future studies that could help delineate molecular premises behind potential impairments in insulin signaling and metabolic disease susceptibility in AA.
AbstractList African Americans (AA) are disproportionately burdened by metabolic diseases. While largely unexplored between Caucasian (C) and AA, differences in mitochondrial bioenergetics may provide crucial insight to mechanisms for increased susceptibility to metabolic diseases. AA display lower total energy expenditure and resting metabolic rate compared to C, but paradoxically have a higher amount of skeletal muscle mass, suggestive of inherent energetic efficiency differences between these races. Such adaptations would increase the chances of overnutrition in AA; however, these disparities would not explain the racial difference in insulin resistance (IR) in healthy subjects. Hallmarks associated with insulin resistance (IR), such as reduced mitochondrial oxidative capacity and metabolic inflexibility are present even in healthy AA without a metabolic disease. These adaptations might be influential of mitochondrial "substrate preference" and could play a role in disproportionate IR rates among races. A higher glycolytic flux and provision of shuttles transferring electrons from cytosol to mitochondrial matrix could be a contributing factor in development of IR via heightened reactive oxygen species (ROS) production. This review highlights the above concepts and provides suggestions for future studies that could help delineate molecular premises behind potential impairments in insulin signaling and metabolic disease susceptibility in AA.African Americans (AA) are disproportionately burdened by metabolic diseases. While largely unexplored between Caucasian (C) and AA, differences in mitochondrial bioenergetics may provide crucial insight to mechanisms for increased susceptibility to metabolic diseases. AA display lower total energy expenditure and resting metabolic rate compared to C, but paradoxically have a higher amount of skeletal muscle mass, suggestive of inherent energetic efficiency differences between these races. Such adaptations would increase the chances of overnutrition in AA; however, these disparities would not explain the racial difference in insulin resistance (IR) in healthy subjects. Hallmarks associated with insulin resistance (IR), such as reduced mitochondrial oxidative capacity and metabolic inflexibility are present even in healthy AA without a metabolic disease. These adaptations might be influential of mitochondrial "substrate preference" and could play a role in disproportionate IR rates among races. A higher glycolytic flux and provision of shuttles transferring electrons from cytosol to mitochondrial matrix could be a contributing factor in development of IR via heightened reactive oxygen species (ROS) production. This review highlights the above concepts and provides suggestions for future studies that could help delineate molecular premises behind potential impairments in insulin signaling and metabolic disease susceptibility in AA.
African Americans (AA) are disproportionately burdened by metabolic diseases. While largely unexplored between Caucasian (C) and AA, differences in mitochondrial bioenergetics may provide crucial insight to mechanisms for increased susceptibility to metabolic diseases. AA display lower total energy expenditure and resting metabolic rate compared to C, but paradoxically have a higher amount of skeletal muscle mass, suggestive of inherent energetic efficiency differences between these races. Such adaptations would increase the chances of overnutrition in AA; however, these disparities would not explain the racial difference in insulin resistance (IR) in healthy subjects. Hallmarks associated with insulin resistance (IR), such as reduced mitochondrial oxidative capacity and metabolic inflexibility are present even in healthy AA without a metabolic disease. These adaptations might be influential of mitochondrial “substrate preference” and could play a role in disproportionate IR rates among races. A higher glycolytic flux and provision of shuttles transferring electrons from cytosol to mitochondrial matrix could be a contributing factor in development of IR via heightened reactive oxygen species (ROS) production. This review highlights the above concepts and provides suggestions for future studies that could help delineate molecular premises behind potential impairments in insulin signaling and metabolic disease susceptibility in AA.
Author Jevtovic, Filip
Lopez, Christian A.
Fisher-Wellman, Kelsey H.
Cortright, Ronald N.
Broskey, Nicholas T.
Krassovskaia, Polina M.
AuthorAffiliation 2 East Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC 27858, USA; fisherwellmank17@ecu.edu
3 Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC 27858, USA
1 Human Performance Laboratory, Department of Kinesiology, East Carolina University, Greenville, NC 27858, USA; jevtovicf21@students.ecu.edu (F.J.); krassovskaiap18@students.ecu.edu (P.M.K.); lopezch19@students.ecu.edu (C.A.L.); cortrightr@ecu.edu (R.N.C.)
AuthorAffiliation_xml – name: 1 Human Performance Laboratory, Department of Kinesiology, East Carolina University, Greenville, NC 27858, USA; jevtovicf21@students.ecu.edu (F.J.); krassovskaiap18@students.ecu.edu (P.M.K.); lopezch19@students.ecu.edu (C.A.L.); cortrightr@ecu.edu (R.N.C.)
– name: 3 Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC 27858, USA
– name: 2 East Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC 27858, USA; fisherwellmank17@ecu.edu
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Snippet African Americans (AA) are disproportionately burdened by metabolic diseases. While largely unexplored between Caucasian (C) and AA, differences in...
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SubjectTerms Adaptation
African American
African Americans
Bioenergetics
Cytosol
Efficiency
Energy
Energy expenditure
Genotype & phenotype
Glucose
Glycolysis
Hispanic Americans
Hypotheses
Inequality
Insulin
Insulin resistance
Metabolic disorders
metabolic flexibility
Metabolic rate
Mitochondria
Mitochondrial DNA
Musculoskeletal system
Obesity
Overnutrition
Oxidation
Phenotypes
Race
Racial differences
Reactive oxygen species
Respiration
Review
Skeletal muscle
Socioeconomic factors
Substrate preferences
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Title Mitochondrial Phenotype as a Driver of the Racial Dichotomy in Obesity and Insulin Resistance
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Volume 10
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