The Impact of Sugar-Sweetened Beverage Consumption on the Liver: A Proteomics-Based Analysis
Cardiometabolic complications such as the metabolic syndrome and Type 2 Diabetes Mellitus (T2DM) are major causes of global morbidity and mortality. As sugar-sweetened beverages (SSBs) are implicated in this process, this study aimed to obtain greater mechanistic insights. Male Wistar rats (~200 g)...
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Published in | Antioxidants Vol. 9; no. 7; p. 569 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Basel
MDPI AG
01.07.2020
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Online Access | Get full text |
ISSN | 2076-3921 2076-3921 |
DOI | 10.3390/antiox9070569 |
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Abstract | Cardiometabolic complications such as the metabolic syndrome and Type 2 Diabetes Mellitus (T2DM) are major causes of global morbidity and mortality. As sugar-sweetened beverages (SSBs) are implicated in this process, this study aimed to obtain greater mechanistic insights. Male Wistar rats (~200 g) were gavaged with a local SSB every day for a period of six months while the control group was gavaged with an iso-volumetric amount of water. Experimental dosages were calculated according to the surface area-to-volume ratio and were equivalent to 125 mL/day (in human terms). A proteomic analysis was performed on isolated liver samples and thereafter, markers of endoplasmic reticulum (ER) stress, antioxidant/oxidant capacity, calcium regulation, and mitochondrial functionality were assessed. These data show that SSB consumption resulted in (a) the induction of mild hepatic ER stress; (b) altered hepatic mitochondrial dynamics; and (c) perturbed calcium handling across mitochondria-associated ER membranes. Despite significant changes in markers of ER stress, the antioxidant response and calcium handling (proteomics data), the liver is able to initiate adaptive responses to counteract such stressors. However, the mitochondrial data showed increased fission and decreased fusion that may put the organism at risk for developing insulin resistance and T2DM in the longer term. |
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AbstractList | Cardiometabolic complications such as the metabolic syndrome and Type 2 Diabetes Mellitus (T2DM) are major causes of global morbidity and mortality. As sugar-sweetened beverages (SSBs) are implicated in this process, this study aimed to obtain greater mechanistic insights. Male Wistar rats (~200 g) were gavaged with a local SSB every day for a period of six months while the control group was gavaged with an iso-volumetric amount of water. Experimental dosages were calculated according to the surface area-to-volume ratio and were equivalent to 125 mL/day (in human terms). A proteomic analysis was performed on isolated liver samples and thereafter, markers of endoplasmic reticulum (ER) stress, antioxidant/oxidant capacity, calcium regulation, and mitochondrial functionality were assessed. These data show that SSB consumption resulted in (a) the induction of mild hepatic ER stress; (b) altered hepatic mitochondrial dynamics; and (c) perturbed calcium handling across mitochondria-associated ER membranes. Despite significant changes in markers of ER stress, the antioxidant response and calcium handling (proteomics data), the liver is able to initiate adaptive responses to counteract such stressors. However, the mitochondrial data showed increased fission and decreased fusion that may put the organism at risk for developing insulin resistance and T2DM in the longer term. Cardiometabolic complications such as the metabolic syndrome and Type 2 Diabetes Mellitus (T2DM) are major causes of global morbidity and mortality. As sugar-sweetened beverages (SSBs) are implicated in this process, this study aimed to obtain greater mechanistic insights. Male Wistar rats (~200 g) were gavaged with a local SSB every day for a period of six months while the control group was gavaged with an iso-volumetric amount of water. Experimental dosages were calculated according to the surface area-to-volume ratio and were equivalent to 125 mL/day (in human terms). A proteomic analysis was performed on isolated liver samples and thereafter, markers of endoplasmic reticulum (ER) stress, antioxidant/oxidant capacity, calcium regulation, and mitochondrial functionality were assessed. These data show that SSB consumption resulted in (a) the induction of mild hepatic ER stress; (b) altered hepatic mitochondrial dynamics; and (c) perturbed calcium handling across mitochondria-associated ER membranes. Despite significant changes in markers of ER stress, the antioxidant response and calcium handling (proteomics data), the liver is able to initiate adaptive responses to counteract such stressors. However, the mitochondrial data showed increased fission and decreased fusion that may put the organism at risk for developing insulin resistance and T2DM in the longer term.Cardiometabolic complications such as the metabolic syndrome and Type 2 Diabetes Mellitus (T2DM) are major causes of global morbidity and mortality. As sugar-sweetened beverages (SSBs) are implicated in this process, this study aimed to obtain greater mechanistic insights. Male Wistar rats (~200 g) were gavaged with a local SSB every day for a period of six months while the control group was gavaged with an iso-volumetric amount of water. Experimental dosages were calculated according to the surface area-to-volume ratio and were equivalent to 125 mL/day (in human terms). A proteomic analysis was performed on isolated liver samples and thereafter, markers of endoplasmic reticulum (ER) stress, antioxidant/oxidant capacity, calcium regulation, and mitochondrial functionality were assessed. These data show that SSB consumption resulted in (a) the induction of mild hepatic ER stress; (b) altered hepatic mitochondrial dynamics; and (c) perturbed calcium handling across mitochondria-associated ER membranes. Despite significant changes in markers of ER stress, the antioxidant response and calcium handling (proteomics data), the liver is able to initiate adaptive responses to counteract such stressors. However, the mitochondrial data showed increased fission and decreased fusion that may put the organism at risk for developing insulin resistance and T2DM in the longer term. |
Audience | Academic |
Author | Laher, Ismail Sher, Lucien Sieck, Gary Marnewick, Jeanine L. Benade, Janina De Klerk, Sheneez Deshpande, Gaurang Essop, M. Faadiel Bester, Dirk |
AuthorAffiliation | 3 Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, Bellville 7535, Cape Town, South Africa 4 Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA; sieck.gary@mayo.edu 5 Department of Anesthesiology, Pharmacology & Therapeutics, University of British Columbia, Vancouver, BC V6T 1Z3, Canada 2 Applied Microbial and Health Biotechnology Institute, Cape Peninsula University of Technology, Bellville 7535, Cape Town, South Africa; besterd@cput.ac.za (D.B.); MarnewickJ@cput.ac.za (J.L.M.) 1 Center for Cardio-Metabolic Research in Africa (CARMA), Department of Physiological Sciences, Stellenbosch University, Stellenbosch 7600, South Africa; janinabenade@gmail.com (J.B.); 18718078@sun.ac.za (L.S.); sheodk@gmail.com (S.D.K.); gaurang1712@gmail.com (G.D.); ismail.laher@ubc.ca (I.L.) |
AuthorAffiliation_xml | – name: 1 Center for Cardio-Metabolic Research in Africa (CARMA), Department of Physiological Sciences, Stellenbosch University, Stellenbosch 7600, South Africa; janinabenade@gmail.com (J.B.); 18718078@sun.ac.za (L.S.); sheodk@gmail.com (S.D.K.); gaurang1712@gmail.com (G.D.); ismail.laher@ubc.ca (I.L.) – name: 2 Applied Microbial and Health Biotechnology Institute, Cape Peninsula University of Technology, Bellville 7535, Cape Town, South Africa; besterd@cput.ac.za (D.B.); MarnewickJ@cput.ac.za (J.L.M.) – name: 4 Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA; sieck.gary@mayo.edu – name: 5 Department of Anesthesiology, Pharmacology & Therapeutics, University of British Columbia, Vancouver, BC V6T 1Z3, Canada – name: 3 Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, Bellville 7535, Cape Town, South Africa |
Author_xml | – sequence: 1 givenname: Janina surname: Benade fullname: Benade, Janina – sequence: 2 givenname: Lucien surname: Sher fullname: Sher, Lucien – sequence: 3 givenname: Sheneez surname: De Klerk fullname: De Klerk, Sheneez – sequence: 4 givenname: Gaurang surname: Deshpande fullname: Deshpande, Gaurang – sequence: 5 givenname: Dirk surname: Bester fullname: Bester, Dirk – sequence: 6 givenname: Jeanine L. surname: Marnewick fullname: Marnewick, Jeanine L. – sequence: 7 givenname: Gary surname: Sieck fullname: Sieck, Gary – sequence: 8 givenname: Ismail orcidid: 0000-0002-3917-4417 surname: Laher fullname: Laher, Ismail – sequence: 9 givenname: M. Faadiel orcidid: 0000-0002-8434-4294 surname: Essop fullname: Essop, M. Faadiel |
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CitedBy_id | crossref_primary_10_3390_antiox10050638 crossref_primary_10_33549_physiolres_935109 crossref_primary_10_3389_fcell_2022_1036225 crossref_primary_10_3390_ijms22136862 |
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SubjectTerms | antioxidant capacity Antioxidants Beverages Calcium (mitochondrial) Calcium signalling Cytochrome Diabetes mellitus (non-insulin dependent) Endoplasmic reticulum endoplasmic reticulum stress Glucose Health aspects Homeostasis Insulin Laboratory animals Liver Metabolic syndrome Metabolism Mitochondria mitochondrial dysfunction mitochondrial fission and fusion Morbidity Oxidants Proteins Proteomics Software sugar-sweetened beverages Water content |
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Title | The Impact of Sugar-Sweetened Beverage Consumption on the Liver: A Proteomics-Based Analysis |
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