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The Intra- or Extracellular Redox State Was Not Affected by a High vs. Low Glycemic Response Diet in Mice.

A low glycemic response (LGR) vs. high glycemic response (HGR) diet helps curtail the development of obesity and diabetes, though the mechanisms are unknown. We hypothesized that consumption of a HGR vs. a LGR diet would lead to a more oxidized circulating redox state and predicted that a HGR diet w... Full description

Journal Title: PloS one 2015, Vol.10(6), p.e0128380
Main Author: Kleckner, Amber S
Other Authors: Wong, Siu , Corkey, Barbara E
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 1932-6203 ; DOI: 10.1371/journal.pone.0128380
Link: http://search.proquest.com/docview/1685755948/?pq-origsite=primo
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title: The Intra- or Extracellular Redox State Was Not Affected by a High vs. Low Glycemic Response Diet in Mice.
format: Article
creator:
  • Kleckner, Amber S
  • Wong, Siu
  • Corkey, Barbara E
subjects:
  • Animals–Drug Effects
  • Behavior, Animal–Drug Effects
  • Body Composition–Drug Effects
  • Body Weight–Adverse Effects
  • Diet–Drug Effects
  • Energy Metabolism–Drug Effects
  • Extracellular Space–Metabolism
  • Glutathione Disulfide–Metabolism
  • Glycemic Index–Drug Effects
  • Insulin Resistance–Metabolism
  • Intracellular Space–Drug Effects
  • Lipid Peroxidation–Drug Effects
  • Male–Drug Effects
  • Mice–Drug Effects
  • Mice, Inbred C57bl–Drug Effects
  • Oxidation-Reduction–Drug Effects
  • Glutathione Disulfide
ispartof: PloS one, 2015, Vol.10(6), p.e0128380
description: A low glycemic response (LGR) vs. high glycemic response (HGR) diet helps curtail the development of obesity and diabetes, though the mechanisms are unknown. We hypothesized that consumption of a HGR vs. a LGR diet would lead to a more oxidized circulating redox state and predicted that a HGR diet would increase fat accumulation, reduce insulin sensitivity, and impair metabolic acclimation to a high fat diet in a mouse model. Hence, male C57BL/6 mice consumed a HGR or LGR diet for 16 weeks and a subset of the mice subsequently consumed a high fat diet for 4 weeks. We found that body mass increased at a faster rate for those consuming the HGR diet. Percent body fat was greater and percent lean mass was lesser in the HGR group starting at 12 weeks. However, the groups did not differ in terms of glucose tolerance at week 14 and metabolic parameters (respiratory exchange ratio, heat production, activity) at weeks 4 or 15. Moreover, mice on either diet did not show differences in metabolic acclimation to the high fat leg of the study. At the termination of the study, the groups did not differ in terms of redox pairs (lactate/pyruvate and [beta]-hydroxybutyrate/acetoacetate) or thioredoxin reductase activity in blood. Also, total and oxidized glutathione levels and lipid peroxidation were similar in blood and liver. Correlations between baseline measures, longitudinal parameters, environmental conditions, and terminal metrics revealed that individual mice have innate propensities to metabolic regulation that may be difficult to perturb with diet alone; for example, starting mass correlated negatively with energy expenditure 4 weeks into the study and total hepatic glutathione at the end of the study. In conclusion, these data suggest that the mechanism by which HGR carbohydrates contributes to obesity is not via prolonged oxidation of the circulating redox state.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 1932-6203 ; DOI: 10.1371/journal.pone.0128380
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titleThe Intra- or Extracellular Redox State Was Not Affected by a High vs. Low Glycemic Response Diet in Mice.
creatorKleckner, Amber S ; Wong, Siu ; Corkey, Barbara E
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subjectAnimals–Drug Effects ; Behavior, Animal–Drug Effects ; Body Composition–Drug Effects ; Body Weight–Adverse Effects ; Diet–Drug Effects ; Energy Metabolism–Drug Effects ; Extracellular Space–Metabolism ; Glutathione Disulfide–Metabolism ; Glycemic Index–Drug Effects ; Insulin Resistance–Metabolism ; Intracellular Space–Drug Effects ; Lipid Peroxidation–Drug Effects ; Male–Drug Effects ; Mice–Drug Effects ; Mice, Inbred C57bl–Drug Effects ; Oxidation-Reduction–Drug Effects ; Glutathione Disulfide
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descriptionA low glycemic response (LGR) vs. high glycemic response (HGR) diet helps curtail the development of obesity and diabetes, though the mechanisms are unknown. We hypothesized that consumption of a HGR vs. a LGR diet would lead to a more oxidized circulating redox state and predicted that a HGR diet would increase fat accumulation, reduce insulin sensitivity, and impair metabolic acclimation to a high fat diet in a mouse model. Hence, male C57BL/6 mice consumed a HGR or LGR diet for 16 weeks and a subset of the mice subsequently consumed a high fat diet for 4 weeks. We found that body mass increased at a faster rate for those consuming the HGR diet. Percent body fat was greater and percent lean mass was lesser in the HGR group starting at 12 weeks. However, the groups did not differ in terms of glucose tolerance at week 14 and metabolic parameters (respiratory exchange ratio, heat production, activity) at weeks 4 or 15. Moreover, mice on either diet did not show differences in metabolic acclimation to the high fat leg of the study. At the termination of the study, the groups did not differ in terms of redox pairs (lactate/pyruvate and [beta]-hydroxybutyrate/acetoacetate) or thioredoxin reductase activity in blood. Also, total and oxidized glutathione levels and lipid peroxidation were similar in blood and liver. Correlations between baseline measures, longitudinal parameters, environmental conditions, and terminal metrics revealed that individual mice have innate propensities to metabolic regulation that may be difficult to perturb with diet alone; for example, starting mass correlated negatively with energy expenditure 4 weeks into the study and total hepatic glutathione at the end of the study. In conclusion, these data suggest that the mechanism by which HGR carbohydrates contributes to obesity is not via prolonged oxidation of the circulating redox state.
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