Whey protein supplementation does not alter plasma branched-chained amino acid profiles but results in unique metabolomics patterns in obese women enrolled in an 8-week weight loss trial

Brian D. Piccolo, Kevin B. Comerford, Siddika E Karakas, Trina A. Knotts, Oliver Fiehn, Sean H. Adams

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Background: It has been suggested that perturbations in branched-chain amino acid (BCAA) catabolism are associated with insulin resistance and contribute to elevated systemic BCAAs. Evidence in rodents suggests dietary protein rich in BCAAs can increase BCAA catabolism, but there is limited evidence in humans. Objective: We hypothesize that a diet rich in BCAAs will increase BCAA catabolism, which will manifest in a reduction of fasting plasma BCAA concentrations. Methods: The metabolome of 27 obese women with metabolic syndrome before and after weight loss was investigated to identify changes in BCAA metabolism using GC-time-of-flight mass spectrometry. Subjects were enrolled in an 8-wk weight-loss study including either a 20-g/d whey (whey group, n = 16) or gelatin (gelatin group, n = 11) protein supplement. When matched for total protein by weight, whey protein has 3 times the amount of BCAAs compared with gelatin protein. Results: Postintervention plasma abundances of Ile (gelatin group:637 ± 18, quantifier ion peak height O 100; whey group:744 ± 65), Leu (gelatin group:1210 ± 33; whey group:1380 ± 79), and Val (gelatin group:2080 ± 59; whey group:2510 ± 230) did not differ between treatment groups. BCAAs were significantly correlated with homeostasis model assessment of insulin resistance at baseline (r = 0.52, 0.43, and 0.49 for Leu, Ile, and Val, respectively; all, P < 0.05), but correlations were no longer significant at postintervention. Pro-and Cys-related pathways were found discriminant of whey protein vs. gelatin protein supplementation in multivariate statistical analyses. Conclusions: These findings suggest that BCAA metabolism is, at best, only modestly affected at a whey protein supplementation dose of 20 g/d. Furthermore, the loss of an association between postintervention BCAA and homeostasis model assessment suggests that factors associated with calorie restriction or protein intake affect howplasma BCAAs relate to insulin sensitivity. This trial was registered at clinicaltrials.gov as NCT00739479.

Original languageEnglish (US)
Pages (from-to)691-700
Number of pages10
JournalJournal of Nutrition
Volume145
Issue number4
DOIs
StatePublished - 2015

Fingerprint

Branched Chain Amino Acids
Metabolomics
Gelatin
Weight Loss
Amino Acids
Insulin Resistance
Proteins
Homeostasis
Metabolome
Dietary Proteins
Whey Proteins
Rodentia
Fasting
Mass Spectrometry
Multivariate Analysis
Whey
Ions
Diet
Weights and Measures

Keywords

  • BCAA
  • Cys
  • Dairy
  • Leu
  • Metabolic syndrome
  • Metabolomics
  • Obesity
  • Pro
  • Protein
  • Weight loss

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Nutrition and Dietetics

Cite this

Whey protein supplementation does not alter plasma branched-chained amino acid profiles but results in unique metabolomics patterns in obese women enrolled in an 8-week weight loss trial. / Piccolo, Brian D.; Comerford, Kevin B.; Karakas, Siddika E; Knotts, Trina A.; Fiehn, Oliver; Adams, Sean H.

In: Journal of Nutrition, Vol. 145, No. 4, 2015, p. 691-700.

Research output: Contribution to journalArticle

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T1 - Whey protein supplementation does not alter plasma branched-chained amino acid profiles but results in unique metabolomics patterns in obese women enrolled in an 8-week weight loss trial

AU - Piccolo, Brian D.

AU - Comerford, Kevin B.

AU - Karakas, Siddika E

AU - Knotts, Trina A.

AU - Fiehn, Oliver

AU - Adams, Sean H.

PY - 2015

Y1 - 2015

N2 - Background: It has been suggested that perturbations in branched-chain amino acid (BCAA) catabolism are associated with insulin resistance and contribute to elevated systemic BCAAs. Evidence in rodents suggests dietary protein rich in BCAAs can increase BCAA catabolism, but there is limited evidence in humans. Objective: We hypothesize that a diet rich in BCAAs will increase BCAA catabolism, which will manifest in a reduction of fasting plasma BCAA concentrations. Methods: The metabolome of 27 obese women with metabolic syndrome before and after weight loss was investigated to identify changes in BCAA metabolism using GC-time-of-flight mass spectrometry. Subjects were enrolled in an 8-wk weight-loss study including either a 20-g/d whey (whey group, n = 16) or gelatin (gelatin group, n = 11) protein supplement. When matched for total protein by weight, whey protein has 3 times the amount of BCAAs compared with gelatin protein. Results: Postintervention plasma abundances of Ile (gelatin group:637 ± 18, quantifier ion peak height O 100; whey group:744 ± 65), Leu (gelatin group:1210 ± 33; whey group:1380 ± 79), and Val (gelatin group:2080 ± 59; whey group:2510 ± 230) did not differ between treatment groups. BCAAs were significantly correlated with homeostasis model assessment of insulin resistance at baseline (r = 0.52, 0.43, and 0.49 for Leu, Ile, and Val, respectively; all, P < 0.05), but correlations were no longer significant at postintervention. Pro-and Cys-related pathways were found discriminant of whey protein vs. gelatin protein supplementation in multivariate statistical analyses. Conclusions: These findings suggest that BCAA metabolism is, at best, only modestly affected at a whey protein supplementation dose of 20 g/d. Furthermore, the loss of an association between postintervention BCAA and homeostasis model assessment suggests that factors associated with calorie restriction or protein intake affect howplasma BCAAs relate to insulin sensitivity. This trial was registered at clinicaltrials.gov as NCT00739479.

AB - Background: It has been suggested that perturbations in branched-chain amino acid (BCAA) catabolism are associated with insulin resistance and contribute to elevated systemic BCAAs. Evidence in rodents suggests dietary protein rich in BCAAs can increase BCAA catabolism, but there is limited evidence in humans. Objective: We hypothesize that a diet rich in BCAAs will increase BCAA catabolism, which will manifest in a reduction of fasting plasma BCAA concentrations. Methods: The metabolome of 27 obese women with metabolic syndrome before and after weight loss was investigated to identify changes in BCAA metabolism using GC-time-of-flight mass spectrometry. Subjects were enrolled in an 8-wk weight-loss study including either a 20-g/d whey (whey group, n = 16) or gelatin (gelatin group, n = 11) protein supplement. When matched for total protein by weight, whey protein has 3 times the amount of BCAAs compared with gelatin protein. Results: Postintervention plasma abundances of Ile (gelatin group:637 ± 18, quantifier ion peak height O 100; whey group:744 ± 65), Leu (gelatin group:1210 ± 33; whey group:1380 ± 79), and Val (gelatin group:2080 ± 59; whey group:2510 ± 230) did not differ between treatment groups. BCAAs were significantly correlated with homeostasis model assessment of insulin resistance at baseline (r = 0.52, 0.43, and 0.49 for Leu, Ile, and Val, respectively; all, P < 0.05), but correlations were no longer significant at postintervention. Pro-and Cys-related pathways were found discriminant of whey protein vs. gelatin protein supplementation in multivariate statistical analyses. Conclusions: These findings suggest that BCAA metabolism is, at best, only modestly affected at a whey protein supplementation dose of 20 g/d. Furthermore, the loss of an association between postintervention BCAA and homeostasis model assessment suggests that factors associated with calorie restriction or protein intake affect howplasma BCAAs relate to insulin sensitivity. This trial was registered at clinicaltrials.gov as NCT00739479.

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KW - Cys

KW - Dairy

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KW - Metabolic syndrome

KW - Metabolomics

KW - Obesity

KW - Pro

KW - Protein

KW - Weight loss

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