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Regulation of energy metabolism and mitochondrial function in skeletal muscle during lipid overfeeding in healthy men.

The Journal of clinical endocrinology and metabolism
July 1, 2014
K Seyssel et al. (14 authors)
Clinical TrialJournal ArticleResearch Support, Non-U.S. Gov'tHuman StudyClinical
Study Details

Study Goal

The researchers aimed to evaluate how lipid overfeeding regulates fuel partitioning and energy metabolism in skeletal muscle of healthy men.

Results Summary

Overfeeding increased body weight and fat mass, shifted substrate use toward carbohydrate oxidation, reduced NAD(+) concentration, and hyperacetylated PGC-1α, but paradoxically increased mitochondrial gene expression and respiration rates.

Population

Thirty-nine healthy male volunteers

Effective Dosage

3180 kJ/day (high-fat diet)

Duration

56 days

Interactions

None mentioned

Extracted Claims (10)
InterventionDirectionEndpointPopulationDosageImpactClaim #
overfeeding with a high-fat diet (3180 kJ/d)
increase
body weight
healthy men
+2.6 kg
increased
#1
overfeeding with a high-fat diet (3180 kJ/d)
increase
fat mass
healthy men
-
increased
#2
overfeeding with a high-fat diet (3180 kJ/d)
increase
use of substrates as energy fuel
healthy men
toward preferential oxidation of carbohydrates instead of lipids
shifted
#3
overfeeding with a high-fat diet (3180 kJ/d)
decrease
pyruvate dehydrogenase kinase 4 expression
healthy men
-
reduction in
#4
overfeeding with a high-fat diet (3180 kJ/d)
decrease
NAD(+) concentration
healthy men
-
decreased
#5
overfeeding with a high-fat diet (3180 kJ/d)
decrease
deacetylase activity of the sirtuins
healthy men
-
reduced
#6
overfeeding with a high-fat diet (3180 kJ/d)
increase
PGC-1α
healthy men
-
hyperacetylation of
#7
overfeeding with a high-fat diet (3180 kJ/d)
decrease
sirtuin PGC-1α pathway
healthy men
-
reduction of the
#8
overfeeding with a high-fat diet (3180 kJ/d)
increase
mitochondrial gene expression
healthy men
-
increased
#9
overfeeding with a high-fat diet (3180 kJ/d)
increase
respiration rate
healthy men
-
higher
#10
Abstract

CONTEXT/OBJECTIVE: The aim of this study was to evaluate the regulation of the fuel partitioning and energy metabolism in skeletal muscle during lipid overfeeding in healthy men. Design/Participants/Intervention: Thirty-nine healthy volunteers were overfed for 56 days with a high-fat diet (3180 kJ/d). Energy metabolism (indirect calorimetry) was characterized in the fasting state and during a test meal before and at the end of the diet. Skeletal muscle biopsies were taken at day 0 and day 56. MAIN OUTCOME MEASURES: Change in gene expression, mitochondrial respiration, nicotinamide adenine dinucleotide (NAD(+)) content, and acetylation of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) in skeletal muscle was measured. RESULTS: Overfeeding increased body weight (+2.6 kg) and fat mass concomitantly with a shift in the use of substrates as energy fuel toward preferential oxidation of carbohydrates instead of lipids. Changes in lipid metabolic gene expression supported this observation, with a reduction in pyruvate dehydrogenase kinase 4 expression that could be the consequences of decreased NAD(+) concentration and reduced deacetylase activity of the sirtuins, as supported by hyperacetylation of PGC-1α after overfeeding. Interestingly, this reduction of the sirtuin PGC-1α pathway was associated with increased mitochondrial gene expression and higher respiration rate under these conditions. CONCLUSION: Adaptation to lipid overfeeding and regulation of fuel partitioning in human muscle appear to rely on a dissociation between the regulatory functions of the sirtuin-PGC-1α pathway on fatty acid oxidation and on mitochondrial regulation. This may facilitate lipid storage during a period of positive energy balance while maintaining mitochondrial functions and oxidative capacities.

Medical Subject Headings (MeSH)
AdultCell RespirationDiet, High-FatDietary FatsEnergy MetabolismHumansLipid MetabolismMaleMitochondria, MuscleMuscle, SkeletalOvernutritionOxidation-Reduction
Study Links
Quality Scores
SafetyNot Assessed
Efficacy75/10
Quality85/10
Citation Metrics
Total Citations28
Citations/Year2.5
Relative Citation Ratio0.90
NIH Percentile46.5%
Research Impact Scores
APT Score0.50
Weight Score1.73
Normalized Score0.67
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