PMID- 8675642
OWN - NLM
STAT- MEDLINE
DCOM- 19960813
LR  - 20181113
IS  - 0021-9738 (Print)
IS  - 0021-9738 (Linking)
VI  - 96
IP  - 6
DP  - 1995 Dec
TI  - Short-term alterations in carbohydrate energy intake in humans. Striking effects 
      on hepatic glucose production, de novo lipogenesis, lipolysis, and whole-body 
      fuel selection.
PG  - 2735-43
AB  - Short-term alterations in dietary carbohydrate (CHO) energy are known to alter 
      whole-body fuel selection in humans, but the metabolic mechanisms remain unknown. 
      We used stable isotope-mass spectrometric methods with indirect calorimetry in 
      normal subjects to quantify the metabolic response to six dietary phases (5 d 
      each), ranging from 50% surplus CHO (+50% CHO) to 50% deficient CHO (-50% CHO), 
      and 50% surplus fat (+50% fat). Fasting hepatic glucose production (HGP) varied 
      by > 40% from deficient to surplus CHO diets (1.78 +/- 0.08 vs 2.43 +/- 0.09 
      mg/kg per min, P < 0.01). Increased HGP on surplus CHO occurred despite 
      significantly higher serum insulin concentrations. Lipolysis correlated inversely 
      with CHO intake as did the proportion of whole-body lipolytic flux oxidized. 
      Fractional de novo hepatic lipogenesis (DNL) increased more than 10-fold on 
      surplus CHO and was unmeasurable on deficient CHO diets; thus, the preceding 5-d 
      CHO intake could be inferred from DNL. Nevertheless, absolute hepatic DNL 
      accounted for < 5g fatty acids synthesized per day even on +50% CHO. Whole-body 
      CHO oxidation increased sixfold and fat oxidation decreased > 90% on surplus CHO 
      diets. CHO oxidation was highly correlated with HGP (r2= 0.60). HGP could account 
      for 85% of fasting CHO oxidation on +25% CHO and 67% on +50% CHO diets. Some 
      oxidation of intracellular CHO stores was therefore also occurring. +50% fat diet 
      had no effects on HGP, DNL, or fuel selection. We conclude that altered CHO 
      intake alters HGP specifically and in a dose-dependent manner, that HGP may 
      mediate the effects of CHO on whole-body fuel selection both by providing 
      substrate and by altering serum insulin concentrations, that altered lipolysis 
      and tissue oxidation efficiency contribute to changes in fat oxidation, and that 
      surplus CHO is not substantially converted by the liver to fat as it spares fat 
      oxidation, but that fractional DNL may nevertheless be a qualitative marker of 
      recent CHO intake.
FAU - Schwarz, J M
AU  - Schwarz JM
AD  - Department of Nutritional Sciences, University of California, Berkeley 
      94720-3104, USA.
FAU - Neese, R A
AU  - Neese RA
FAU - Turner, S
AU  - Turner S
FAU - Dare, D
AU  - Dare D
FAU - Hellerstein, M K
AU  - Hellerstein MK
LA  - eng
GR  - RR-0083/RR/NCRR NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Clin Invest
JT  - The Journal of clinical investigation
JID - 7802877
RN  - 0 (Dietary Carbohydrates)
RN  - 0 (Dietary Fats)
RN  - 0 (Insulin)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Body Weight
MH  - *Dietary Carbohydrates
MH  - Dietary Fats
MH  - Energy Intake
MH  - *Energy Metabolism
MH  - *Gluconeogenesis
MH  - Glucose/metabolism
MH  - Humans
MH  - Insulin/blood
MH  - Least-Squares Analysis
MH  - *Lipolysis
MH  - Liver/*metabolism
MH  - Models, Biological
MH  - Oxidation-Reduction
MH  - Reference Values
MH  - Regression Analysis
MH  - Time Factors
PMC - PMC185982
EDAT- 1995/12/01 00:00
MHDA- 1995/12/01 00:01
PMCR- 1995/12/01
CRDT- 1995/12/01 00:00
PHST- 1995/12/01 00:00 [pubmed]
PHST- 1995/12/01 00:01 [medline]
PHST- 1995/12/01 00:00 [entrez]
PHST- 1995/12/01 00:00 [pmc-release]
AID - 10.1172/JCI118342 [doi]
PST - ppublish
SO  - J Clin Invest. 1995 Dec;96(6):2735-43. doi: 10.1172/JCI118342.