PMID- 20714332
OWN - NLM
STAT- MEDLINE
DCOM- 20110630
LR  - 20220408
IS  - 1476-5497 (Electronic)
IS  - 0307-0565 (Linking)
VI  - 35
IP  - 4
DP  - 2011 Apr
TI  - A free-choice high-fat high-sugar diet induces glucose intolerance and insulin 
      unresponsiveness to a glucose load not explained by obesity.
PG  - 595-604
LID - 10.1038/ijo.2010.164 [doi]
AB  - OBJECTIVES: In diet-induced obesity, it is not clear whether impaired glucose 
      metabolism is caused directly by the diet, or indirectly via obesity. This study 
      examined the effects of different free-choice, high-caloric, obesity-inducing 
      diets on glucose metabolism. In these free-choice diets, saturated fat and/or a 
      30% sugar solution are provided in an addition to normal chow pellets. METHOD: In 
      the first experiment, male rats received a free-choice high-fat high-sugar 
      (HFHS), free-choice high-fat (HF) or a chow diet. In a second experiment, male 
      rats received a free-choice high-sugar (HS) diet or chow diet. For both 
      experiments, after weeks 1 and 4, an intravenous glucose tolerance test was 
      performed. RESULTS: Both the HFHS and HF diets resulted in obesity with 
      comparable plasma concentrations of free fatty acids. Interestingly, the HF diet 
      did not affect glucose metabolism, whereas the HFHS diet resulted in 
      hyperglycemia, hyperinsulinemia and in glucose intolerance because of a 
      diminished insulin response. Moreover, adiposity in rats on the HF diet 
      correlated positively with the insulin response to the glucose load, whereas 
      adiposity in rats on the HFHS diet showed a negative correlation. In addition, 
      total caloric intake did not explain differences in glucose tolerance. To test 
      whether sugar itself was crucial, we next performed a similar experiment in rats 
      on the HS diet. Rats consumed three times as much sugar when compared with rats 
      on the HFHS diet, which resulted in obesity with basal hyperinsulinemia. Glucose 
      tolerance, however, was not affected. CONCLUSION: Together, these results suggest 
      that not only obesity or total caloric intake, but the diet content also is 
      crucial for the glucose intolerance that we observed in rats on the HFHS diet.
FAU - la Fleur, S E
AU  - la Fleur SE
AD  - Department of Neuroscience and Pharmacology, Rudolf Magnus Institute of 
      Neuroscience, University Medical Center Utrecht, Utrecht, The Netherlands. 
      s.e.lafleur@amc.uva.nl
FAU - Luijendijk, M C M
AU  - Luijendijk MC
FAU - van Rozen, A J
AU  - van Rozen AJ
FAU - Kalsbeek, A
AU  - Kalsbeek A
FAU - Adan, R A H
AU  - Adan RA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100817
PL  - England
TA  - Int J Obes (Lond)
JT  - International journal of obesity (2005)
JID - 101256108
RN  - 0 (Blood Glucose)
RN  - 0 (Dietary Fats)
RN  - 0 (Dietary Sucrose)
RN  - 0 (Insulin)
SB  - IM
MH  - Animals
MH  - Blood Glucose/*metabolism
MH  - Dietary Fats/administration & dosage/*adverse effects/blood
MH  - Dietary Sucrose/administration & dosage/*adverse effects/blood
MH  - Energy Intake
MH  - Glucose Intolerance/*etiology
MH  - Glucose Tolerance Test
MH  - Insulin/metabolism
MH  - Male
MH  - Obesity/blood/*complications
MH  - Rats
MH  - Rats, Wistar
EDAT- 2010/08/18 06:00
MHDA- 2011/07/01 06:00
CRDT- 2010/08/18 06:00
PHST- 2010/08/18 06:00 [entrez]
PHST- 2010/08/18 06:00 [pubmed]
PHST- 2011/07/01 06:00 [medline]
AID - ijo2010164 [pii]
AID - 10.1038/ijo.2010.164 [doi]
PST - ppublish
SO  - Int J Obes (Lond). 2011 Apr;35(4):595-604. doi: 10.1038/ijo.2010.164. Epub 2010 
      Aug 17.