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Diet, Insulin Sensitivity And the Brain (DISAB)

This study has been completed.
Sponsor:
ClinicalTrials.gov Identifier:
NCT01297738
First Posted: February 17, 2011
Last Update Posted: January 24, 2013
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
Collaborator:
Netherlands Organisation for Scientific Research
Information provided by (Responsible Party):
K.E.M. Koopman, Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA)
February 16, 2011
February 17, 2011
January 24, 2013
February 2011
July 2012   (Final data collection date for primary outcome measure)
Cerebral binding of [123I]FP-CIT to serotonin- and dopamine transporters and correlation with changes in in vivo and ex vivo insulin sensitivity [ Time Frame: At baseline and after 6 weeks of hypercaloric HFHS or HS diet ]
Difference in cerebral binding of the radioligand [123I]FP-CIT to serotonin- and dopamine transporters before and after dietary manipulations and correlation of cerebral dopamine and serotonin transporter binding with changes in in vivo and ex vivo insulin sensitivity.
Same as current
Complete list of historical versions of study NCT01297738 on ClinicalTrials.gov Archive Site
  • Abdominal fat mass [ Time Frame: At baseline and after 6 weeks of HFHS or HS hypercaloric diet ]
    Changes in accumulated amount of abdominal (visceral) and liver fat
  • Glucoregularoty hormones [ Time Frame: At baseline and after 6 weeks of hypercaloric HFHS- or HS diet ]
    Changes in glucoregulatory hormones such as glucagon and leptin
  • Insulin signalling pathways [ Time Frame: At baseline and after 6 weeks of hypercaloric HFHS- or HS diet ]
    Changes in insulin signalling pathways in peripheral fat and muscle tissue
Same as current
Not Provided
Not Provided
 
Diet, Insulin Sensitivity And the Brain
The Effect of Dietary Patterns and Diet Composition on Insulin Sensitivity and Cerebral Dopamine- and Serotonin Transporters
Obesity and insulin resistance may be in part explained by an altered reward system with changes in the serotonin/dopamine system. These changes might be caused by changes in dietary habits, especially by an increased intake of liquid sugar and an increase in meal frequency. The investigators hypothesize that increasing meal frequency compared to increasing meal size and when consuming a hypercaloric high-sugar diet (HS) compared to a hypercaloric high-fat-high-sugar diet (HFHS) will result in a reduction in cerebral serotonin and dopamine transporters and in a more prominent increase in insulin resistance. In addition, the investigators hypothesize that the changes in insulin sensitivity will be independent of changes in abdominal (visceral) and liver fat and that changes in insulin sensitivity due to the dietary manipulation will co-occur with changes in insulin signaling pathways in peripheral fat and muscle tissue.
Lean, healthy, young men will follow a hypercaloric HF- or HFHS diet for 6 weeks. Before and after the dietary intervention, the investigators will perform a SPECT-scan for serotonin and dopamine transporters with the radioligand [123I]FP-CIT, administered intravenously. The investigators will also perform a structural MRI for localization. Furthermore the investigators will perform a liver MRS and abdominal MRI for liver fat- and abdominal visceral fat measurement. The investigators will also perform a euglycemic, hyperinsulinemic clamp to measure insulin sensitivity and muscle- and fat biopsies to examine changes in insulin signaling pathways and fat metabolism. After the hypercaloric diet subjects will follow a hypocaloric diet until their weight is back to baseline.
Interventional
Not Provided
Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: None (Open Label)
Primary Purpose: Basic Science
  • Obesity
  • Diabetes Mellitus Type 2
  • Other: Meal size increase with HFHS
    On top of a healthy, eucaloric diet, study subjects consume a 40% calory surplus by consuming a high-fat, high-sugar liquid medical food supplement (Nutridrink®). Subjects consume the Nutridrink® with their meals, which results in an increase in meal size.
    Other Name: Nutridrink
  • Other: Meal size increase with HS
    On top of a healthy, eucaloric diet, study subjects consume a 40% calory surplus by consuming commercially available sugar-sweetened beverages. Subjects consume these sugar-sweetened beverages with their meals, which results in an increase in meal size.
  • Other: Meal frequency increase with HFHS
    On top of a healthy, eucaloric diet, study subjects consume a 40% calory surplus by consuming a high-fat, high-sugar liquid medical food supplement (Nutridrink®). Subjects consume the Nutridrink® 3 times a day in between meals, which results in an increase in meal frequency.
    Other Name: Nutridrink
  • Other: Meal frequency increase with HS
    On top of a healthy, eucaloric diet, study subjects consume a 40% calory surplus by consuming commercially available sugar-sweetened beverages. Subjects consume these sugar-sweetened beverages 3 times a day in between meals, which results in an increase in meal frequency.
  • Experimental: Meal size increase with HFHS
    On top of a healthy, eucaloric diet, study subjects consume a 40% calory surplus by consuming a liquid meal which is high in fat and sugar (Nutridrink®)
    Intervention: Other: Meal size increase with HFHS
  • Experimental: Meal size increase with HS
    On top of a healthy, eucaloric diet, study subjects consume a 40% calory surplus by consuming commercially available sugar-sweetened beverages. Subjects consume this caloric surplus with their meals, which results in an increase in meal size.
    Intervention: Other: Meal size increase with HS
  • Experimental: Meal frequency increase with HFHS
    On top of a healthy, eucaloric diet, study subjects consume a 40% calory surplus by consuming a liquid meal which has a high fat and sugar content(Nutridrink®). Subjects consume the Nutridrink 3 times a day in between meals. which results in an increase in meal frequency.
    Intervention: Other: Meal frequency increase with HFHS
  • Experimental: Meal frequency increase with HS
    On top of a healthy, eucaloric diet, study subjects consume a 40% calory surplus by consuming commercially available sugar-sweetened beverages. Subjects consume these sugar-sweetened beverages 3 times a day in between meals, which results in an increase in meal frequency.
    Intervention: Other: Meal frequency increase with HS
  • No Intervention: Control group
    Subjects will not follow any diet but their own ad-libitum, healty diet.
Koopman KE, Caan MW, Nederveen AJ, Pels A, Ackermans MT, Fliers E, la Fleur SE, Serlie MJ. Hypercaloric diets with increased meal frequency, but not meal size, increase intrahepatic triglycerides: a randomized controlled trial. Hepatology. 2014 Aug;60(2):545-53. doi: 10.1002/hep.27149. Epub 2014 May 13.

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
39
July 2012
July 2012   (Final data collection date for primary outcome measure)

Inclusion Criteria:

  • BMI 19-26 kg/m2
  • Age 18-40 years old
  • Male gender
  • Caucasian
  • Stable weight 3 months prior to start study participation

Exclusion Criteria:

  • Abnormal oral glucose tolerance test (OGTT)
  • Lipid disorders, renal disorders, thyroid disorders, elevated liver enzymes
  • Use of medication
  • Use of alcohol > 3/day
  • Use of ecstasy, amphetamines or cocaine
  • Smoking
  • History of eating disorder or psychiatric disorder
  • Any medical condition, intensive sports ( >3 times/week), shift work
Sexes Eligible for Study: Male
18 Years to 40 Years   (Adult)
Yes
Contact information is only displayed when the study is recruiting subjects
Netherlands
 
 
NCT01297738
DISAB
No
Not Provided
Not Provided
K.E.M. Koopman, Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA)
Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA)
Netherlands Organisation for Scientific Research
Study Director: Mireille JM Serlie, Dr Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA)
Principal Investigator: Karin EM Koopman, MD Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA)
Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA)
January 2013

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP