n-3 Fatty Acid Infusion and Type 2 Diabetes

This study has been completed.
Sponsor:
Collaborators:
Norwegian University of Science and Technology
Norwegian Foundation for Health and Rehabilitation
Novo Nordisk A/S
Norwegian Diabetes Association
Information provided by (Responsible Party):
St. Olavs Hospital
ClinicalTrials.gov Identifier:
NCT00829569
First received: January 26, 2009
Last updated: November 3, 2011
Last verified: November 2011

January 26, 2009
November 3, 2011
January 2004
May 2004   (final data collection date for primary outcome measure)
insulin sensitivity [ Time Frame: 4 hours ] [ Designated as safety issue: No ]
insulin sensitivity [ Time Frame: 4 hours ] [ Designated as safety issue: Yes ]
Complete list of historical versions of study NCT00829569 on ClinicalTrials.gov Archive Site
  • n-3 fatty acid distribution [ Time Frame: 4 hours ] [ Designated as safety issue: No ]
  • insulin secretion [ Time Frame: 4 hours ] [ Designated as safety issue: No ]
  • energy metabolism [ Time Frame: 4 hours ] [ Designated as safety issue: No ]
  • oxidative stress [ Time Frame: 4 hours ] [ Designated as safety issue: No ]
  • n-3 fatty acid distribution [ Time Frame: 4 hours ] [ Designated as safety issue: Yes ]
  • insulin secretion [ Time Frame: 4 hours ] [ Designated as safety issue: Yes ]
  • energy metabolism [ Time Frame: 4 hours ] [ Designated as safety issue: Yes ]
  • oxidative stress [ Time Frame: 4 hours ] [ Designated as safety issue: Yes ]
Not Provided
Not Provided
 
n-3 Fatty Acid Infusion and Type 2 Diabetes
Effects of Marine n-3 Fatty Acid Infusion on Insulin Sensitivity and Insulin Secretion in Type 2 Diabetes

The purpose of this experimental study is to investigate whether an acute lipid infusion added marine n-3 fatty acids produces effects on insulin sensitivity in subjects with type 2 diabetes, when compared with an acute lipid infusion without marine n-3 fatty acids. Furthermore other effects on intermediary metabolism are tested for.

Evidence indicates that n-3 fatty acids exert several beneficial effects. However, the effects of marine n-3 fatty acids on intermediary metabolism have not been completely elucidated. In a previous study of a high intake of marine n-3 fatty acids during 9 wk we demonstrated reduced insulin sensitivity and altered proportion of carbohydrate vs. fat oxidation in subjects with type 2 diabetes. These results question the use of high doses of n-3 supplements in type 2 diabetes. It is not known to what extent such effects in type 2 diabetes can be reproduced by intravenous administration of n-3 fatty acids and/or whether short term intravenous administration has other effects.

Interventional
Not Provided
Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Crossover Assignment
Masking: Double Blind (Subject, Caregiver, Investigator)
Primary Purpose: Treatment
Type 2 Diabetes
Dietary Supplement: Intralipid +/- Omegaven

Intralipid®: the 500 ml 20% Intralipid will be infused during a hyperinsulinemic clamp. Infusion rate will increase from 50 to 100 ml/hour the first 30 min and then continue at 100 ml/hour for the next 210 min, infusion duration 240 min (4 hours) in all.

Intralipid® + Omegaven®: In the 500 ml 20% Intralipid 100 ml will be replaced by 100 ml 10% Omegaven and infused during the hyperinsulinemic clamp as described for Intralipid only. Heparin (0.4 U/kg/min) will be added to both lipid emulsions.

Content of marine n-3 fatty acids in 100 ml Omegaven will be 1.25-2.82 g EPA and 1.44-3.09 g DHA (seasoning variations of n-3 fatty acids in fish oil).

Other Names:
  • Fresenius Kabi, ATC main group B05B A 02
  • Intralipid Vnr 42 79 55
  • Omegaven Vnr 55 25 54
Experimental: Intralipid with/without Omegaven
Lipid infusion with/without marine n-3 fatty acids
Intervention: Dietary Supplement: Intralipid +/- Omegaven
Mostad IL, Bjerve KS, Basu S, Sutton P, Frayn KN, Grill V. Addition of n-3 fatty acids to a 4-hour lipid infusion does not affect insulin sensitivity, insulin secretion, or markers of oxidative stress in subjects with type 2 diabetes mellitus. Metabolism. 2009 Dec;58(12):1753-61. Epub 2009 Aug 27.

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
11
October 2008
May 2004   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Type 2 diabetes defined by clinical criteria and by absence of antibodies to glutamic acid decarboxylase.
  • HbA1c 5,5 - 8,5 %
  • Blood pressure ≤ 170 mm Hg systolic and/or ≤ 105 mm Hg diastolic

Exclusion Criteria:

  • insulin treatment
  • hypertriglyceridemia (> 2,1 mmol/l TG)
  • proliferative retinopathy, renal insufficiency (Se-Creatinine > 150 μmol/l)
  • alcoholism, congestive heart failure or other serious diseases affecting the possibility of the subject to participate
  • supplement with fish oil or marine n-3 fatty acids during the last 6 months before baseline
  • Dicumarol treatment
  • allergy to soya, fish or egg
  • pregnancy or lactation
  • smoking
Both
30 Years to 75 Years
No
Contact information is only displayed when the study is recruiting subjects
Norway
 
NCT00829569
4.2003.169, 03-14463, 15759, 03/05008
No
St. Olavs Hospital
St. Olavs Hospital
  • Norwegian University of Science and Technology
  • Norwegian Foundation for Health and Rehabilitation
  • Novo Nordisk A/S
  • Norwegian Diabetes Association
Principal Investigator: Valdemar Grill, M.D. St. Olavs Hospital, NTNU
St. Olavs Hospital
November 2011

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