NCT00342303

Activity of Essential Fatty Acid Elongation/Desaturation Pathway During Early Life in Human Infants, In Vivo

Completed Last updated 2 July 2017

What this trial tests

trial in Fatty Acid Metabolism in 110 participants. Completed in 13 July 2010.

Timeline

8 June 1993

13 July 2010

Quick facts

Lead sponsor	National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Status	Completed
Study type	OBSERVATIONAL
Enrollment	110
Start date	8 June 1993
Estimated completion	13 July 2010
Sites	2 locations across Chile

Conditions studied

• Fatty Acid Metabolism — all drugs for Fatty Acid Metabolism →

Sponsor

National Institute on Alcohol Abuse and Alcoholism (NIAAA)

Who can join

Eligibility, any sex, with Fatty Acid Metabolism. Patients with the condition only — healthy volunteers not accepted.

Sponsor's own description

We will test the following hypotheses:

1. The activity of the desaturating/elongating enzymes assessed by the in vivo conversion of deuterated a-linolenic and linoleic acids to DHA and AA, respectively, will be related to the duration of gestation and to postnatal age.
2. Dietary w-3 and w-6 LCPUFAs in human milk or DHA and AA supplemented formula will inhibit the desaturation/elongation of deuterated a-linolenic and linoleic acids demonstrating in vivo inhibition of the metabolic pathway by respective products.

Present evidence suggests that the parent essential fatty acids (EFA), linoleic acid (18:2 w-6) and a-linolenic acids (18:3 w-3) are insufficient to fully satisfy EFA nutrition during early life in the human. A possible need for long chain (LC, longer than 18 C chain length) EFAs in the human is suggested by the accretion rates of elongated and desaturated products in the developing fetus; the altered plasma and red cell fatty acid patterns, and the abnormal visual function observed in infants receiving solely the parent EFAs; and by the relatively high concentration of LC EFAs in human milk. Most milk formula, as compared to human milk, are lower in oleic acid, higher in linoleic, have little a-linolenic acid and virtually no LC w-3 or w-6 polyunsaturated FA (LC PUFA). This study will evaluate the capacity of human infants to form w-3 and w-6 LCPUFAs from the parent EFAs as affected by developmental stage and dietary EFA supply. The precursors will be labeled with deuterium and the products analyzed by gas chromatography / mass spectrometry GC/MS. The main products of the desaturation / elongation pathway are docosahexaenoic (DHA) and arachidonic (AA) acids for the w-3 and w-6 series, respectively. Infants will be fed human milk or formulas with or without supplemental LCPUFAs as part of a study to evaluate the effect of EFAs on CNS functional development. Infants included in this study of the effect of developmental stage on EFA desaturation/elongation will be 2-5 days of age (before any fat is administered enterally or parenterally) and 28, 32, 36 or 40 weeks gestation. In addition, infants born at 28 and 40 weeks gestation will be studied 2 and 6 weeks postnatally after dietary fat has been provided for at least 7 days and energy intake is sufficient to assure growth. To evaluate the effect of dietary EFA on DHA and AA formation we will assess elongation/ desaturation in infants receiving 3 diets: human milk (which contains w-3 and w-6 LCPUFAs); cow milk based formula providing 18:2 w-6 and 18:3 w-3 but no LCPUFAs; or formula supplemented with added LCPUFAs (DHA and AA). This study should provide new information on the effects of developmental stage and w-3 and w-6 LCPUFA supply in determining the activity of EFA elongation/desaturation in the human. This knowledge may help in improving early neonatal nutritional practices to assure meeting the EFA needs of the developing CNS.

Publications & conference data

No peer-reviewed publications indexed yet for this trial. Completed trials usually publish results within 12-18 months.