Is Fructose Linked to Adiposity in Babies?

NCT ID: NCT01262781

Last Updated: 2014-04-10

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

Get a concise snapshot of the trial, including recruitment status, study phase, enrollment targets, and key timeline milestones.

Recruitment Status

COMPLETED

Total Enrollment

40 participants

Study Classification

OBSERVATIONAL

Study Start Date

2011-01-31

Study Completion Date

2013-01-31

Brief Summary

Review the sponsor-provided synopsis that highlights what the study is about and why it is being conducted.

The obesity epidemic has reached down into the infant and toddler age group. Dietary indiscretion during pregnancy, particularly in our current food environment, is a major risk factor for both gestational diabetes and neonatal macrosomia (\>4kg newborns), which is itself a risk factor for obesity and metabolic syndrome in the offspring, possibly even during childhood. Temporal increases in fructose consumption in the last two decades coincide with temporal increases weight gain during pregnancy and with increased birth weight, including a higher prevalence of macrosomic newborns. Our central hypothesis is that higher fructose consumption during pregnancy is a risk factor for infant obesity and metabolic syndrome.

Detailed Description

Dive into the extended narrative that explains the scientific background, objectives, and procedures in greater depth.

The "fetal origins hypothesis" suggests that an individual's risk for obesity and metabolic disorders begins in utero; that fetal or early postnatal exposure to environmental factors, such as maternal nutrition or endocrine disrupting chemicals, adversely influences early development and results in permanent changes affecting energy storage and expenditure.

Most studies on "fetal origins" of obesity in the offspring have focused on maternal high-fat diets; yet dietary fat consumption has not changed appreciably in the last two decades. One chemical exposure in both pregnant mothers and newborns that has been steadily increasing worldwide is fructose. Although ostensibly a carbohydrate, fructose is a potent lipogenic substrate, and in the hypercaloric state, as much as 30% of an ingested fructose load undergoes de novo lipogenesis to form triglyceride thus the effects of high-fat and high-fructose diets in terms of physiology and outcome are comparable. Substituting sucrose (fructose + glucose) for glucose alone increases visceral adiposity, insulin resistance, and dyslipidemia in adult animals and humans. For humans, fructose is ubiquitous in the food environment, especially for pregnant mothers, who are often counseled to drink juice during pregnancy, as it is deemed to be healthier than soda. The effects of fructose consumption during pregnancy on infant birth weight and adiposity has not yet been studied.

Conditions

See the medical conditions and disease areas that this research is targeting or investigating.

Obesity Metabolic Syndrome

Study Design

Understand how the trial is structured, including allocation methods, masking strategies, primary purpose, and other design elements.

Observational Model Type

COHORT

Study Time Perspective

PROSPECTIVE

Eligibility Criteria

Check the participation requirements, including inclusion and exclusion rules, age limits, and whether healthy volunteers are accepted.

Inclusion Criteria

* Agreement to participate in all measurements
* Plans to remain in the area through delivery
* Ability to understand and give informed consent in either English or Spanish.

Exclusion Criteria

* Presence of diabetes prior to the index pregnancy
* Presence of gestational diabetes during a previous pregnancy
* Presence of diabetes or of other chronic metabolic disease such as cardiovascular disease, active thyroid disease, liver disease, pulmonary or psychiatric disorders, HIV
* Any disorder requiring diet therapy (i.e., renal insufficiency)
* Multiple gestation
* Prior history of intrauterine growth retardation
* Use of substances known to cause intrauterine growth retardation (e.g., smoking or drug use). -
* Once recruited, any ultrasonographic evidence of intrauterine growth retardation during the course of the pregnancy would also lead to exclusion.
Minimum Eligible Age

18 Years

Maximum Eligible Age

40 Years

Eligible Sex

FEMALE

Accepts Healthy Volunteers

Yes

Sponsors

Meet the organizations funding or collaborating on the study and learn about their roles.

San Francisco General Hospital

OTHER

Sponsor Role collaborator

University of California, San Francisco

OTHER

Sponsor Role lead

Responsible Party

Identify the individual or organization who holds primary responsibility for the study information submitted to regulators.

Responsibility Role SPONSOR

Principal Investigators

Learn about the lead researchers overseeing the trial and their institutional affiliations.

Robert Lustig, MD

Role: PRINCIPAL_INVESTIGATOR

University of California, San Francisco

Anjali Jain, MD

Role: STUDY_DIRECTOR

University of California, San Francisco

Locations

Explore where the study is taking place and check the recruitment status at each participating site.

San Francisco General Hospital

San Francisco, California, United States

Site Status

Countries

Review the countries where the study has at least one active or historical site.

United States

Other Identifiers

Review additional registry numbers or institutional identifiers associated with this trial.

SFGH 6281

Identifier Type: -

Identifier Source: org_study_id

More Related Trials

Additional clinical trials that may be relevant based on similarity analysis.

Fructose Intestinal Gluconeogenesis
NCT07209202 NOT_YET_RECRUITING NA
High Fructose Corn Syrup
NCT02018237 COMPLETED NA