Mitochondrial Function in Pediatric Obesity

The recruitment status of this study is unknown because the information has not been verified recently.
Verified April 2012 by Massachusetts General Hospital.
Recruitment status was  Active, not recruiting
Sponsor:
Collaborators:
Lawson Wilkins Pediatric Endocrine Society
Children's Hospital Boston
Information provided by (Responsible Party):
Amy Fleischman, MD, Massachusetts General Hospital
ClinicalTrials.gov Identifier:
NCT00577174
First received: December 18, 2007
Last updated: April 27, 2012
Last verified: April 2012
  Purpose

The prevalence of pediatric obesity is increasing at an unprecedented rate. Obese children are at risk for the development of insulin resistance, relative insulin deficiency and type 2 diabetes mellitus. However, the cause of insulin resistance remains an area of scientific interest. The study of type 2 diabetes in children is limited by the lack of a non-invasive method to evaluate insulin resistance. Recent studies have suggested that mitochondrial dysfunction is associated with, and perhaps predictive of insulin resistance in adult relatives of individuals with type 2 diabetes. Mitochondria generate energy in muscle tissue through the production of ATP, and are important in the metabolism of both glucose and fat. This study evaluates a novel, non invasive, safe method for predicting insulin resistance and diabetes in children using a magnetic resonance imaging (MRI) based technique to measure mitochondrial function. We propose to investigate mitochondrial function and glucose metabolism in obese and non-obese children in early, mid and late puberty. Analyses will be conducted to investigate the presence of mitochondrial dysfunction in obese children, to evaluate the contribution of mitochondrial dysfunction to insulin resistance, and to determine the contribution of pubertal status to mitochondrial dysfunction and insulin resistance. The successful completion of this study would provide evidence to support the hypothesis that mitochondrial dysfunction plays a role in insulin resistance and diabetes in children. In addition, it would provide a new technique for the prediction of disease states and perhaps lead to the development of preventative therapeutics for insulin resistance and type 2 diabetes in children.

We hypothesize that mitochondrial dysfunction will mirror the progression of insulin resistance and precede and predict abnormal glucose metabolism in a population with pediatric obesity


Condition
Obesity
Insulin Resistance

Study Type: Observational
Study Design: Observational Model: Case Control
Official Title: Mitochondrial Function in Pediatric Obesity

Resource links provided by NLM:


Further study details as provided by Massachusetts General Hospital:

Primary Outcome Measures:
  • Determine whether children with pediatric obesity have impaired mitochondrial function based on 31P magnetic resonance spectroscopy when compared to healthy non-obese control children [ Time Frame: 4 years ] [ Designated as safety issue: No ]
  • Examine the relationship between mitochondrial function and insulin resistance in obese and non-obese children [ Time Frame: four years ] [ Designated as safety issue: No ]

Secondary Outcome Measures:
  • Determine the impact of pubertal stage, dietary intake, activity recall, inflammatory markers and metabolic markers on mitochondrial function in obese and non-obese children [ Time Frame: four years ] [ Designated as safety issue: No ]
  • Evaluate the relationship of obesity, timing of puberty and related changes in hormone levels to mitochondrial function and the development of insulin resistance and/or impaired glucose tolerance in longitudinal analyses [ Time Frame: four years ] [ Designated as safety issue: No ]

Biospecimen Retention:   Samples With DNA

Whole blood, serum, white blood cells


Estimated Enrollment: 110
Study Start Date: June 2007
Estimated Study Completion Date: October 2012
Primary Completion Date: August 2011 (Final data collection date for primary outcome measure)
Groups/Cohorts
1. Controls
Healthy children ages 8 to 18 years
2. Obese childrens
Obese children, ages 8 to 18 years

Detailed Description:

Aim I: A cross sectional study to evaluate baseline mitochondrial function in obese children compared to non-obese children. Determine whether children with pediatric obesity have impaired mitochondrial function based on 31P magnetic resonance spectroscopy when compared to healthy non-obese control children.Examine the relationship between mitochondrial function and insulin resistance in obese and non-obese children. Determine the impact of pubertal stage on mitochondrial function in obese and non-obese children.

Aim II:A prospective evaluation to determine in a longitudinal cohort study the timing and relationship of mitochondrial dysfunction to the development of insulin resistance in prepubertal/early pubertal obese children compared to prepubertal/early pubertal non-obese children. Determine in a longitudinal cohort study if obese children with mitochondrial dysfunction develop greater insulin resistance and/or impaired glucose tolerance at an earlier time point. Evaluate the relationship of obesity, timing of puberty and related changes in hormone levels to mitochondrial function and the development of insulin resistance and/or impaired glucose tolerance in longitudinal analyses.

  Eligibility

Ages Eligible for Study:   8 Years to 18 Years
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   Yes
Sampling Method:   Non-Probability Sample
Study Population

Healthy and obese children from clinical practices and the local community

Criteria

Inclusion Criteria:

  1. Girls and boys ages 8 to 18 years old
  2. Non-obese cohort: body mass index less than 75th percentile for age
  3. Obese cohort: body mass index more than 95th percentile for age

Exclusion Criteria:

  1. Underlying medical problem with potential to affect growth, pubertal development or glucose homeostasis
  2. Chronic medical therapy with glucocorticoids, growth hormone, estrogen, progesterone, testosterone, or other medications with the potential to alter growth, pubertal development or glucose homeostasis within the proceeding 6 months
  3. Personal history of diabetes
  4. Family history of diabetes in first degree relative
  5. Inability to have MRI scan performed due to metal prosthesis or implant
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT00577174

Locations
United States, Massachusetts
Massachusetts General Hospital
Boston, Massachusetts, United States, 02114
Sponsors and Collaborators
Massachusetts General Hospital
Lawson Wilkins Pediatric Endocrine Society
Children's Hospital Boston
Investigators
Principal Investigator: Amy D Fleischman, MD, MMSc Massachusetts General Hospital
  More Information

Publications:
Responsible Party: Amy Fleischman, MD, Assistant Professor, Massachusetts General Hospital
ClinicalTrials.gov Identifier: NCT00577174     History of Changes
Other Study ID Numbers: 1K23DK080658, 2006p001067, Partners IRB, 575, MIT IRB
Study First Received: December 18, 2007
Last Updated: April 27, 2012
Health Authority: United States: Institutional Review Board

Keywords provided by Massachusetts General Hospital:
Children
Obesity
Insulin resistance
Diabetes
Mitochondrial Function

Additional relevant MeSH terms:
Insulin Resistance
Obesity
Hyperinsulinism
Glucose Metabolism Disorders
Metabolic Diseases
Overnutrition
Nutrition Disorders
Overweight
Body Weight
Signs and Symptoms

ClinicalTrials.gov processed this record on July 20, 2014