There has been a recent increase in incidence of obesity and its associated morbidities, including T2 DM, hypertension and hepatic steatosis. Hepatic steatosis is a precursor to non-alcoholic steatohepatitis, cirrhosis and end-stage liver disease. The 1st reported case of pediatric hepatic steatosis was in 1980 and it is now affects 30-77% of overweight children. In addition to its association with obesity, hepatic steatosis has been associated with the metabolic syndrome, insulin resistance, and post-prandial hyperglycemia. Current treatment of hepatic steatosis includes weight loss with a hypocaloric low fat diet. Given the association with insulin resistance and post-prandial hyperglycemia, adult patients with hepatic steatosis that does not respond to weight loss are placed on insulin sensitizing drugs. We hypothesize that weight loss with a diet designed to decrease insulin resistance and post-prandial hyperglycemia, a low glycemic load diet, will provide a safe and effective way to decrease hepatic fat content in the pediatric population. This hypothesis will be tested with a randomized control trial comparing the effect of a low fat diet with a low glycemic load diet.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
NONE
Enrollment
40
Outpatient behavioral counseling
Outpatient behavioral counseling
Children's Hospital
Boston, Massachusetts, United States
percent liver fat as determined by nMR spectroscopy
Time frame: 6 months
hepatic steatosis as measured by T1 weighted MRI images
Time frame: 6 monhts
visceral fat
Time frame: 6 months
liver function tests
Time frame: 6 months
measures of oxidative stress
Time frame: 6 months
measures of chronic inflammation
Time frame: 6 months
insulin resistance
Time frame: 6 months
serum lipids
Time frame: 6 months
blood pressure
Time frame: 6 months
insulin secretion
Time frame: baseline
measures of glucose tolerance
Time frame: 6 months
adiponectin
Time frame: 6 months
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