Study Results
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Basic Information
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COMPLETED
NA
24 participants
INTERVENTIONAL
2007-09-01
2013-12-31
Brief Summary
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Detailed Description
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Using detailed in vivo, serial measurements of fuel metabolism (GC/MS and NMR) fatty acid metabolism will be measured in the liver and periphery. This will be the first study in which these two methodologies are used together to assess both glucose and fatty acid metabolism in the same subjects. Subjects will be tested before and after a dietary weight-loss intervention producing 6% body weight loss over 5 months.
The specific aims are as follows:
AIM 1: Determine the contribution of peripheral and dietary fat to liver-TG in Hispanics and African Americans with metabolic syndrome.
Hypothesis: De novo lipogenesis will contribute to liver-TG in greater quantities compared to African Americans.
AIM 2: Determine the effects of low-CHO and low-fat diets on liver fat regression.
Hypothesis: Compared to a low-fat diet, a low-CHO diet will markedly decrease markers of inflammation coincident with greater improvements in insulin sensitivity as assessed by an intravenous glucose tolerance test.
Conditions
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Study Design
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RANDOMIZED
FACTORIAL
BASIC_SCIENCE
NONE
Study Groups
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Hispanic subjects
Subjects will identify as Hispanic ethnicity.
Low-fat diet
The subject will consume a diet that is calorically restricted to cause at least a 6% body weight loss over 4 months. Fat will make up less than 30% of dietary energy.
Low-carbohydrate diet
The diet will be restricted in energy to cause at least a 6% loss of body weight over a 4 month period. Carbohydrate will provide less than 40% of total dietary energy.
African American subjects
Subjects will self-identify as African American in origin.
Low-fat diet
The subject will consume a diet that is calorically restricted to cause at least a 6% body weight loss over 4 months. Fat will make up less than 30% of dietary energy.
Low-carbohydrate diet
The diet will be restricted in energy to cause at least a 6% loss of body weight over a 4 month period. Carbohydrate will provide less than 40% of total dietary energy.
Interventions
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Low-fat diet
The subject will consume a diet that is calorically restricted to cause at least a 6% body weight loss over 4 months. Fat will make up less than 30% of dietary energy.
Low-carbohydrate diet
The diet will be restricted in energy to cause at least a 6% loss of body weight over a 4 month period. Carbohydrate will provide less than 40% of total dietary energy.
Eligibility Criteria
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Inclusion Criteria
* African American or Hispanic
* Nondiabetic
* Men or women
* Smokers and nonsmokers
* Pre- and post-menopausal (+/- HRT)
* Stable body weight
* Age 20-65 years
* BMI between 25-45 kg/m2
Exclusion Criteria
* Ethanol intake: males \> 140 g/week, females \> 70 g/week
* Chronic hepatitis B or chronic hepatitis C
* Hemochromatosis or Wilson's Disease
* Autoimmune hepatitis or primary biliary cirrhosis
20 Years
65 Years
ALL
No
Sponsors
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University of Texas Southwestern Medical Center
OTHER
Responsible Party
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Elizabeth Parks
Associate Professor
Principal Investigators
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Elizabeth J Parks, PhD
Role: PRINCIPAL_INVESTIGATOR
UTSW Medical Center
Locations
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Center for Human Nutrition
Dallas, Texas, United States
Countries
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References
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Shetty S, Ramos-Roman MA, Cho YR, Brown J, Plutzky J, Muise ES, Horton JD, Scherer PE, Parks EJ. Enhanced fatty acid flux triggered by adiponectin overexpression. Endocrinology. 2012 Jan;153(1):113-22. doi: 10.1210/en.2011-1339. Epub 2011 Nov 1.
Ramos-Roman MA, Sweetman L, Valdez MJ, Parks EJ. Postprandial changes in plasma acylcarnitine concentrations as markers of fatty acid flux in overweight and obesity. Metabolism. 2012 Feb;61(2):202-12. doi: 10.1016/j.metabol.2011.06.008. Epub 2011 Aug 5.
Sunny NE, Parks EJ, Browning JD, Burgess SC. Excessive hepatic mitochondrial TCA cycle and gluconeogenesis in humans with nonalcoholic fatty liver disease. Cell Metab. 2011 Dec 7;14(6):804-10. doi: 10.1016/j.cmet.2011.11.004.
Satapati S, Kucejova B, Duarte JA, Fletcher JA, Reynolds L, Sunny NE, He T, Nair LA, Livingston KA, Fu X, Merritt ME, Sherry AD, Malloy CR, Shelton JM, Lambert J, Parks EJ, Corbin I, Magnuson MA, Browning JD, Burgess SC. Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver. J Clin Invest. 2016 Apr 1;126(4):1605. doi: 10.1172/JCI86695. Epub 2016 Apr 1. No abstract available.
Lee JJ, Lambert JE, Hovhannisyan Y, Ramos-Roman MA, Trombold JR, Wagner DA, Parks EJ. Palmitoleic acid is elevated in fatty liver disease and reflects hepatic lipogenesis. Am J Clin Nutr. 2015 Jan;101(1):34-43. doi: 10.3945/ajcn.114.092262. Epub 2014 Nov 19.
Lambert JE, Parks EJ. Getting the label in: practical research strategies for tracing dietary fat. Int J Obes Suppl. 2012 Dec;2(Suppl 2):S43-50. doi: 10.1038/ijosup.2012.22. Epub 2012 Dec 11.
Lambert JE, Ramos-Roman MA, Valdez MJ, Browning JD, Rogers T, Parks EJ. Weight loss in MASLD restores the balance of liver fatty acid sources. J Clin Invest. 2025 May 1;135(9):e174233. doi: 10.1172/JCI174233. eCollection 2025 May 1.
Ramos-Roman MA, Lapidot SA, Phair RD, Parks EJ. Insulin activation of plasma nonesterified fatty acid uptake in metabolic syndrome. Arterioscler Thromb Vasc Biol. 2012 Aug;32(8):1799-808. doi: 10.1161/ATVBAHA.112.250019. Epub 2012 Jun 21.
Other Identifiers
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5RL-1DK081187
Identifier Type: -
Identifier Source: org_study_id
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