NAFLDNCT03783195
Genetic-specific Effects of Fructose on Liver Lipogenesis
A study testing Sugar drink in people with NAFLD, run by University of North Carolina, Chapel Hill at 1 site in United States.
Trial summary
The primary goal of this study is to identify a set of genotypes that increase the risk for nonalcoholic fatty liver disease (NAFLD) and predispose individuals to increased de novo lipogenesis (DNL) and liver fat accumulation when exposed to fructose intake. Read more about this study
- Who is it for?
- Ages 12 to 40 yearsHealthy volunteers can take part
- Conditions the study is for
- NAFLD
- What is being tested?
- Sugar drink
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 15 participants
- Where
- 1 siteUnited States
- Study dates
- 25 Jan 2019to 25 Apr 2023
- Phase
- Interventional
- Are there results?
- Yes, posted in the registrySummary in the doctors' view
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 12 to 40 years
- All sexes
- Healthy volunteers accepted
- Child, Adult
Who may be able to join
- Subjects 12 - 40 years
- No history of alcohol abuse (> 7 drinks per week)
- History of fructose intake of < 14 drinks per week
- Caucasian ethnicity
- BMI > 25kg/m² - 32kg/m² or 85th -99th percentile but otherwise healthy
Who cannot join
- ages < 12 and > 40 years
- Pregnant/lactating
- known alcohol abuse or fructose intake > 14 drinks per week
- not of Caucasian ethnicity
- glucose levels > 100 mg/dL if fasting, > 140mg/dL if within 2 hours post meal and > 200 mg/dL if random sample
- taking anti-hypertensive, anti-diabetic, uric acid and/or lipid-lowering medications
Show all 9Show fewer
- known diagnosis of diabetes, fructose intolerance, chronic kidney disease, NAFLD or any liver-related disease, hypertriglyceridemia, polycystic ovary syndrome, hypothyroidism, obstructive sleep apnea, hypopituitarism and hypogonadism
- BMI < 25kg/m² or > 32 kg/m² or < 85th or > 99th percentile
- Liver fat fraction >5% as per baseline MRI scan
Trial locations and contacts
1 site in 1 country.
United States1 site
UNC Nutrition Research Institute
Kannapolis, North Carolina, 28081
About this study
The primary goal of this study is to identify a set of genotypes that increase the risk for nonalcoholic fatty liver disease (NAFLD) and predispose individuals to increased de novo lipogenesis (DNL) and liver fat accumulation when exposed to fructose intake. The proposed goal will be achieved through the completion of following aims:
- To determine the impact of prolonged exposure of fructose on hepatic lipid accumulation in Caucasian individuals with high and low genetic risk for NAFLD,
- to determine the impact of acute exposure of fructose on hepatic DNL, and
- to determine the relationship between markers of DNL, liver fat accumulation and serum concentrations of lipids, uric acid and liver function markers before and after the fructose challenge.
Read the detailed description
BACKGROUND AND RATIONALE Non-alcoholic fatty liver disease (NAFLD) is characterized by fat accumulation in liver cells not caused by alcohol. A leading cause of chronic liver disease in the US, NAFLD represents a group of disorders including steatosis, nonalcoholic steatohepatitis with fibrosis. It has substantially risen in prevalence over the last two decades with the estimated prevalence being 20% among US adults and 25% in young adults (18-39 years). Over 64 million individuals are believed to have NAFLD with annual medical costs rising to more $100 billion. More common in individuals who are obese or diabetic and/or have metabolic syndrome, NAFLD has been associated with increased cirrhosis, liver-related mortality and hepatocellular carcinoma.
Both genetic and environmental, including nutritional, factors contribute to the onset and progression of NAFLD. Increased consumption of sugar-sweetened, fructose-rich beverages has been linked to NAFLD. Fructose, commonly found in soft drinks, fruit juices and energy drinks, affects many metabolic processes, foremost being an increase in fat accumulation in the liver and hence, NAFLD. Genome-wide and candidate gene studies have identified several genes associated with NAFLD. However, none of these studies have shown the cumulative effects of single nucleotide polymorphisms (SNPs) on changes in liver fat when exposed to fructose. The results from this study can be extrapolated to larger cohorts and other ethnicities and are therefore, expected to lay the foundation for developing personalized nutritional plans.
- Conditions
- NAFLD
- Being tested
- Sugar drink
- Keywords
- Glucose, Fructose, Fatty-liver, Polymorphisms, Imaging, Fibroscan
- Medical subject headings
- Non-alcoholic Fatty Liver Disease, Fatty Liver
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Sugar drinkOther
A sugar drink made with 1.2 g/kg body weight of added sugar( 0.75g/kg body weight of fructose + 0.45g/kg body weight of glucose) and 24oz water
| Study group | Role | What they receive |
|---|---|---|
| High GRS group | Experimental | This group consists of individuals who are in the highest quartile of the genetic risk score (GRS) and will ingest one sugar drink (equal to 2 soft drinks) per day for 3 weeks. The GRS is computed by adding the number of alleles that increase the risk for liver lipogenesis or fatty liver. Receives: Other: Sugar drink |
| Low GRS group | Experimental | This groups consists of individuals who are in the lowest quartile of the genetic risk score (GRS) and will ingest one sugar drink (equal to 2 soft drinks) per day for 3 weeks. The GRS is computed by adding the number of alleles that increase the risk for liver lipogenesis or fatty liver. Receives: Other: Sugar drink |
What is being measured
The primary outcome is the main question the study is designed to answer.
Mean Change in Liver Fat Content Based on Elastography
Elastography (Fibroscan) will be used to measure changes in liver fat.
Measured: between week 0 (Baseline) and week 3
Mean Percent Change in Liver Fat Content Based on MRI
Magnetic resonance imaging (MRI) will be used to measure changes in liver fat (% change in fat fraction).
Measured: between week 0 (Baseline) and week 3
Mean Change in Serum Concentrations of Very Low Density Lipoprotein-triglycerides (VLDL-TG)
VLDL-TG measurement in serum (mg/dl) at week 0 and Week 3.
Measured: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Very Low Density Lipoprotein-triglycerides (VLDL-TG)
Area under curve (AUC) (mg*hr/dl) of serum VLDL-TG for baseline and 3hr time points at week 0 and Week 3.
Measured: between week 0 (Baseline) and week 3
Secondary outcomes (18)
Mean Change in Serum Concentrations of Triglycerides
Fasting concentrations of serum triglycerides (mg/dl) will be measured at week 0 and 3
Measured: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Triglycerides
Area under curve (AUC) (mg*hr/dl) of serum VLDL-TG for baseline and 3hr time points at week 0 and Week 3.
Measured: between week 0 (Baseline) and week 3
Mean Change in Serum Concentrations of HDL Cholesterol
Fasting concentrations of serum HDL cholesterol (mg/dl) will be measured at week 0 and week 3.
Measured: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum HDL Cholesterol
Area under curve (AUC) (mg*hr/dl) of serum HDL cholesterol for baseline and 3hr time points at week 0 and Week 3.
Measured: between week 0 (baseline) and week 3
Mean Change in Serum Concentrations of LDL Cholesterol
Fasting concentrations of serum LDL cholesterol (mg/dl) will be measured.at week 0 and week 3
Measured: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum LDL Cholesterol
Area under curve (AUC) (mg*hr/dl) of serum LDL cholesterol for baseline and 3hr time points at week 0 and Week 3.
Measured: Week 0 (baseline) and week 3
Mean Change in Serum Concentrations of Total Cholesterol
Fasting serum concentrations of total cholesterol (mg/dl) will be measured at week 0 and week 3
Measured: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Total Cholesterol
Area under curve (AUC) (mg*hr/dl) of serum total cholesterol for baseline and 3hr time points at week 0 and Week 3.
Measured: week 0 and week 3
Mean Changes in Serum Concentrations of Uric Acid
Fasting concentrations of serum uric acid (ng/ml) will be measured at week 0 and week 3
Measured: between week 0 (Baseline) and week 3
Mean Changes in AUC of Serum Uric Acid
Area under curve (AUC) (ng*hr/ml) of serum uric acid for baseline and 3hr time points at week 0 and Week 3.
Measured: between week 0 (Baseline) and week 3
Mean Change in Serum Concentrations of Liver Function Marker (Alanine Transaminase- ALT).
Fasting concentrations of serum ALT (nmol) will be measured at week 0 and week 3
Measured: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Alanine Transaminase (ALT)
Area under curve (AUC) (nmol/hr) of serum ALT for baseline and 3hr time points at week 0 and Week 3.
Measured: between week 0 (Baseline) and week 3
Mean Change in Serum Concentrations of Liver Function Marker (Aspartate Transaminase-AST).
Serum concentrations of serum AST will be measured at week 0 and week 3
Measured: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Aspartate Transaminase (AST).
Area under curve (AUC) (IU*hr/L) of serum AST for baseline and 3hr time points at week 0 and Week 3.
Measured: between week 0 (Baseline) and week 3
Mean Change in Serum Concentrations of Liver Function Marker (Alkaline Phosphatase-ALP)
Fasting concentrations of serum ALP (nmol) will be measured at week 0 and week3
Measured: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Alkaline Phosphatase (ALP)
Area under curve (AUC) (nmol/hr) of serum ALP for baseline and 3hr time points at week 0 and Week 3.
Measured: between week 0 (Baseline) and week 3
Mean Change in Serum Concentrations of Liver Function Marker (Gamma Glutamyl Transpeptidase-GGT)
Serum concentrations of GGT will be measured at week 0 and week 3
Measured: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Gamma Glutamyl Transpeptidase (GGT)
Area under curve (AUC) (IU*hr/dl) of serum VLDL-TG for baseline and 3hr time points at week 0 and Week 3.
Measured: between week 0 (Baseline) and week 3
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted20 Dec 2018
- Study start25 Jan 2019
- Primary completion25 Apr 2023
- Study completion25 Apr 2023
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Posted resultsParticipant flow, outcome measures and adverse events reported by the sponsor.
- Publications (27)Papers the sponsor has linked to this study.
- Other trials for NAFLDStudies of the same condition, open and under way.
- More trials run by University of North Carolina, Chapel HillThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Model description
- Participants are assigned to high genetic risk score group in parallel to low genetic risk score group
- Masking
- None (open label)
- Enrolment
- 15 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of North Carolina, Chapel Hill
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Saroja Voruganti, Principal investigator, University of North Carolina, Chapel Hill
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03783195
- Sponsor's protocol ID
- 17-3348
- Other IDs
- P30DK056336-16S1
- Status last verified
- May 2023
- First submitted
- 17 Dec 2018
- Last updated
- 23 Oct 2024
- Results posted
- Yes, on ClinicalTrials.gov
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Yes: Deidentified individual data that supports the results will be shared beginning 9 to 36 months following publication provided the investigator who proposes to use the data has approval from an Institutional Review Board (IRB), Independent Ethics Committee (IEC), or Research Ethics Board (REB), as applicable, and executes a data use/sharing agreement with University of North Carolina (UNC).
Publications
Younossi ZM, Blissett D, Blissett R, Henry L, Stepanova M, Younossi Y, Racila A, Hunt S, Beckerman R. The economic and clinical burden of nonalcoholic fatty liver disease in the United States and Europe. Hepatology. 2016 Nov;64(5):1577-1586. doi: 10.1002/hep.28785. Epub 2016 Sep 26.
PubMed 27543837Vos MB, Kimmons JE, Gillespie C, Welsh J, Blanck HM. Dietary fructose consumption among US children and adults: the Third National Health and Nutrition Examination Survey. Medscape J Med. 2008 Jul 9;10(7):160.
PubMed 18769702Moore JB, Gunn PJ, Fielding BA. The role of dietary sugars and de novo lipogenesis in non-alcoholic fatty liver disease. Nutrients. 2014 Dec 10;6(12):5679-703. doi: 10.3390/nu6125679.
PubMed 25514388Faeh D, Minehira K, Schwarz JM, Periasamy R, Park S, Tappy L. Effect of fructose overfeeding and fish oil administration on hepatic de novo lipogenesis and insulin sensitivity in healthy men. Diabetes. 2005 Jul;54(7):1907-13. doi: 10.2337/diabetes.54.7.1907.
PubMed 15983189Alwahsh SM, Gebhardt R. Dietary fructose as a risk factor for non-alcoholic fatty liver disease (NAFLD). Arch Toxicol. 2017 Apr;91(4):1545-1563. doi: 10.1007/s00204-016-1892-7. Epub 2016 Dec 19.
PubMed 27995280Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May;119(5):1322-34. doi: 10.1172/JCI37385. Epub 2009 Apr 20.
PubMed 19381015Stanhope KL, Medici V, Bremer AA, Lee V, Lam HD, Nunez MV, Chen GX, Keim NL, Havel PJ. A dose-response study of consuming high-fructose corn syrup-sweetened beverages on lipid/lipoprotein risk factors for cardiovascular disease in young adults. Am J Clin Nutr. 2015 Jun;101(6):1144-54. doi: 10.3945/ajcn.114.100461. Epub 2015 Apr 22.
PubMed 25904601Softic S, Gupta MK, Wang GX, Fujisaka S, O'Neill BT, Rao TN, Willoughby J, Harbison C, Fitzgerald K, Ilkayeva O, Newgard CB, Cohen DE, Kahn CR. Divergent effects of glucose and fructose on hepatic lipogenesis and insulin signaling. J Clin Invest. 2017 Nov 1;127(11):4059-4074. doi: 10.1172/JCI94585. Epub 2017 Oct 3.
PubMed 28972537Basaranoglu M, Basaranoglu G, Bugianesi E. Carbohydrate intake and nonalcoholic fatty liver disease: fructose as a weapon of mass destruction. Hepatobiliary Surg Nutr. 2015 Apr;4(2):109-16. doi: 10.3978/j.issn.2304-3881.2014.11.05.
PubMed 26005677Johnson RJ, Nakagawa T, Sanchez-Lozada LG, Shafiu M, Sundaram S, Le M, Ishimoto T, Sautin YY, Lanaspa MA. Sugar, uric acid, and the etiology of diabetes and obesity. Diabetes. 2013 Oct;62(10):3307-15. doi: 10.2337/db12-1814.
PubMed 24065788Zhou Y, Wei F, Fan Y. High serum uric acid and risk of nonalcoholic fatty liver disease: A systematic review and meta-analysis. Clin Biochem. 2016 May;49(7-8):636-42. doi: 10.1016/j.clinbiochem.2015.12.010. Epub 2015 Dec 29.
PubMed 26738417Goran MI, Walker R, Allayee H. Genetic-related and carbohydrate-related factors affecting liver fat accumulation. Curr Opin Clin Nutr Metab Care. 2012 Jul;15(4):392-6. doi: 10.1097/MCO.0b013e3283544477.
PubMed 22617559Speliotes EK, Yerges-Armstrong LM, Wu J, Hernaez R, Kim LJ, Palmer CD, Gudnason V, Eiriksdottir G, Garcia ME, Launer LJ, Nalls MA, Clark JM, Mitchell BD, Shuldiner AR, Butler JL, Tomas M, Hoffmann U, Hwang SJ, Massaro JM, O'Donnell CJ, Sahani DV, Salomaa V, Schadt EE, Schwartz SM, Siscovick DS; NASH CRN; GIANT Consortium; MAGIC Investigators; Voight BF, Carr JJ, Feitosa MF, Harris TB, Fox CS, Smith AV, Kao WH, Hirschhorn JN, Borecki IB; GOLD Consortium. Genome-wide association analysis identifies variants associated with nonalcoholic fatty liver disease that have distinct effects on metabolic traits. PLoS Genet. 2011 Mar;7(3):e1001324. doi: 10.1371/journal.pgen.1001324. Epub 2011 Mar 10.
PubMed 21423719Davis JN, Le KA, Walker RW, Vikman S, Spruijt-Metz D, Weigensberg MJ, Allayee H, Goran MI. Increased hepatic fat in overweight Hispanic youth influenced by interaction between genetic variation in PNPLA3 and high dietary carbohydrate and sugar consumption. Am J Clin Nutr. 2010 Dec;92(6):1522-7. doi: 10.3945/ajcn.2010.30185. Epub 2010 Oct 20.
PubMed 20962157Santoro N, Caprio S, Pierpont B, Van Name M, Savoye M, Parks EJ. Hepatic De Novo Lipogenesis in Obese Youth Is Modulated by a Common Variant in the GCKR Gene. J Clin Endocrinol Metab. 2015 Aug;100(8):E1125-32. doi: 10.1210/jc.2015-1587. Epub 2015 Jun 4.
PubMed 26043229
Study at a glance
From the registry record, last updated by the sponsor on 23 Oct 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Genetic-specific Effects of Fructose on Liver Lipogenesis
- ClinicalTrials.gov ID
- NCT03783195
- Acronym / sponsor ID
- 17-3348
- Conditions
- NAFLD
- Keywords
- Glucose, Fructose, Fatty-liver, Polymorphisms, Imaging, Fibroscan
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 15 participants (actual)
- Lead sponsor
- University of North Carolina, Chapel HillUniversity, hospital or other
- Collaborators
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
- Study start
- 25 Jan 2019 (actual)
- Primary completion
- 25 Apr 2023 (actual)
- Study completion
- 25 Apr 2023 (actual)
- First posted
- 20 Dec 2018 (actual)
- Results
- Posted 23 Oct 2024
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The primary goal of this study is to identify a set of genotypes that increase the risk for nonalcoholic fatty liver disease (NAFLD) and predispose individuals to increased de novo lipogenesis (DNL) and liver fat accumulation when exposed to fructose intake. The proposed goal will be achieved through the completion of following aims:
- To determine the impact of prolonged exposure of fructose on hepatic lipid accumulation in Caucasian individuals with high and low genetic risk for NAFLD,
- to determine the impact of acute exposure of fructose on hepatic DNL, and
- to determine the relationship between markers of DNL, liver fat accumulation and serum concentrations of lipids, uric acid and liver function markers before and after the fructose challenge.
Detailed description
BACKGROUND AND RATIONALE Non-alcoholic fatty liver disease (NAFLD) is characterized by fat accumulation in liver cells not caused by alcohol. A leading cause of chronic liver disease in the US, NAFLD represents a group of disorders including steatosis, nonalcoholic steatohepatitis with fibrosis. It has substantially risen in prevalence over the last two decades with the estimated prevalence being 20% among US adults and 25% in young adults (18-39 years). Over 64 million individuals are believed to have NAFLD with annual medical costs rising to more $100 billion. More common in individuals who are obese or diabetic and/or have metabolic syndrome, NAFLD has been associated with increased cirrhosis, liver-related mortality and hepatocellular carcinoma.
Both genetic and environmental, including nutritional, factors contribute to the onset and progression of NAFLD. Increased consumption of sugar-sweetened, fructose-rich beverages has been linked to NAFLD. Fructose, commonly found in soft drinks, fruit juices and energy drinks, affects many metabolic processes, foremost being an increase in fat accumulation in the liver and hence, NAFLD. Genome-wide and candidate gene studies have identified several genes associated with NAFLD. However, none of these studies have shown the cumulative effects of single nucleotide polymorphisms (SNPs) on changes in liver fat when exposed to fructose. The results from this study can be extrapolated to larger cohorts and other ethnicities and are therefore, expected to lay the foundation for developing personalized nutritional plans.
Study design
- Primary purpose
- Basic science
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Number of arms
- 2
- Model description
- Participants are assigned to high genetic risk score group in parallel to low genetic risk score group
| Arm | Type | Receives |
|---|---|---|
| High GRS group | Experimental | Other: Sugar drinkThis group consists of individuals who are in the highest quartile of the genetic risk score (GRS) and will ingest one sugar drink (equal to 2 soft drinks) per day for 3 weeks. The GRS is computed by adding the number of alleles that increase the risk for liver lipogenesis or fatty liver. |
| Low GRS group | Experimental | Other: Sugar drinkThis groups consists of individuals who are in the lowest quartile of the genetic risk score (GRS) and will ingest one sugar drink (equal to 2 soft drinks) per day for 3 weeks. The GRS is computed by adding the number of alleles that increase the risk for liver lipogenesis or fatty liver. |
Who may qualify
- Ages
- 12 to 40 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Child, Adult
Key inclusion criteria (5 listed)
- Subjects 12 - 40 years
- No history of alcohol abuse (> 7 drinks per week)
- History of fructose intake of < 14 drinks per week
- Caucasian ethnicity
- BMI > 25kg/m² - 32kg/m² or 85th -99th percentile but otherwise healthy
Key exclusion criteria (9 listed)
- ages < 12 and > 40 years
- Pregnant/lactating
- known alcohol abuse or fructose intake > 14 drinks per week
- not of Caucasian ethnicity
- glucose levels > 100 mg/dL if fasting, > 140mg/dL if within 2 hours post meal and > 200 mg/dL if random sample
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Sugar drinkA sugar drink made with 1.2 g/kg body weight of added sugar( 0.75g/kg body weight of fructose + 0.45g/kg body weight of glucose) and 24oz water | Other | High GRS group, Low GRS group |
Primary outcome
Mean Change in Liver Fat Content Based on Elastography
Time frame: between week 0 (Baseline) and week 3
Elastography (Fibroscan) will be used to measure changes in liver fat.
Mean Percent Change in Liver Fat Content Based on MRI
Time frame: between week 0 (Baseline) and week 3
Magnetic resonance imaging (MRI) will be used to measure changes in liver fat (% change in fat fraction).
Mean Change in Serum Concentrations of Very Low Density Lipoprotein-triglycerides (VLDL-TG)
Time frame: between week 0 (Baseline) and week 3
VLDL-TG measurement in serum (mg/dl) at week 0 and Week 3.
Mean Change in AUC of Serum Very Low Density Lipoprotein-triglycerides (VLDL-TG)
Time frame: between week 0 (Baseline) and week 3
Area under curve (AUC) (mg*hr/dl) of serum VLDL-TG for baseline and 3hr time points at week 0 and Week 3.
18 secondary outcomes
Mean Change in Serum Concentrations of Triglycerides
Time frame: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Triglycerides
Time frame: between week 0 (Baseline) and week 3
Mean Change in Serum Concentrations of HDL Cholesterol
Time frame: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum HDL Cholesterol
Time frame: between week 0 (baseline) and week 3
Mean Change in Serum Concentrations of LDL Cholesterol
Time frame: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum LDL Cholesterol
Time frame: Week 0 (baseline) and week 3
Mean Change in Serum Concentrations of Total Cholesterol
Time frame: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Total Cholesterol
Time frame: week 0 and week 3
Mean Changes in Serum Concentrations of Uric Acid
Time frame: between week 0 (Baseline) and week 3
Mean Changes in AUC of Serum Uric Acid
Time frame: between week 0 (Baseline) and week 3
Mean Change in Serum Concentrations of Liver Function Marker (Alanine Transaminase- ALT).
Time frame: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Alanine Transaminase (ALT)
Time frame: between week 0 (Baseline) and week 3
Mean Change in Serum Concentrations of Liver Function Marker (Aspartate Transaminase-AST).
Time frame: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Aspartate Transaminase (AST).
Time frame: between week 0 (Baseline) and week 3
Mean Change in Serum Concentrations of Liver Function Marker (Alkaline Phosphatase-ALP)
Time frame: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Alkaline Phosphatase (ALP)
Time frame: between week 0 (Baseline) and week 3
Mean Change in Serum Concentrations of Liver Function Marker (Gamma Glutamyl Transpeptidase-GGT)
Time frame: between week 0 (Baseline) and week 3
Mean Change in AUC of Serum Gamma Glutamyl Transpeptidase (GGT)
Time frame: between week 0 (Baseline) and week 3
Results and safety
Loading the posted results from ClinicalTrials.gov…
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 23 Oct 2024.
- Posted resultsParticipant flow, baseline, all outcome measures and adverse events.
- Background: PubMed 27543837Younossi ZM, Blissett D, Blissett R, Henry L, Stepanova M, Younossi Y, Racila A, Hunt S, Beckerman R. The economic and clinical burden of nonalcoholic fatty liver disease in the United States and Europe. Hepatology. 2016 Nov;64(5):1577-1586. doi: 10.1002/hep.28785. Epub 2016 Sep 26.
- Background: PubMed 18769702Vos MB, Kimmons JE, Gillespie C, Welsh J, Blanck HM. Dietary fructose consumption among US children and adults: the Third National Health and Nutrition Examination Survey. Medscape J Med. 2008 Jul 9;10(7):160.
- Background: PubMed 25514388Moore JB, Gunn PJ, Fielding BA. The role of dietary sugars and de novo lipogenesis in non-alcoholic fatty liver disease. Nutrients. 2014 Dec 10;6(12):5679-703. doi: 10.3390/nu6125679.
- Background: PubMed 15983189Faeh D, Minehira K, Schwarz JM, Periasamy R, Park S, Tappy L. Effect of fructose overfeeding and fish oil administration on hepatic de novo lipogenesis and insulin sensitivity in healthy men. Diabetes. 2005 Jul;54(7):1907-13. doi: 10.2337/diabetes.54.7.1907.
- Background: PubMed 27995280Alwahsh SM, Gebhardt R. Dietary fructose as a risk factor for non-alcoholic fatty liver disease (NAFLD). Arch Toxicol. 2017 Apr;91(4):1545-1563. doi: 10.1007/s00204-016-1892-7. Epub 2016 Dec 19.
- Background: PubMed 19381015Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May;119(5):1322-34. doi: 10.1172/JCI37385. Epub 2009 Apr 20.
- Background: PubMed 25904601Stanhope KL, Medici V, Bremer AA, Lee V, Lam HD, Nunez MV, Chen GX, Keim NL, Havel PJ. A dose-response study of consuming high-fructose corn syrup-sweetened beverages on lipid/lipoprotein risk factors for cardiovascular disease in young adults. Am J Clin Nutr. 2015 Jun;101(6):1144-54. doi: 10.3945/ajcn.114.100461. Epub 2015 Apr 22.
- Background: PubMed 28972537Softic S, Gupta MK, Wang GX, Fujisaka S, O'Neill BT, Rao TN, Willoughby J, Harbison C, Fitzgerald K, Ilkayeva O, Newgard CB, Cohen DE, Kahn CR. Divergent effects of glucose and fructose on hepatic lipogenesis and insulin signaling. J Clin Invest. 2017 Nov 1;127(11):4059-4074. doi: 10.1172/JCI94585. Epub 2017 Oct 3.
- Background: PubMed 26005677Basaranoglu M, Basaranoglu G, Bugianesi E. Carbohydrate intake and nonalcoholic fatty liver disease: fructose as a weapon of mass destruction. Hepatobiliary Surg Nutr. 2015 Apr;4(2):109-16. doi: 10.3978/j.issn.2304-3881.2014.11.05.
- Background: PubMed 24065788Johnson RJ, Nakagawa T, Sanchez-Lozada LG, Shafiu M, Sundaram S, Le M, Ishimoto T, Sautin YY, Lanaspa MA. Sugar, uric acid, and the etiology of diabetes and obesity. Diabetes. 2013 Oct;62(10):3307-15. doi: 10.2337/db12-1814.
- Background: PubMed 26738417Zhou Y, Wei F, Fan Y. High serum uric acid and risk of nonalcoholic fatty liver disease: A systematic review and meta-analysis. Clin Biochem. 2016 May;49(7-8):636-42. doi: 10.1016/j.clinbiochem.2015.12.010. Epub 2015 Dec 29.
- Background: PubMed 22617559Goran MI, Walker R, Allayee H. Genetic-related and carbohydrate-related factors affecting liver fat accumulation. Curr Opin Clin Nutr Metab Care. 2012 Jul;15(4):392-6. doi: 10.1097/MCO.0b013e3283544477.
- Individual participant dataSharing planned: Yes. Deidentified individual data that supports the results will be shared beginning 9 to 36 months following publication provided the investigator who proposes to use the data has approval from an Institutional Review Board (IRB), Independent Ethics Committee (IEC), or Research Ethics Board (REB), as applicable, and executes a data use/sharing agreement with University of North Carolina (UNC).
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Saroja Voruganti principal investigator
University of North Carolina, Chapel Hill
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Sugar drink in people with NAFLD, run by University of North Carolina, Chapel Hill at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 9 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 23 Oct 2024. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Yes. Results are posted in the registry (first posted 23 Oct 2024). A summary is in the For doctors view, and the full results are on ClinicalTrials.gov.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Mean Change in Liver Fat Content Based on Elastography (time frame: between week 0 (Baseline) and week 3). The study lists 4 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT03783195, which also lists 27 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 23 Oct 2024.