Fructose Consumption and Metabolic Dysregulation

NCT01445730 | Completed Results

• 1 other identifier: T1010K0029
• Study Type: interventional
• Target: 82
• Locations: 4 countries
• Sites: 4

Brief Summary

High fructose intake is increasingly recognized as causative in development of prediabetes, metabolic syndrome and cardiovascular disease (CVD). The mechanisms underlying fructose-induced metabolic disturbances are unclear but are beginning to be unraveled. In contrast to metabolism of glucose, the breakdown of fructose leads to the generation of metabolites that stimulate hepatic de novo lipogenesis (DNL) and increased levels of both fasting and postprandial triglycerides. The key lipogenic transcription factor seems to be activated by fructose independently of insulin. However, it is still controversial whether fructose consumption increases DNL in man to the extent that it induces metabolic disturbances. Animal studies have shown that also the adipose tissue is responsive to fructose feeding fructose, and that high fructose-feeding induces insulin resistance and inflammation in the adipose tissue. The role of intestinal insulin resistance in fructose-induced dysmetabolism has not been studied in detail. The critical question is whether the metabolic disturbances are induced by calorie excess or by fructose per se.

Conditions

Central Obesity; Hypertriglyceridemia

Keywords

fructose; hypertriglyceridemia; postprandial lipids; de novo lipogenesis; stable isotopes

Outcome Measures

Primary Outcomes (3)

• TG Plasma AUC

  Before vs. after fructose challenge: Triglycerides (TG) plasma Area Under Curve (AUC)

  Form the baseline (time point 1) to end of treatment at 3 months (time point 2)

• B48 Plasma AUC

  Before vs. after fructose challenge: apolipoprotein (apo)B48 plasma Area Under Curve (AUC)

  Form the baseline (time point 1) to end of treatment at 3 months (time point 2)

• TG Plasma iAUC

  Before vs. after fructose challenge:Triglycerides (TG) plasma incremental Area Under Curve (iAUC)

  Form the baseline (time point 1) to end of treatment at 3 months (time point 2)

Secondary Outcomes (4)

• DNL

  Form the baseline (time point 1) to end of treatment at 3 months (time point 2)

• ApoC-III

  Form the baseline (time point 1) to end of treatment at 3 months (time point 2)

• β-OH Butyrate

  Form the baseline (time point 1) to end of treatment at 3 months (time point 2)

• Liver Fat

  Form the baseline (time point 1) to end of treatment at 3 months (time point 2)

Study Arms (1)

After fructose feeding

EXPERIMENTAL

After 3 month fructose diet 75 g/day

Dietary Supplement: Fructose

Interventions

Fructose DIETARY_SUPPLEMENT

3 month fructose diet 75 g/day

After fructose feeding

Eligibility Criteria

• Age: 20 Years - 60 Years
• Sex: male
• Healthy Volunteers: Yes
• Age Groups: Adult (18-64)

You may qualify if:

• Body mass index 27-40
• Waist \> 96 cm
• Age 20-60 years
• Male

You may not qualify if:

• Smoking
• Active health problems
• Contraindications to MRI scanning
• Bleeding tendency
• Abnormal liver or renal function tests
• Type 2 diabetes
• Evidence of metabolic or viral liver disease
• Alcohol intake \> 21 units per week
• Chronic medication except ones needed for stable hypertension

Sponsors & Collaborators

• Marja-Riitta Taskinen: lead
• Sahlgrenska University Hospital: collaborator
• Lund University: collaborator
• University of Naples: collaborator
• Laval University: collaborator

Study Sites (4)

Université Laval

Québec, Canada

Location

Helsinki University Central Hospital, Biomedicum

Helsinki, 00290, Finland

Location

University of Naples, Federico II, and Faculty of Medicine

Naples, Italy

Location

Sahlgrenska Academy at University of Gothenburg and Sahlgrenska University Hospital

Gothenburg, Sweden

Location

Related Publications (1)

• Taskinen MR, Bjornson E, Matikainen N, Soderlund S, Ramo J, Ainola MM, Hakkarainen A, Sihlbom C, Thorsell A, Andersson L, Bergh PO, Henricsson M, Romeo S, Adiels M, Ripatti S, Laakso M, Packard CJ, Boren J. Postprandial metabolism of apolipoproteins B48, B100, C-III, and E in humans with APOC3 loss-of-function mutations. JCI Insight. 2022 Oct 10;7(19):e160607. doi: 10.1172/jci.insight.160607.

  PMID: 36040803 DERIVED

MeSH Terms

Conditions

Obesity, Abdominal; Hypertriglyceridemia

Interventions

Fructose

Condition Hierarchy (Ancestors)

Obesity; Overweight; Overnutrition; Nutrition Disorders; Nutritional and Metabolic Diseases; Body Weight; Signs and Symptoms; Pathological Conditions, Signs and Symptoms; Hyperlipidemias; Dyslipidemias; Lipid Metabolism Disorders; Metabolic Diseases

Intervention Hierarchy (Ancestors)

Hexoses; Monosaccharides; Sugars; Carbohydrates; Ketoses

Results Point of Contact

• Title: Prof. Marja-Riitta Taskinen
• Organization: Helsinki University and Helsinki University Hospital

marja-riitta.taskinen@helsinki.fi

+358-9-4717 1990

Study Officials

• Marja-Riitta Taskinen, Professor

  Helsinki University Central Hospital, Biomedicum

  PRINCIPAL INVESTIGATOR

Publication Agreements

• PI is Sponsor Employee: Yes

Study Design

• Study Type: interventional
• Phase: not applicable
• Allocation: NA
• Masking: NONE
• Purpose: BASIC SCIENCE
• Intervention Model: SINGLE GROUP
• Sponsor Type: OTHER
• Responsible Party: SPONSOR INVESTIGATOR
• PI Title: Professor

Study Record Dates

• First Submitted: September 28, 2011
• First Posted: October 4, 2011
• Study Start: August 1, 2011
• Primary Completion: May 1, 2015
• Study Completion: June 1, 2015
• Last Updated: June 15, 2021
• Results First Posted: June 15, 2021

Record last verified: 2021-05

Locations

SE (1); FI (1); IT (1); CA (1)