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Potential Association of a Common L-FABP Polymorphism With Lipid-induced Hepatic Insulin Resistance

This study has been completed.
Information provided by:
German Institute of Human Nutrition Identifier:
First received: January 12, 2006
Last updated: May 3, 2012
Last verified: August 2006
The investigators hypothesise that a common A277G polymorphism of the liver fatty acid binding protein (L-FABP) gene, which leads to an amino acid exchange, may be associated with alterations of lipid-induced hepatic insulin resistance. In the present study the investigators will investigate potential differences in lipid-induced hepatic insulin resistance, and in the relation between glycogenolysis and gluconeogenesis, in healthy subjects with the A277G polymorphism vs. subjects carrying the wildtype.

Condition Intervention
Wildtype Polymorphism Liver FABP Procedure: measurement of lipid-induced hepatic insulin resistance

Study Type: Interventional
Study Design: Allocation: Randomized
Intervention Model: Single Group Assignment
Masking: Single
Primary Purpose: Diagnostic

Resource links provided by NLM:

Further study details as provided by German Institute of Human Nutrition:

Primary Outcome Measures:
  • lipid-induced hepatic insulin resistance(WT vs.SNP L-FABP)
  • changes in the relation GNG to GL

Secondary Outcome Measures:
  • changes in peripheral plasma glucose and lipid responses

Estimated Enrollment: 18
Study Start Date: January 2006
Estimated Study Completion Date: April 2006
Detailed Description:
Liver fatty acid binding protein (L-FABP) is an abundant cytosolic lipid-binding protein that regulates lipid transport and metabolism. Only one common non-synonymous polymorphism (A227G) leading to an amino-acid exchange in the exonic region of the L-FABP gene has been previously identified. Experimental elevations of free fatty acids (FFAs) have been shown to impair insulin mediated suppression of endogenous glucose production (EGP). Deletion of the L-FABP gene shows no obvious phenotype in mice receiving a low fat chow diet, but leads to decreased hepatic triglyceride accumulation in the prolonged fasted state, which exposes mice to an increased fatty acid flux to the liver. The function of the L-FABP gene may be altered by polymorphisms in coding regions of the gene, probably leading to modifications in hepatic triglyceride accumulation and hepatic insulin resistance.We hypothesize that carriers of the A277G SNP, when compared to matched wild-type subjects, may show altered responses of hepatic glucose production upon exposure to increased peripheral fatty acid concentrations, as achieved by lipid / heparin infusions. Because it is known that free fatty acids potently increase insulin secretion, we use somatostatin clamps in our experiments, followed by replacement of postabsorptive insulin and glucagon concentrations.

Ages Eligible for Study:   18 Years to 70 Years   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes

Inclusion Criteria:

  • healthy subjects with normal glucose tolerance (NGT)

Exclusion Criteria:

  • any severe cardiac, liver, or kidney diseases
  • pregnant or lactating women, menstrual irregularities
  • cortisone, antidiabetic drugs
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Please refer to this study by its identifier: NCT00277342

German Institute of Human Nutrition DIfE, Dpt. of Clinical Nutrition, Potsdam-Rehbrücke
Nuthetal, Germany, 14558
Sponsors and Collaborators
German Institute of Human Nutrition
Principal Investigator: Martin O Weickert, MD German Institute of Human Nutrition; Charité Campus Benjamin Franklin
Principal Investigator: Matthias Möhlig, MD German Institute of Human Nutrition; Charité Campus Benjamin Franklin
Study Chair: Andreas FH Pfeiffer, MD German Institute of Human Nutrition; Charité Campus Benjamin Franklin
  More Information

Additional Information:
Publications: Identifier: NCT00277342     History of Changes
Other Study ID Numbers: MOW_MM_LFABP
Study First Received: January 12, 2006
Last Updated: May 3, 2012

Keywords provided by German Institute of Human Nutrition:
lipid induced hepatic insulin resistance
polymorphisms liver fatty-acid-binding-protein
endogenous glucose production

Additional relevant MeSH terms:
Insulin Resistance
Glucose Metabolism Disorders
Metabolic Diseases
Insulin, Globin Zinc
Hypoglycemic Agents
Physiological Effects of Drugs processed this record on August 18, 2017