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Genetic Polymorphisms, Steatosis and Diabetes

Genetic Polymorphisms, Hepatic Steatosis and Lipid Anomalies in Diabetic Patients

Status
Completed
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT02045563
Enrollment
507
Registered
2014-01-27
Start date
2007-10-15
Completion date
2015-03-25
Last updated
2024-02-21

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Type 1 and 2 Diabetes

Brief summary

* Our research hypothesis is to show that a certain number of genetic polymorphisms of the proteins involved in glucose, lipid and adipocyte metabolism are factors that favour the development of steatosis in patients with Type 2 diabetes. * We also wish to evaluate more thoroughly lipid anomalies associated with the presence of steatosis, notably with regard to monocyte expression of LDL receptors. We hypothesize that hepatic steatosis is accompanied by activation of transcription factors involved in lipogenesis, notably SREBP factors. The activation of these factors could cause an increase in the expression of LDL receptors, leading to increased LDL catabolism. * Chronological description of the study During an outpatient consultation at the endocrinology department, diabetic patients, programmed to undergo an examination to assess their diabetes will be invited to participate in the study. Once written informed consent has been provided and clinical data has been recorded, patients with type 1 or type 2 diabetes will have standard biological examination, which is systematically done in such patients (Fasting glycemia, HBA1c, aspartate aminotransferase, alanine amino transferase, Gammaglutamyl-transferases, PAL, bilirubin, blood proteins, albuminemia, Total Cholesterol total, HDL cholesterol, triglycerides, Sedimentation Rate, C-reactive protein, fibrinogen). As well as the systematic biological tests, 3 additional tubes will be taken to screen for genetic polymorphism in 3 proteins (Microsomal Transfer Protein, Adiponectin receptor - 1, Apolipoprotein A - II). IN addition, magnetic resonance imaging and magnetic resonance spectroscopy will be done to look for the presence of liver steatosis and to measure carotid intima-media thickness.

Interventions

OTHERmagnetic resonance imaging and magnetic resonance spectroscopy

Sponsors

Centre Hospitalier Universitaire Dijon
Lead SponsorOTHER

Study design

Observational model
OTHER
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
Yes

Inclusion criteria

Inclusion criteria Type-2 diabetics: * Type 2 diabetes * HbA1C\>6.5% * 27\<BMI\<55 Inclusion criteria Type-1 diabetics: * Type 1 diabetes * BMI\<55 Diagnosis of type-1 diabetes based on the clinical history of the patient and/or the presence of anti-glutamate decarboxylase auto antibodies and/or a plasma level of C peptide below 0,5 ng/l. Inclusion criteria healthy volunteers: * Non diabetic * Alcohol consumption \< 2 glasses per day * Without hyperglycemic treatment (corticoids, ...) * Without liver disease (cirrhosis, hepatitis, ...)

Exclusion criteria

* Pacemaker * Daily alcohol consumption above 4 glasses per day * Patients treated with Glitazones during the 3 months preceding inclusion * Presence of implants * Claustrophobia * Patient \< 18 years * Patient under guardianship or not intellectually independent * Pregnancy

Design outcomes

Primary

MeasureTime frame
Determination of the existence of liver steatosis measured by magnetic resonance spectroscopy spectrometryAt inclusion

Secondary

MeasureTime frame
Measurement of monocyte expression of LDL receptorsAt inclusion

Countries

France

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026