Abstract | BACKGROUND: MATERIAL AND METHODS: A population of 76 patients with NAFLD was recruited in a cross sectional study. A biochemical analysis of serum was measured. Genotype of LEPR gene Lys656Asn was studied. RESULTS: Nineteen patients (25%) had the genotype Lys656Asn and 4 patients genotype Asn656Asn (mutant type group) and 53 patients (69.7%) Lys656Lys (wild type group). Body mass index, weight, fat mass, waist circumference, waist to hip ratio, glucose levels and HOMA-IR were higher in mutant than wild type group. LEPR polymorphism is in any way related with liver lesions. The multivariate analysis adjusted by age, sex, BMI and genotype showed an independently association of lobular inflammation 4.19 (CI95%: 1.37-12.77), portal inflammation 1.97 (CI95%: 1.05-3.74) and steatosis 9.23 (CI95%: 1.47-57.83) with HOMA. Liver steatosis was associated with leptin levels (1.09 (CI95%: 1.06-1.18)), too. CONCLUSION:
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Authors | R Aller, D A De Luis, O Izaola, M González Sagrado, R Conde, D Pacheco, M C Velasco, H F Ovalle |
Journal | European review for medical and pharmacological sciences
(Eur Rev Med Pharmacol Sci)
Vol. 16
Issue 3
Pg. 335-41
(Mar 2012)
ISSN: 1128-3602 [Print] Italy |
PMID | 22530350
(Publication Type: Journal Article)
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Chemical References |
- Blood Glucose
- Leptin
- Receptors, Leptin
- Triglycerides
- DNA
- Cholesterol
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Topics |
- Adult
- Anthropometry
- Biopsy
- Blood Glucose
(metabolism)
- Body Weight
(physiology)
- Cholesterol
(blood)
- DNA
(genetics)
- Fatty Liver
(blood, genetics, physiopathology)
- Female
- Genotype
- Humans
- Insulin Resistance
(genetics, physiology)
- Leptin
(blood)
- Liver
(pathology)
- Male
- Middle Aged
- Overweight
(blood, genetics, physiopathology)
- Polymorphism, Genetic
- Receptors, Leptin
(genetics)
- Risk Factors
- Sample Size
- Triglycerides
(blood)
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