Published online Aug 28, 2016. doi: 10.4254/wjh.v8.i24.1019
Peer-review started: April 28, 2016
First decision: May 17, 2016
Revised: June 26, 2016
Accepted: July 14, 2016
Article in press: July 18, 2016
Published online: August 28, 2016
Processing time: 120 Days and 12.9 Hours
To assess lactase gene (LCT)-13910C>T polymorphisms in Brazilian non-alcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) patients in comparison with healthy controls.
This was a transverse observational clinical study with NAFLD patients who were followed at the Hepatology Outpatient Unit of the Hospital das Clínicas, São Paulo, Brazil. The polymorphism of lactase non-persistence/lactase persistence (LCT-13910C>T) was examined by PCR-restriction fragment length polymorphism technique in 102 liver biopsy-proven NAFLD patients (steatosis in 9 and NASH in 93) and compared to those of 501 unrelated healthy volunteers. Anthropometric, clinical, biochemical and liver histology data were analyzed. Continuous variables were compared using the t or Mann-Whitney tests, and categorical data were compared with the Fisher’s exact test. Univariate logistic regression and multivariate logistic regression adjusted for gender and age were performed.
No differences in the LCT-13910 genotype frequencies were noted between the NAFLD patients (66.67% of the patients with steatosis were CC, 33.33% were CT, and none were TT; 55.91% of the patients with NASH were CC, 39.78% were CT, and 4.3% were TT; P = 0.941) and the healthy controls (59.12% were CC, 35.67% were CT, and 5.21% were TT) or between the steatosis and NASH patients. That is, the distribution of the lactase non-persistence/lactase persistence polymorphism (LCT-13910C>T) in the patients with NAFLD was equal to that in the general population. In the NASH patients, the univariate analysis revealed that the lactase non-persistence (low lactase activity or hypolactasia) phenotype was associated with higher insulin levels (23.47 ± 15.94 μU/mL vs 15.8 ± 8.33 μU/mL, P = 0.027) and a higher frequency of insulin resistance (91.84% vs 72.22%, P = 0.02) compared with the lactase persistence phenotype. There were no associations between the LCT genotypes and diabetes (P = 0.651), dyslipidaemia (P = 0.328), hypertension (P = 0.507) or liver histology in these patients. Moreover, in the NASH patients, hypolactasia was an independent risk factor for insulin resistance even after adjusting for gender and age [OR = 5.0 (95%CI: 1.35-20; P = 0.017)].
The LCT-13910 genotype distribution in Brazilian NAFLD patients was the same as that of the general population, but hypolactasia increased the risk of insulin resistance in the NASH patients.
Core tip: Non-alcoholic fatty liver disease (NAFLD) exhibits a close relationship with metabolic syndrome (MetS), but the associations of the lactase non-persistence/lactase persistence genotypes with MetS components are controversial. Therefore, we assessed hypolactasia (LCT-13910CC) and lactase persistence genotypes in 102 Brazilian NAFLD patients in comparison with 501 healthy controls, the associations of these polymorphisms were verified with the results of biochemical tests, MetS and severity of liver histology in nonalcoholic steatohepatitis (NASH) patients. No differences in the LCT-13910C>T polymorphisms were noted between the NAFLD and controls, but hypolactasia increased the risk of insulin resistance in the NASH patients.