The LEPR K109R and Q223R Might Contribute to the Risk of NAFLD: A Meta-Analysis

Leptin and insulin resistance have been pointed out to play a role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Increasing genes were shown to be associated with the risk of NAFLD.

The study aimed to investigate the genetic association between two leptin receptor (LEPR) polymorphisms (Q223R and K109R) and the NAFLD risk.

Studies were retrieved and included by using PubMed, Web of Science, the Cochrane Library databases, Chinese National Knowledge Infrastructure (CNKI) and EMBASE database. Genetic associations were assessed with pooled odds ratios (ORs) with 95% confidence intervals (CIs).

Five case-control studies with 1711 NAFLD patients and 1732 healthy controls were included in this meta-analysis. The K109R was significantly associated with NAFLD in allelic model in Southeast Asian subgroup (p=0.01, OR=0.59, 95% CI [0.39- 0.90]), but not in Chinese subgroup (p=0.24, OR=1.10, 95% CI [0.94-1.29]). The Q223R was significantly associated with NAFLD in both allelic and recessive models (allelic model: p<0.001, OR=0.57, 95% CI [0.50-0.65]; recessive model: p=0.001, OR=0.67, 95% CI [0.52-0.85]). However, subgroup analysis showed that the significant association between Q223R and NAFLD in allelic model cannot be found in Southeast Asians subgroup (p=0.07, OR=0.67, 95% CI [0.52-0.85]).

LEPR K109R might be a susceptible factor for NAFLD in Southeast Asian population. And LEPR Q223R might be a susceptible factor for NAFLD in Chinese population.