Influence of adiponectin gene polymorphisms in Japanese patients with non-alcoholic fatty liver disease

Tokushige, Katsutoshi; Hashimoto, Etsuko; Noto, Haruka; Yatsuji, Satoru; Taniai, Makiko; Torii, Nobuyuki; Shiratori, Keiko

doi:10.1007/s00535-009-0085-z

Cited by 58 publications

(52 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The share of heterozygotes +276G/T at 1.53 times higher (p < 0.001) than the theoretically expected value at equilibrium [42]. Our data correspond in part to the Передова стаття /Leading Articlе/ other study which revealed that adiponectin +276 G/T polymorphism was not significantly different between NAFLD and controls, but among females, the GG geno type was reported to be significantly more prevalent in patients with NAFLD [43].…”

Section: Discussionsupporting

confidence: 83%

Однонуклеотидні Поліморфізми Гена Адипонектину У Хворих На Цукровий Діабет 2-Го Типу Та Неалкогольну Жирову Хворобу Печінки

Karachentsev¹,

Gorshunska²,

Tyzhnenko³

et al. 2021

Mìžnarodnij endokrinologìčnij žurnal

View full text Add to dashboard Cite

Abstract. Background. It is generally believed that environmental and genetic factors interact with the formation of nonalcoholic fatty liver disease (NAFLD) phenotype and determine its progression. Both NAFLD and type 2 diabetes (T2D) are heterogeneous diseases with common pathogenic pathways. Adiponectin is an adipokine, which increases the sensitivity of hepatocytes and muscle to insulin NAFLD (190.18 ± 22.15 vs 133.32 ± 13.58 mmol/L·pmol/L, p < 0.02), with negative correlation between Adipo-IR and adiponectin level in T2D patients with NAFLD only (r s = -0.350, p = 0.021). Stratification of non-NAFLD patients by +276G/T genotype suggests the prevalence of GT-and TT-genotypes. Thus, the rs1501299 G-allele increased the risk of NAFLD in comparison with p < 0.05). We also found a significant difference in the frequency of -11391G/A between T2D and control groups, but not between the patients with and without NAFLD. We observed that the haplotype of GT/GG had been more common in T2D with NAFLD, and twice less often detected in patients without hepatic disease (33 and 16.49 %, respectively, p < 0.05). (rs1501299 G-allele, rs17300539 and rs1501299 GG/GG and GT/GG haplotypes, respectively) Conclusions. We can recommend Adipo-IR index as a predictive marker for the NAFLD development and the indicator for therapy success in T2D patients. We established new genetic markers

show abstract

Section: Discussionsupporting

confidence: 83%

Однонуклеотидні Поліморфізми Гена Адипонектину У Хворих На Цукровий Діабет 2-Го Типу Та Неалкогольну Жирову Хворобу Печінки

Karachentsev¹,

Gorshunska²,

Tyzhnenko³

et al. 2021

Mìžnarodnij endokrinologìčnij žurnal

View full text Add to dashboard Cite

show abstract

“…In a subsequent Japanese study of 119 histologically proven NAFLD (54 females) and 115 age-and gendermatched healthy controls (57 females), the only association found with the adiponectin 276 SNP was among females, where a higher allele frequency of 276G in NAFLD was observed (0.78 versus 0.65 in controls, P = 0.03) ( 200 ). More 45 and 276G homozygotes were seen among patients with severe fi brosis (23.4%) than among patients with mild fi brosis (2.8%).…”

Section: Adiponectin and Adiponectin Receptormentioning

confidence: 94%

Genetic determinants of hepatic steatosis in man

Hooper

Adams

Burnett

2011

Journal of Lipid Research

119

View full text Add to dashboard Cite

in childhood in some individuals, with a prevalence of 10% found in an autopsy study of 2-19 year olds from the United States ( 5 ). The prevalence of NAFLD increases with advancing age, with a peak between 40 and 69 years of age ( 2, 6 ).A cut-off of 5.5% hepatic steatosis has been accepted as the threshold to diagnose fatty liver, based on the 95th centile of hepatic fat content in low-risk subjects [normal body mass index (BMI), normal glucose tolerance, lack of excessive alcohol ingestion, and normal liver function tests] ( 1, 7 ). Subjects with NAFLD may have a range of histopathological changes (

show abstract

“…Musoo et al demonstrated that in an Italian cohort, an adiponectin genotype (?45T/G) was associated with hepatic steatosis, necroinflammatory grade, and postprandial adiponectin levels [50]. Similarly, associations between ?45T/G and HOMA-IR and liver fibrosis were reported among Japanese NAFLD patients [51]. In an Indian population, -11377GG and ?45T/G were associated with NAFLD [52].…”

Section: Adiponectinmentioning

confidence: 97%

Significance of genetic polymorphisms in patients with nonalcoholic fatty liver disease

Miyaaki

Nakao

2017

Clin J Gastroenterol

View full text Add to dashboard Cite

Because of recent advances in genetic research such as genome-wide association studies, the underlying genetic mechanisms of nonalcoholic fatty liver disease (NAFLD) pathophysiology have been elucidated. Here, we present a review of the current literature on the impact of genetic polymorphisms in patients with NAFLD. These genetic polymorphisms, which regulate lipid metabolism, glucose metabolism, and the renin-angiotensin system, are involved in NAFLD onset, steatosis, inflammation, fibrosis, and hepatocellular carcinoma (HCC). Among these genetic polymorphisms, many studies and meta-analyses have demonstrated that position 148 (rs738409 C/G) of the patatin-like phospholipase domain-containing protein (PNPLA3) is a genetic factor associated with NAFLD pathophysiological features, such as hepatic fat level, hepatic inflammation, fibrosis, and HCC. However, the impact of genetic polymorphisms on NAFLD pathophysiology appears to differ among ethnic groups. Therefore, further studies with larger sample sizes are needed for each ethnic group.

show abstract

Influence of adiponectin gene polymorphisms in Japanese patients with non-alcoholic fatty liver disease

Abstract: Adiponectin SNPs were found to be associated with the progression of liver fibrosis and insulin resistance, suggesting that adiponectin SNPs might play roles in the occurrence and progression of NAFLD.

Cited by 58 publications

References 40 publications

Однонуклеотидні Поліморфізми Гена Адипонектину У Хворих На Цукровий Діабет 2-Го Типу Та Неалкогольну Жирову Хворобу Печінки

Однонуклеотидні Поліморфізми Гена Адипонектину У Хворих На Цукровий Діабет 2-Го Типу Та Неалкогольну Жирову Хворобу Печінки

Genetic determinants of hepatic steatosis in man

Significance of genetic polymorphisms in patients with nonalcoholic fatty liver disease

Contact Info

Product

Resources

About