Ask about this productRelated genes to: LENG4 antibody
- Gene:
- MBOAT7 NIH gene
- Name:
- membrane bound O-acyltransferase domain containing 7
- Previous symbol:
- LENG4
- Synonyms:
- BB1, hMBOA-7, LPLAT
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-28
- Date modifiied:
- 2018-03-06
Related products to: LENG4 antibody
Related articles to: LENG4 antibody
- Lifestyle factors (i.e. obesity) worsen infertility in both sexes. Metabolic dysfunction-associated steatotic liver disease (MASLD) in particular and adverse metabolic profile in general seem to be related to infertility, for the relationship with the over-weight and the endocrinological dysregulation as in Polycystic Ovary Syndrome, erectile disfunction and hypogonadism. - Source: PubMed
Publication date: 2026/06/15
Aquino Carmen ImmaVercellino NicoleFortina ElisabettaFerrante DanielaRigamonti CristinaMinisini RosalbaPirisi MarioRemorgida ValentinoBellan MattiaSurico Daniela - Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized during adolescence and exhibits sex-specific characteristics. Its prevalence in late adolescent females is around 10% in the general population and exceeds 30% in obesity. Genetic variants in , , and modulate hepatic fat accumulation and liver injury in adults, but evidence in adolescent females remains limited. This study examined MASLD-related variants ( rs738409, rs641738, rs2642438) in relation to metabolic and immune-inflammation indices in a late-adolescent female cohort. A cross-sectional analysis was performed in a prospectively assembled female cohort ( = 150; age 16-19 years). Ultrasound-defined MASLD prevalence was 16.7%. Although genotype-wise differences did not reach statistical significance, MASLD prevalence was directionally higher among G- and T-allele carriers, while a non-uniform, directionally favorable pattern was observed for the A allele. Nominal, unadjusted differences were observed for low-density lipoprotein cholesterol (LDL-c) and systemic immune-inflammation index (SII) across . Cumulative risk-allele burden analyses identified nominal trends for triglycerides (K-W = 0.05; J-T = 0.014) and triglyceride-glucose (TyG) index (K-W = 0.034; J-T = 0.008), which were not retained after adjustment for age and body mass index. Overall, these findings indicate modest, exploratory genotype-related patterns in metabolic and hematological immune-inflammation indices within a relatively healthy, late-adolescent female population. TyG and SII exhibited substantial inter-individual variability but did not demonstrate independent predictive value. Larger, longitudinal studies with advanced imaging are required to clarify the role of genetic variation and simple hematological metabolic-inflammation indices in early MASLD risk assessment in adolescent females. - Source: PubMed
Publication date: 2026/05/27
Jurkovic Mlakar SimonaKlisic AleksandraMarc JanjaOstanek Barbara - Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a primary driver of hepatocellular carcinoma (HCC). However, the synergistic impact of ancestral genetic susceptibility and socio-demographic transitions on the global MASLD-HCC landscape remains insufficiently quantified. - Source: PubMed
Publication date: 2026/06/11
Wu NaXiong XinyingWang XinyueWei ShuangShi XinyuChen YilinZhou WenjunWang JianyingZhang LeiLiu BaochengSong HualingYu HuitingJi Guang - Metabolic dysfunction-associated steatotic liver disease (MASLD), previously called non-alcoholic fatty liver disease, has emerged as the most common chronic liver disease in children and adolescents. This is happening in parallel to the global rise in paediatric obesity. Prevalence estimates are 13% in the general population and 47% among children with obesity, with higher rates observed in certain ethnic groups and in males. MASLD is often silent in early stages but may progress to steatohepatitis, fibrosis, cirrhosis and liver failure in a subset of patients. The pathophysiology of MASLD is multifactorial, involving excess calorie intake, insulin resistance and altered lipid metabolism. Genetic variants, particularly in , and influence disease susceptibility and disease severity, with some increasing the risk while others exhibiting a protective effect. The gut-liver axis, through mechanisms like increased intestinal permeability and dysbiosis, also contributes to hepatic fat accumulation and inflammation. The natural history of MASLD in children is variable. Some children may remain in remission while others may progress to advanced liver disease. Management is centred on lifestyle modification. A balanced, calorie-controlled diet, particularly a Mediterranean diet, has been shown to be beneficial in children and adolescents with MASLD, along with regular physical activity. Weight loss has been associated with histological improvement. Role of pharmacotherapy remains limited in the management of MASLD. Interventions like vitamin E, omega-3 fatty acids and GLP-1 receptor agonists are being explored in clinical trials with positive results. This narrative review is timely and relevant, as the growing burden of MASLD in children and adolescents calls for greater awareness and updated knowledge among clinicians and researchers. Despite notable progress in understanding the condition, important gaps remain regarding its natural history, early identification, and effective therapeutic options in the younger population. By bringing together current evidence and highlighting these areas of uncertainty, this review aims to support ongoing research and inform more age-appropriate approaches to care. - Source: PubMed
Publication date: 2026/05/20
Venu SwathilakshmiRaj Manu - Metabolic dysfunction-associated steatotic liver disease (MASLD) is the hepatic expression of systemic metabolic derangement; however, we have limited understanding of its progression or improvement, and there's a lack of adequate tools to monitor these changes. Metabolomics can provide dynamic biomarkers that reflect pathophysiological change. - Source: PubMed
Publication date: 2026/04/18
Troisi JTorre PSchiavo LMotta B MLombardi MFesta MSarcina TMasarone MPersico M