Role of neuropeptide Y gene variant (rs161477) in liver histology in obese patients with non-alcoholic fatty liver disease

Aller, R.; López-Gómez, Juan José; Izaola, Olatz; Primo, David; Luis, Daniel de

doi:10.1016/j.endinu.2018.10.007

Cited by 7 publications

(4 citation statements)

References 32 publications

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“…Additional research is needed to identify whether it is necessary to assess various polymorphisms in the patient with NAFLD at the time of diagnosis and before starting therapy. However, the authors know that the NPY gene polymorphism rs16147 is independently related to a reduced proportion of steatohepatitis and lobulillar inflammation in obese people with biopsy-verified NAFLD [ 26 ].…”

Section: Resultsmentioning

confidence: 99%

Significant roles of potential genes and their mutations in nonalcoholic fatty liver disease

Sokouti¹

2023

ceh

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In addition to having inflammation in the liver, overweight people also have changes in the composition of their immune systems and subsets of their immune systems. There are several genes involved in liver metabolism that have been implicated in nonalcoholic fatty liver disease (NAFLD), a liver disease associated with obesity, which is caused by high triglycerides and liver transaminases. NAFLD, a global liver disease, may differ in gene expression depending on where a person lives. In some alleles, the risk factors were independent. Finally, the researchers identified many genetic variations connected to fatty liver disease in those who did not drink alcohol regularly. These variants were located in genes involved in RNA metabolism, protein catabolism, and energy metabolism.

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Section: Resultsmentioning

confidence: 99%

Significant roles of potential genes and their mutations in nonalcoholic fatty liver disease

Sokouti¹

2023

ceh

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“…For example, Patel et al [23] have described in a cross-sectional study a strong association between this genetic variant. Besides, Aller et al [24] reported a lower percentage of liver damage in A allele carriers with non-alcoholic fatty liver disease. Moreover, it have reported [25e27] an association of rs16147 variant with metabolic syndrome and its related phenotypes, such as central obesity and hyperglycemia.…”

Section: Discussionmentioning

confidence: 97%

Allele a of the rs16147 variant of neuropeptide Y predicts early metabolic improvements after bariatric surgery with biliopancreatic diversion in morbid obese subjects

Pacheco

Izaola

Primo

et al. 2021

Clinical Nutrition Open Science

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“…Despite its central, appetite-regulating actions, Y2R are also involved in oxidative fuel selection and lipid metabolism in peripheral tissues like fat, bones, and liver [ 41 ]. Genetic polymorphisms of the NPY gene (particullary the rs164147 polymorphism) have previously shown an association with insulin resistance and the development of steatohepatitis (the latter in obese subjects) [ 42 , 43 ]. As the JNJ-31020028-treated animals in the present study almost exclusively consumed a HFD [ 27 ] but did not develop liver steatosis, Y2R antagonists may be beneficial for liver health in an energy-rich setting as described before [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of NPY-2 Receptor Antagonists, Semaglutide, PYY3-36, and Empagliflozin on Early MASLD in Diet-Induced Obese Rats

Kloock,

Haerting,

Herzog

et al. 2024

Nutrients

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(1) Background: Modulators of the Neuropeptide Y (NPY) system are involved in energy metabolism, but the effect of NPY receptor antagonists on metabolic-dysfunction-associated steatotic liver disease (MASLD), a common obesity-related comorbidity, are largely unknown. In this study, we report on the effects of antagonists of the NPY-2 receptor (Y2R) in comparison with empagliflozin and semaglutide, substances that are known to be beneficial in MASLD. (2) Methods: Diet-induced obese (DIO) male Wistar rats were randomized into the following treatment groups: empagliflozin, semaglutide ± PYY3-36, the Y2R antagonists JNJ 31020028 and a food-restricted group, as well as a control group. After a treatment period of 8 weeks, livers were weighed and histologically evaluated. QrtPCR was performed to investigate liver inflammation and de novo lipogenesis (in liver and adipose tissue). Serum samples were analysed for metabolic parameters. (3) Results: Semaglutide + PYY3-36 led to significant weight loss, reduced liver steatosis (p = 0.05), and decreased inflammation, insulin resistance, and leptin levels. JNJ-31020028 prevented steatosis (p = 0.03) without significant weight loss. Hepatic downregulation of de novo lipogenesis-regulating genes (SREBP1 and MLXIPL) was observed in JNJ-31020028-treated rats (p ≤ 0.0001). Food restriction also resulted in significantly reduced weight, steatosis, and hepatic de novo lipogenesis. (4) Conclusions: Body weight reduction (e.g., by food restriction or drugs like semaglutide ± PYY3-36) is effective in improving liver steatosis in DIO rats. Remarkably, the body-weight-neutral Y2R antagonists may be effective in preventing liver steatosis through a reduction in de novo lipogenesis, making this drug class a candidate for the treatment of (early) MASLD.

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Role of neuropeptide Y gene variant (rs161477) in liver histology in obese patients with non-alcoholic fatty liver disease

Cited by 7 publications

References 32 publications

Significant roles of potential genes and their mutations in nonalcoholic fatty liver disease

Significant roles of potential genes and their mutations in nonalcoholic fatty liver disease

Allele a of the rs16147 variant of neuropeptide Y predicts early metabolic improvements after bariatric surgery with biliopancreatic diversion in morbid obese subjects

Effects of NPY-2 Receptor Antagonists, Semaglutide, PYY3-36, and Empagliflozin on Early MASLD in Diet-Induced Obese Rats

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