{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,12]],"date-time":"2025-11-12T14:25:17Z","timestamp":1762957517475,"version":"build-2065373602"},"reference-count":36,"publisher":"MDPI AG","issue":"21","license":[{"start":{"date-parts":[[2024,10,29]],"date-time":"2024-10-29T00:00:00Z","timestamp":1730160000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nutrients"],"abstract":"<jats:p>Background\/Objectives: Fatty acids are involved in some hepatic disorders. The proprotein convertase subtilisin kexin 9 (PCSK9) inhibits the uptake of low-density lipoproteins (LDLs), which contain lipids, into the liver and may thus be associated with nonalcoholic fatty liver disease (NAFLD), a cardiovascular disorder (CVD) risk. Statins reduce blood LDL\u2013cholesterol (LDL-C) levels and CVD risk and can attenuate the development of NAFLD while increasing blood PCSK9 levels. Methods: We investigated the correlation between PCSK9 and liver conditions in patients with familial hypercholesterolemia (FH), a CVD risk population with elevated blood LDL-C levels, under statin treatment. Blood tests for lipids, PCSK9, and liver function (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) were performed in patients with FH taking statins (n = 25, mean age = 57 years, 12% of males). The ALT:AST ratio was used as a marker of NAFLD risk. Results: The mean LDL-C level was 3.38 mmol\/L, and the median PCSK9 level was 312 ng\/mL. The median ALT:AST ratio was 0.88. A significant negative correlation was observed between the PCSK9 and ALT:AST ratio (\u03b2 = \u22120.67, p &lt; 0.05). Conclusions: Their negative correlation might give a hypothetical insight into the effect of statin treatment on the development of NAFLD, in relation to PCSK9 behavior, in patients with FH.<\/jats:p>","DOI":"10.3390\/nu16213686","type":"journal-article","created":{"date-parts":[[2024,10,29]],"date-time":"2024-10-29T08:42:09Z","timestamp":1730191329000},"page":"3686","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Nonalcoholic Fatty Liver Disease Risk and Proprotein Convertase Subtilisin Kexin 9 in Familial Hypercholesterolemia Under Statin Treatment"],"prefix":"10.3390","volume":"16","author":[{"given":"Masato","family":"Hamasaki","sequence":"first","affiliation":[{"name":"Division of Community and Family Medicine, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke 329-0498, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2625-571X","authenticated-orcid":false,"given":"Naoki","family":"Sakane","sequence":"additional","affiliation":[{"name":"Division of Preventive Medicine, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, 1-1 Fushimi-Ku, Kyoto 612-8555, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8119-633X","authenticated-orcid":false,"given":"Kazuhiko","family":"Kotani","sequence":"additional","affiliation":[{"name":"Division of Community and Family Medicine, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke 329-0498, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2024,10,29]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"2075","DOI":"10.1093\/jn\/135.9.2075","article-title":"Mechanisms by Which Dietary Fatty Acids Modulate Plasma Lipids","volume":"135","author":"Fernandez","year":"2005","journal-title":"J. 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