{"title":"Preβ1-HDL binds to TG-rich lipoproteins and its release is impaired in the postprandial state among patients with poorly controlled type 2 diabetes.","authors":"Yuna Horiuchi, Satoshi Hirayama, Atsushi Hori, Yuri Ichikawa, Satoshi Soda, Utako Seino, Kazumasa Sekihara, Tsuyoshi Ueno, Yoshifumi Fukushima, Katsuo Kubono, Takashi Miida","doi":"10.1177/00045632251328154","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Although preβ1-high-density lipoprotein (preβ1-HDL) promotes cholesterol efflux, high fasting preβ1-HDL levels after breakfast are reduced in patients with poorly controlled type 2 diabetes.</p><p><strong>Objective: </strong>This study investigated whether preβ1-HDL binds to triglyceride (TG)-rich lipoproteins (TGRLs) in the postprandial state and is released during lipolysis.</p><p><strong>Methods: </strong>We measured preβ1-HDL concentrations, lecithin-cholesterol acyltransferase (LCAT) activity, and LCAT-dependent preβ1-HDL conversion before and after breakfast in patients with diabetes. We also performed in vitro studies using TGRLs. Preβ1-HDL was quantified by enzyme-linked immunosorbent assay and native two-dimensional gradient gel (N-2D-gel) electrophoresis.</p><p><strong>Results: </strong>Before breakfast, the diabetes group had higher preβ1-HDL concentrations than the healthy controls; after breakfast, levels in the two groups were similar. Neither LCAT mass nor the LCAT-dependent preβ1-HDL conversion rate changed after breakfast. Mixing of fasting plasma with chylomicrons or very-low-density lipoprotein (VLDL) reduced the preβ1-HDL level by 15% ± 4% and 45% ± 10%, respectively. N-2D-gel electrophoresis showed that preβ1-HDL was generated by bacteria-derived TG lipase only from postprandial VLDL of patients with type 2 diabetes.</p><p><strong>Conclusion: </strong>Preβ1-HDL binds to TGRLs in the postprandial state and is released during lipolysis, implying that postprandial hyperlipidemia impairs reverse cholesterol transport in patients with poorly controlled type 2 diabetes.</p>","PeriodicalId":8005,"journal":{"name":"Annals of Clinical Biochemistry","volume":" ","pages":"45632251328154"},"PeriodicalIF":2.1000,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of Clinical Biochemistry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/00045632251328154","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICAL LABORATORY TECHNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Although preβ1-high-density lipoprotein (preβ1-HDL) promotes cholesterol efflux, high fasting preβ1-HDL levels after breakfast are reduced in patients with poorly controlled type 2 diabetes.
Objective: This study investigated whether preβ1-HDL binds to triglyceride (TG)-rich lipoproteins (TGRLs) in the postprandial state and is released during lipolysis.
Methods: We measured preβ1-HDL concentrations, lecithin-cholesterol acyltransferase (LCAT) activity, and LCAT-dependent preβ1-HDL conversion before and after breakfast in patients with diabetes. We also performed in vitro studies using TGRLs. Preβ1-HDL was quantified by enzyme-linked immunosorbent assay and native two-dimensional gradient gel (N-2D-gel) electrophoresis.
Results: Before breakfast, the diabetes group had higher preβ1-HDL concentrations than the healthy controls; after breakfast, levels in the two groups were similar. Neither LCAT mass nor the LCAT-dependent preβ1-HDL conversion rate changed after breakfast. Mixing of fasting plasma with chylomicrons or very-low-density lipoprotein (VLDL) reduced the preβ1-HDL level by 15% ± 4% and 45% ± 10%, respectively. N-2D-gel electrophoresis showed that preβ1-HDL was generated by bacteria-derived TG lipase only from postprandial VLDL of patients with type 2 diabetes.
Conclusion: Preβ1-HDL binds to TGRLs in the postprandial state and is released during lipolysis, implying that postprandial hyperlipidemia impairs reverse cholesterol transport in patients with poorly controlled type 2 diabetes.
期刊介绍:
Annals of Clinical Biochemistry is the fully peer reviewed international journal of the Association for Clinical Biochemistry and Laboratory Medicine.
Annals of Clinical Biochemistry accepts papers that contribute to knowledge in all fields of laboratory medicine, especially those pertaining to the understanding, diagnosis and treatment of human disease. It publishes papers on clinical biochemistry, clinical audit, metabolic medicine, immunology, genetics, biotechnology, haematology, microbiology, computing and management where they have both biochemical and clinical relevance. Papers describing evaluation or implementation of commercial reagent kits or the performance of new analysers require substantial original information. Unless of exceptional interest and novelty, studies dealing with the redox status in various diseases are not generally considered within the journal''s scope. Studies documenting the association of single nucleotide polymorphisms (SNPs) with particular phenotypes will not normally be considered, given the greater strength of genome wide association studies (GWAS). Research undertaken in non-human animals will not be considered for publication in the Annals.
Annals of Clinical Biochemistry is also the official journal of NVKC (de Nederlandse Vereniging voor Klinische Chemie) and JSCC (Japan Society of Clinical Chemistry).