Circulating Apolipoprotein L1 is associated with insulin resistance-induced abnormal lipid metabolism.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
16 10 2019
Historique:
received: 23 11 2018
accepted: 23 09 2019
entrez: 18 10 2019
pubmed: 18 10 2019
medline: 3 11 2020
Statut: epublish

Résumé

Circulating ApolipoproteinL1 (ApoL1) is a component of pre-β-high-density lipoprotein (HDL), however little is known about the relationship of ApoL1 with cardiometabolic factors. Considering previous studies reporting the correlation of ApoL1 to triglyceride, we have hypothesized that ApoL1 associates with insulin-related metabolism. The current study examined their associations in 126 non-diabetic subjects and 36 patients with type 2 diabetes (T2DM). Non-diabetic subjects demonstrated triglyceride (standardized coefficients [s.c.] = 0.204, p < 0.05), body mass index (s.c. =0.232, p < 0.05) and HDL cholesterol (s.c. = -0.203, p < 0.05) as independent determinant of ApoL1 levels, and the significant elevation of ApoL1 in metabolic syndrome. Lipoprotein fractionation analysis revealed the predominant distribution of ApoL1 in large HDL fraction, and the significant increase of ApoL1 in large LDL fraction in high ApoL1 samples with insulin resistance. In T2DM, ApoL1 was higher in T2DM with metabolic syndrome, however ApoL1 was lower with β cell dysfunction. Insulin significantly promotes ApoL1 synthesis and secretion in HepG2 cells. In conclusion, circulating ApoL1 may be associated with abnormal HDL metabolism in insulin resistant status. This may suggest a regulation of insulin signal on the ApoL1 level, leading to offer a novel insight to the ApoL1 biology.

Identifiants

pubmed: 31619724
doi: 10.1038/s41598-019-51367-7
pii: 10.1038/s41598-019-51367-7
pmc: PMC6795879
doi:

Substances chimiques

APOL1 protein, human 0
Apolipoprotein L1 0
Cholesterol, HDL 0
Cholesterol, LDL 0
Insulin 0
Triglycerides 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

14869

Commentaires et corrections

Type : ErratumIn

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Auteurs

Kenji Nishimura (K)

Department of Nephrology, Graduate School of Biomedical Science, Tokushima University, Tokushima, Japan.

Taichi Murakami (T)

Department of Nephrology, Graduate School of Biomedical Science, Tokushima University, Tokushima, Japan. c-tamurakami@eph.pref.ehime.jp.

Toshihiro Sakurai (T)

Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.

Masashi Miyoshi (M)

Division of Medical Technology, Tokushima University Hospital, Tokushima, Japan.

Kiyoe Kurahashi (K)

Department of Hematology, Endocrinology and Metabolism, Graduate School of Biomedical Sciences, Tokushima University, Tokushima, Japan.

Seiji Kishi (S)

Department of Nephrology, Graduate School of Biomedical Science, Tokushima University, Tokushima, Japan.

Masanori Tamaki (M)

Department of Nephrology, Graduate School of Biomedical Science, Tokushima University, Tokushima, Japan.

Tatsuya Tominaga (T)

Department of Chronomedicine, Graduate School of Biomedical Science, Tokushima University, Tokushima, Japan.

Sumiko Yoshida (S)

Department of Hematology, Endocrinology and Metabolism, Graduate School of Biomedical Sciences, Tokushima University, Tokushima, Japan.

Kojiro Nagai (K)

Department of Nephrology, Graduate School of Biomedical Science, Tokushima University, Tokushima, Japan.

Hideharu Abe (H)

Department of Nephrology, Graduate School of Biomedical Science, Tokushima University, Tokushima, Japan.

Shu-Ping Hui (SP)

Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.

Kazuhiko Kotani (K)

Division of Community and Family Medicine, Center for Community Medicine, Jichi Medical University, Shimotsuke, Japan.

Toshio Doi (T)

Department of Nephrology, Graduate School of Biomedical Science, Tokushima University, Tokushima, Japan.

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Classifications MeSH