Lipoprotein Insulin Resistance Index Reflects Liver Fat Content in Patients With Nonalcoholic Fatty Liver Disease.

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Citation: Hepatology Communications. 5(4):589-597, 2021 04.Hepatology Communications. 5(4):589-597, 2021 Apr.PMID: 33860117Institution: MedStar Union Memorial Hospital | MedStar Washington Hospital CenterDepartment: Internal Medicine ResidencyForm of publication: Journal ArticleMedline article type(s): Journal ArticleSubject headings: *Insulin Resistance | *Lipoproteins/bl [Blood] | *Liver/pa [Pathology] | *Non-alcoholic Fatty Liver Disease/bl [Blood] | *Non-alcoholic Fatty Liver Disease/pa [Pathology] | Adipose Tissue/pa [Pathology] | Adult | Aged | Diabetes Complications | Female | Humans | Male | Middle Aged | Retrospective StudiesYear: 2021ISSN:
  • 2471-254X
Name of journal: Hepatology communicationsAbstract: The recently developed lipoprotein insulin resistance index (LP-IR) incorporates lipoprotein particle numbers and sizes and is considered to reflect both hepatic and peripheral IR. As tissue IR is a strong component of nonalcoholic fatty liver disease (NAFLD) pathogenesis, we aimed to assess the degree by which LP-IR associates with hepatic fat content. This was a single-center retrospective analysis of patients with NAFLD. LP-IR, the homeostasis model assessment of insulin resistance (HOMA-IR), and adipose tissue IR (Adipo-IR) were measured simultaneously. Liver fat content was estimated by FibroScan controlled attenuated parameter. Associations were assessed using Spearman's correlation and multivariate linear regression. The study included 61 patients. LP-IR was correlated with HOMA-IR (rho = 0.30; P = 0.02), typically thought to reflect hepatic IR, but not with Adipo-IR (rho = 0.15; P = 0.25). Liver fat content was significantly associated with Adipo-IR (rho = 0.48; P < 0.001), LP-IR (rho = 0.35; P = 0.005), and to a lesser degree with HOMA-IR (rho = 0.25; P = 0.051). The association of liver fat with LP-IR was limited to patients without diabetes (rho = 0.60; P < 0.0001), whereas no association was seen in those with diabetes. In a multivariate model, Adipo-IR, LP-IR, and diabetes were independently associated with liver fat and together explained 35% of the variability in liver fat. Conclusion: LP-IR is a reasonable measure of IR in non-diabetic patients with NAFLD and is associated with hepatic fat content. Although adipose tissue is the major contributor to liver fat, the additional contribution of nonadipose tissues can be easily estimated using LP-IR. Copyright (c) 2020 The Authors. Hepatology Communications published by Wiley Periodicals LLC on behalf of the American Association for the Study of Liver Diseases.All authors: Ben Yakov G, Lee W, Rotman Y, Sampson M, Shapses M, Sharma B, Sharma D, Sun Q, Vittal AOriginally published: Hepatology Communications. 5(4):589-597, 2021 Apr.Fiscal year: FY2021Fiscal year of original publication: FY2021Digital Object Identifier: Date added to catalog: 2021-06-07
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Journal Article MedStar Authors Catalog Article 33860117 Available 33860117

The recently developed lipoprotein insulin resistance index (LP-IR) incorporates lipoprotein particle numbers and sizes and is considered to reflect both hepatic and peripheral IR. As tissue IR is a strong component of nonalcoholic fatty liver disease (NAFLD) pathogenesis, we aimed to assess the degree by which LP-IR associates with hepatic fat content. This was a single-center retrospective analysis of patients with NAFLD. LP-IR, the homeostasis model assessment of insulin resistance (HOMA-IR), and adipose tissue IR (Adipo-IR) were measured simultaneously. Liver fat content was estimated by FibroScan controlled attenuated parameter. Associations were assessed using Spearman's correlation and multivariate linear regression. The study included 61 patients. LP-IR was correlated with HOMA-IR (rho = 0.30; P = 0.02), typically thought to reflect hepatic IR, but not with Adipo-IR (rho = 0.15; P = 0.25). Liver fat content was significantly associated with Adipo-IR (rho = 0.48; P < 0.001), LP-IR (rho = 0.35; P = 0.005), and to a lesser degree with HOMA-IR (rho = 0.25; P = 0.051). The association of liver fat with LP-IR was limited to patients without diabetes (rho = 0.60; P < 0.0001), whereas no association was seen in those with diabetes. In a multivariate model, Adipo-IR, LP-IR, and diabetes were independently associated with liver fat and together explained 35% of the variability in liver fat. Conclusion: LP-IR is a reasonable measure of IR in non-diabetic patients with NAFLD and is associated with hepatic fat content. Although adipose tissue is the major contributor to liver fat, the additional contribution of nonadipose tissues can be easily estimated using LP-IR. Copyright (c) 2020 The Authors. Hepatology Communications published by Wiley Periodicals LLC on behalf of the American Association for the Study of Liver Diseases.

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