Author Correction: Apolipoprotein J is a hepatokine regulating muscle glucose metabolism and insulin sensitivity

Seo, Ji A; Kang, Moon Seong; Yang, Won Mo; Hwang, Won Min; Kim, Sang Soo; Hong, Soo Hyun; Heo, Jee In; Vijyakumar, Achana; Moura, Leandro Pereira de; Üner, Aykut Göktürk; Hu, Huang; Lee, Seung Hwan; Lima, Inês S.; Park, Kyong Soo; Kim, Min Seon; Dagon, Yossi; Willnow, Thomas E.; Aroda, Vanita R.; Ciaraldi, Theodore P.; Henry, Robert R.; Kim, Young–Bum

doi:10.1038/s41467-020-16305-6

Cited by 6 publications

(3 citation statements)

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“…The results of animal studies appeared to support our speculation. Seo et al ( 18 ) discovered that clusterin was mostly released by the liver and functioned in a paracrine manner in skeletal muscle by binding to its receptor LRP2, consequently modulating systemic glucose homeostasis.…”

Section: Discussionmentioning

confidence: 99%

“…One study has suggested that clusterin was a novel adipokine that linked cardiometabolic disease and obesity ( 17 ). In addition, liver-derived clusterin played an important role in regulating insulin-dependent muscle glucose uptake, hence regulating systemic metabolic homeostasis ( 18 ). However, the relationship between serum clusterin levels and NAFLD has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Associations between serum clusterin levels and non-alcoholic fatty liver disease

Wang

Shen

et al. 2023

Endocrine Connections

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Objective: Clusterin is closely correlated with insulin resistance and its associated comorbidities. This study aimed to investigate the correlation between serum clusterin levels and non-alcoholic fatty liver disease (NAFLD) and further explore the mediating role of insulin resistance in this relationship. Methods: This study enrolled 195 inpatients (41 males and 154 females) aged 18-61 years. Twenty-four patients were followed up for 12 months after bariatric surgery. Serum clusterin levels were measured using a sandwich enzyme-linked immunosorbent assay. Fatty liver disease was diagnosed on the basis of liver ultrasonography. The fatty liver index (FLI) was calculated to quantify the degree of hepatic steatosis. The mediating role of homeostasis model assessment-insulin resistance (HOMA-IR) was assessed using mediation analysis. Results: Participants with NAFLD had significantly higher serum clusterin levels than those without NAFLD (444.61 [325.76-611.52] mg/L versus 294.10 [255.20-373.55] mg/L, P < 0.01). With increasing tertiles of serum clusterin levels, the prevalence of NAFLD displayed an upward trend (P < 0.01). Multivariate linear regression analysis showed that serum clusterin levels were a positive determinant of FLI (standardized β = 0.271, P < 0.001) after adjusting for multiple metabolic risk factors. Serum clusterin levels significantly decreased after bariatric surgery (298.77 [262.56-358.10] mg/L versus 520.55 [354.94-750.21] mg/L, P < 0.01). In the mediation analysis, HOMA-IR played a mediating role in the correlation between serum clusterin levels and FLI; the estimated percentage of the total effect was 17.3%. Conclusion: Serum clusterin levels were associated with NAFLD. In addition, insulin resistance partially mediated the relationship between serum clusterin levels and FLI.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Associations between serum clusterin levels and non-alcoholic fatty liver disease

Wang

Shen

et al. 2023

Endocrine Connections

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“…Within the brain, clusterin is ubiquitously expressed in neurons and glia, and is especially abundant in astrocytes, while being absent from microglia (Yao et al, 2020) 1 . Circulating clusterin levels are very high in serum, predominantly derived from the liver (Seo et al, 2020), and approximate 100 µg/ml (about 1.6 µM). Although at much lower levels than in plasma, clusterin is also abundant in the CSF, with normal levels between 2-9 µg/ml (30-150 nM) (Sihlbom et al, 2008;Přikrylová Vranová et al, 2016).…”

Section: Structure and Expressionmentioning

confidence: 99%

Secreted Chaperones in Neurodegeneration

Chaplot

Jarvela

Lindberg

2020

Front. Aging Neurosci.

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Protein homeostasis, or proteostasis, is a combination of cellular processes that govern protein quality control, namely, protein translation, folding, processing, and degradation. Disruptions in these processes can lead to protein misfolding and aggregation. Proteostatic disruption can lead to cellular changes such as endoplasmic reticulum or oxidative stress; organelle dysfunction; and, if continued, to cell death. A majority of neurodegenerative diseases involve the pathologic aggregation of proteins that subverts normal neuronal function. While prior reviews of neuronal proteostasis in neurodegenerative processes have focused on cytoplasmic chaperones, there is increasing evidence that chaperones secreted both by neurons and other brain cells in the extracellular – including transsynaptic – space play important roles in neuronal proteostasis. In this review, we will introduce various secreted chaperones involved in neurodegeneration. We begin with clusterin and discuss its identification in various protein aggregates, and the use of increased cerebrospinal fluid (CSF) clusterin as a potential biomarker and as a potential therapeutic. Our next secreted chaperone is progranulin; polymorphisms in this gene represent a known genetic risk factor for frontotemporal lobar degeneration, and progranulin overexpression has been found to be effective in reducing Alzheimer’s- and Parkinson’s-like neurodegenerative phenotypes in mouse models. We move on to BRICHOS domain-containing proteins, a family of proteins containing highly potent anti-amyloidogenic activity; we summarize studies describing the biochemical mechanisms by which recombinant BRICHOS protein might serve as a therapeutic agent. The next section of the review is devoted to the secreted chaperones 7B2 and proSAAS, small neuronal proteins which are packaged together with neuropeptides and released during synaptic activity. Since proteins can be secreted by both classical secretory and non-classical mechanisms, we also review the small heat shock proteins (sHsps) that can be secreted from the cytoplasm to the extracellular environment and provide evidence for their involvement in extracellular proteostasis and neuroprotection. Our goal in this review focusing on extracellular chaperones in neurodegenerative disease is to summarize the most recent literature relating to neurodegeneration for each secreted chaperone; to identify any common mechanisms; and to point out areas of similarity as well as differences between the secreted chaperones identified to date.

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Insulin resistance in Alzheimer’s disease: The genetics and metabolomics links

Amin

Mostafa

Khojah

2023

Clinica Chimica Acta

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Author Correction: Apolipoprotein J is a hepatokine regulating muscle glucose metabolism and insulin sensitivity

Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Cited by 6 publications

References 0 publications

Associations between serum clusterin levels and non-alcoholic fatty liver disease

Associations between serum clusterin levels and non-alcoholic fatty liver disease

Secreted Chaperones in Neurodegeneration

Insulin resistance in Alzheimer’s disease: The genetics and metabolomics links

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