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Association of CTRP13 With Liver Enzymes and Cognitive Symptoms in Nonalcoholic Fatty Liver Disease

An, Kyungeh; Starkweather, Angela; Sturgill, Jamie; Salyer, Jeanne; Sterling, Richard K.

doi: 10.1097/NNR.0000000000000319
FEATURE ARTICLES
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Background Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease in which patients present with metabolic dysregulation and obesity as well as fat accumulation in the liver. Those with NAFLD frequently have symptoms of fatigue, sleep disturbance, depression, and cognitive dysfunction. C1q/TNF-related protein 13 (CTRP13) regulates glucose metabolism and obesity in mice, yet the role of CTRP13 in human NAFLD has not been elucidated.

Aims Our aims were to examine whether the plasma levels of CTRP13 are (a) increased in patients with NAFLD; (b) associated with metabolic dysregulation, obesity, liver enzymes, and dyslipidemia; and (c) associated with putative symptoms of NAFLD.

Methods An observational study was conducted with 23 adults with confirmed NAFLD. Plasma levels of CTRP13, insulin resistance, insulin sensitivity, HbA1C, lipid profile, and liver enzymes were collected. Anthropometric analysis (body mass index, waist–hip circumference ratio) and bioelectrical impedance analysis of body composition were used to assess obesity. Symptom questionnaires were used to assess putative symptoms of NAFLD. Plasma levels of CTRP13 were measured in 21 age- and sex-matched control samples from a biobank. Paired t test was used for comparison of the CTRP13 between NAFLD and controls. Pearson’s correlation coefficients were used to examine associations among variables.

Results Plasma levels of CTRP13 were significantly higher in patients with NAFLD than in normal controls (p < .001), were associated with higher levels of aspartate aminotransferase, alanine aminotransferase (both p < .05), triglycerides (p < .001), and poorer cognitive function, particularly visuospatial memory (p < .001).

Conclusions CTRP13 may be a surrogate biomarker of NAFLD symptoms and associated with hepatocellular damage, dyslipidemia, and cognitive dysfunction.

Kyungeh An, PhD, RN, is Associate Professor, Virginia Commonwealth University School of Nursing, Richmond.

Angela Starkweather, PhD, RN, ACNP-BC, CNRN, FAAN, is Professor, University of Connecticut School of Nursing, Storrs. At the time this research was completed, she was Associate Professor, Virginia Commonwealth University School of Nursing, Richmond.

Jamie Sturgill, PhD, is Assistant Professor, University of Kentucky College of Medicine, Lexington. At the time this research was completed, she was Assistant Professor, Virginia Commonwealth University School of Nursing, Richmond.

Jeanne Salyer, PhD, RN, is Associate Professor, Virginia Commonwealth University School of Nursing, Richmond.

Richard K. Sterling, MD, MSc, is Professor, Virginia Commonwealth University Health Systems, Richmond.

Accepted for publication June 9, 2018.

Research reported in this publication was supported by the Virginia Commonwealth University Center for Clinical and Translational Research’s Endowment Grant under Award UL1TR000058. The content is solely the responsibility of the authors and does not necessarily represent the official views of the Virginia Commonwealth University Center for Clinical and Translational Research.

This study followed the ethical conduct of human subject studies, and the study protocol has been approved by Virginia Commonwealth University Institutional Review Board (HM20000329).

The study protocol has been registered to the Clinical Trials.gov. Autonomic Dysfunction in Nonalcoholic Fatty Liver Disease, NCT02132780, registered on May 7, 2014, and the first subject was recruited on June 12, 2014, https://clinicaltrials.gov/ct2/show/NCT02132780?recrs=e&type=Obsr&cond=NAFLD&age=1&fund=3&rank=6

The authors have no conflicts of interest to report.

Corresponding author: Kyungeh An, PhD, RN, Virginia Commonwealth University School of Nursing, 1100 E. Leigh St., Richmond, VA 23289 (e-mail: kan@vcu.edu).

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