Association of plasma dipeptidyl peptidase-4 activity with non-alcoholic fatty liver disease in nondiabetic Chinese population |
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| Institution: | 1. Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, PR China;2. Department of Human Anatomy, Southwest Medical University, Luzhou, Sichuan, PR China;3. Center of Diabetic Systems Medicine, Guilin Medical University, Guilin, Guangxi, PR China;4. Department of Laboratory Medicine, The Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, PR China;5. Department of Epidemiology and Health Statistics, Guilin Medical University, Guilin, Guangxi, China;1. Dept. of Medicine, Duke University Medical Center, Durham, NC, United States;2. Dept. of Surgery, Duke University Medical Center, Durham, NC, United States;3. Dept. of Biostatistics and Bioinformatics, Duke University, United States;4. Duke Cancer Institute, Duke University Medical Center, United States;5. Duke Clinical Research Institute, Duke University Medical Center, United States;1. Unit of Nutritional Epidemiology, The National Institute for Environmental Medicine, Karolinska Institutet, Box 210, 171 77, Stockholm, Sweden;2. Department of Surgical Sciences, Section of Orthopedics, Uppsala University, Akademiska sjukhuset, 751 85 Uppsala, Sweden;3. Department of Public Health, Environmental Medicine, University of Southern Denmark, Winsløws Vej 17, Odense, Denmark;4. Department of Molecular Medicine and Surgery, Karolinska University Hospital Solna, 171 76 Stockholm, Sweden;1. Nutritional Epidemiology Institute and School of Public Health, Tianjin Medical University, Tianjin, China;2. Tianjin University of Traditional Chinese Medicine, Tianjin, China;3. Health Management Centre, Tianjin Medical University General Hospital, Tianjin, China;1. Department of Endocrinology, 424 General Military Hospital, Thessaloniki, Greece;2. Department of Cardiology, 424 General Military Hospital, Thessaloniki, Greece;3. Department of Cardiology, Skaraborg Hospital, Skovde, Sweden;4. Department of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece;5. Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA;6. Department of Hygiene and Epidemiology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece;7. Department of Pharmacology, 424 General Military Hospital, Thessaloniki, Greece |
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| Abstract: | ObjectiveThe pathogenesis of non-alcoholic fatty liver disease (NAFLD) is attributed to a “multi-hits hypothesis” involving insulin resistance, oxidative stress and inflammation. Dipeptidyl peptidase-4 (DPP4) was identified as a novel adipokine capable of enhancing the“multi-hits”. Hence, we investigated the association between plasma DPP4 activity and NAFLD in nondiabetic Chinese population.Design and methodsWe performed a cross-sectional study using data from 1105 subjects (36–79 years) in Guilin between 2015 and 2016. Plasma DPP4 activity, homeostatic model assessment of insulin resistance (HOMA-IR), oxidative stress parameters, and inflammatory markers were measured in all participants. NAFLD and its severity were diagnosed by ultrasound after the exclusion of alcohol abuse and other liver diseases.ResultsParticipants in the highest quartile of DPP4 activity had higher HOMA-IR, nitrotyrosine, 8-iso-PGF2a, interleukin-6, CRP, alanine aminotransferase, aspartate aminotransferase and γ-glutamyltransferase compared with those in the lowest quartile (all P < 0.05). Plasma DPP4 activity gradually increased across the groups according to the ultrasonographic severity of steatosis (P < 0.001 for the trend). In the highest DPP4 quartile, NAFLD risk was higher (odds ratio 1.88; 95% CI 1.04–3.37) than in the lowest quartile after adjustment for confounders. The risk for NAFLD increased more with higher levels of DPP4 activity, HOMA-IR, nitrotyrosine, 8-iso-PGF2a, interleukin-6 and CRP.ConclusionsPlasma DPP4 activity is significantly associated with NAFLD. The underlying mechanisms may be partly attributed to the interactions between insulin resistance, oxidative stress, inflammation, and DPP4. |
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