Skip to main content
Download PDF

Association of serum asprosin with metabolic dysfunction-associated fatty liver disease in older adult type 2 diabetic patients: a cross-sectional study

BMC Endocrine Disorders volume 24, Article number: 27 (2024) Cite this article

Abstract

Background

To explore the association of serum asprosin levels with metabolic dysfunction-associated fatty liver disease (MAFLD) in older adults with type 2 diabetes mellitus (T2DM).

Methods

The cross-sectional study enrolled patients ≥ 65 years old diagnosed with T2DM at two community health service centers between November 2019 and July 2021. Logistic regression was applied to analyze the influencing factors of MAFLD.

Results

Totally 219 cases were included. Compared with diabetic individuals without MAFLD (n = 105), diabetics with MAFLD (n = 114) had younger ages, higher body mass index values, shorter time from T2DM diagnosis, increased waist-to-hip ratios, elevated triglycerides, reduced high-density lipoprotein cholesterol (HDL-C), elevated alanine aminotransferase (ALT), elevated γ-glutaryl transferase, elevated fasting insulin, and elevated HOMA-IR (all P < 0.05). Serum asprosin levels were elevated in diabetics with MAFLD in comparison with the non-MAFLD group (291.71 ± 73.69 vs. 255.24 ± 82.52 pg/ml, P = 0.001). Multivariable analysis revealed, after adjusted for age, time from T2DM diagnosis, HDL-C, and ALT, serum asprosin level (OR = 1.006, 95%CI: 1.001–1.010, P = 0.014) were independently associated with MAFLD in T2DM.

Conclusions

High asprosin level are associated with MAFLD in older patients with T2DM, after adjusted for age, time from T2DM diagnosis, WHR, TG, HDL-C, ALT, GGT, FINS, and HOMA-IR.

Peer Review reports

Background

Metabolic dysfunction-associated fatty liver disease (MAFLD) results from fatty liver changes unrelated to alcohol intake [1,2,3]. The reported prevalence of MAFLD is 24–45% [1,2,3]. MAFLD has significant associations with insulin resistance, obesity, weight gain, and type 2 diabetes mellitus (T2DM). Metabolic dysfunction-associated steatohepatitis (MASH) is the advanced stage of MAFLD, and MASH, in turn, can progress to cirrhosis [1,2,3]. Of all patients with T2DM, 76% and 56% have MAFLD and MASH, respectively [1,2,3]. Progression from MASH to cirrhosis may be uncommon but could be promoted by obesity and diabetes [4]. MASH is associated with elevated mortality compared with MAFLD [5]. T2DM was affecting 9% and 7.9% of adult men and women in 2014 globally, respectively [6], but showed a prevalence of 14.6% in 2017–2018 in the United States of America (USA) [7] and 12.4% in 2018 in China [8]. The detrimental complications of T2DM include cardiovascular disease, neuropathy, nephropathy, retinopathy, and even mortality [9,10,11,12,13]. Patients with T2DM and MAFLD require very aggressive management to prevent T2DM complications and the progression of MAFLD to MASH, but caution must be taken to avoid overtreatment and drug side effects in T2DM patients without MAFLD [14,15,16].

Asprosin represents a novel protein hormone produced by the white fat tissue, which promotes glucose release by the liver. In T2DM, asprosin levels are elevated and positively correlated with insulin resistance and may serve as a biomarker to predict T2DM onset and monitor treatment effects [17]. Asprosin and adiponectin are elevated in obese children with MAFLD [18], and their combination is considered a diagnostic marker of MAFLD [19].

Indeed, MAFLD diagnosis relies on imaging and histopathology. Biopsy remains the gold standard for MAFLD diagnosis but represents an invasive tool not easily accepted by patients [20] and cannot be performed routinely for screening purposes [21]. Ultrasound is considered the first-line imaging modality for MAFLD, with a sensitivity of 60–94% and a specificity of 84–95%, both of which increase with MAFLD severity [21]. Computed tomography (CT) is more expensive and involves radiation, which is not feasible for screening or follow-up [1, 21]. Magnetic resonance imaging (MRI) constitutes the most accurate imaging tool for MAFLD detection but is even more expensive than CT and less readily available [1, 21]. Previous studies have indicated that various blood markers, e.g., alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutaryl transferase (GGT), triglycerides (TG), and C-reactive protein (CRP), are elevated in MAFLD, albeit with low sensitivity and specificity [1, 21, 22]. Hence, asprosin could be a diagnostic biomarker for MAFLD, but its association with MAFLD in the context of T2DM is poorly described.

Therefore, this study explored the association of asprosin with MAFLD in older adults with T2DM. The findings could help improve the clinical management of MAFLD.

Methods

Study design and patients

This cross-sectional study included elderly individuals diagnosed with T2DM at Zhuoma Community Health Service Station and Chengbei Xijie Community Health Service Center in Changzhi City (Shanxi Province) from November 2019 to July 2021. This study had approval from the Ethics Committee of the First Hospital of Shanxi Medical University (2019 [K056]). The study kept patient data confidential and complied with the Declaration of Helsinki.

Inclusion criteria were (1) age ≥ 65 years, (2) meeting the 1999 World Health Organization (WHO) diagnostic criteria for T2DM [23], and (3) available asprosin measurements and clinical data (detailed in the “Data collection and definitions” section below). Exclusion criteria were (1) acute complications of T2DM (e.g., hypoglycemia, diabetic ketoacidosis, and hyperosmolar hyperglycemic syndrome), (2) tumors, (3) acute heart failure, (4) acute renal failure, (5) steroid-induced diabetes, or (6) pulmonary infection.

Cases were assigned to the MAFLD and non-MAFLD groups. A diagnosis of MAFLD was made based on the available literature [24]: (1) weekly alcohol intake below 140 and 70 g in men and women, respectively, (2) no primary or secondary cause of fatty liver, and (3) liver biopsy revealing fatty liver. Since not all patients accepted liver biopsy, MAFLD could be clinically diagnosed [24]: (1) idiopathic fatty liver according to liver ultrasound or (2) idiopathic serum ALT, AST, and/or GGT elevations for ≥ 6 months in patients with metabolic syndrome.

Data collection and definitions

Demographic (age and sex), clinical (BMI, waist-to-hip ratio [WHR], drinking history, time from T2DM diagnosis, systolic [SBP] and diastolic [DBP] blood pressure), and biochemistry (total cholesterol [TC], TG, high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], ALT, AST, GGT, creatinine [CRE], glycated hemoglobin [HbA1C], fasting plasma glucose [FPG], estimated glomerular filtration rate [eGFR], 2-hour postprandial plasma glucose [2hPG], fasting insulin [FINS], homeostasis model assessment of insulin resistance [HOMA-IR], fasting C-peptide [FC-P], and asprosin) data were collected from patient charts. HOMA-IR was calculated as (glucose×insulin)/22.5 (SI measurements) [25].

Statistical analysis

It was a retrospective study, and we included all eligible patients during the study period. Nevertheless, we use α = 0.05, power of 90%, Zα=1.96, Zpower=1.28, σ = 0.43, and δ = 0.3 and the formula below, a minimum of 27 patients were required for each group.

$$ n = \frac{{{{(1.96 + 1.28)}^2}*2*0.43*0.43}}{{{{(0.3)}^2}}} \approx 27$$

Data analysis was carried out with SPSS 22.0 (IBM Corp., Armonk, NY, USA). Continuous data were assessed for normality by the Kolmogorov-Smirnov test. Those with normal distribution were presented as mean ± standard deviation, and between-group comparisons used the independent Student’s t-test. Non-normally distributed continuous data were expressed by median (25th percentile, 75th percentile) and compared between groups by the Mann-Whitney U test. Categorical variables were expressed by number (percentage) and compared by the chi-square test. Factors associated with MAFLD were determined by logistic regression analysis. The multivariable model included parameters with P < 0.05 in univariable analysis using the Enter method. The associations of serum asprosin level with various factors were assessed by Spearman analysis. Two-tail P < 0.05 indicated statistical significance.

Results

Totally 219 patients were analyzed. In comparison with diabetics without MAFLD (n = 105), patients in the MAFLD group (n = 114) had younger ages (median, 71.0 vs. 72.0 years, P = 0.045) and higher BMI values (median, 26.1 vs. 23.8 kg/m2, P < 0.001). In addition, the MAFLD group showed a shorter time from T2DM diagnosis (median, 10.0 vs. 14.0 years, P < 0.001) and larger WHRs (median, 0.92 vs. 0.90, P = 0.018). Regarding biochemistry parameters, MAFLD cases had higher TG levels (median, 1.57 vs. 1.26 mM, P < 0.001), decreased HDL-C (median, 0.97 vs. 1.04 mM, P = 0.002), elevated ALT (median, 17.0 vs. 14.0 IU/L, P = 0.001), elevated GGT (median, 24.0 vs. 18.0 IU/L, P < 0.001), elevated FINS (median, 4.96 vs. 2.84 mIU/L, P < 0.001), and elevated HOMA-IR (median, 1.71 vs. 1.07, P < 0.001). Serum asprosin levels were elevated in diabetics with MAFLD compared with those without MAFLD (291.71 ± 73.69 vs. 255.24 ± 82.52 pg/ml, P = 0.001) (Table 1).

Table 1 Patient characteristics
Full size table

The multivariable analysis is summarized in Table 2. After adjusted for age (OR = 0.923, 95%CI: 0.853–0.999; P = 0.046), time from T2DM diagnosis (OR = 0.919, 95%CI: 0.876–0.965; P = 0.001), HDL-C (OR = 0.089, 95%CI: 0.018–0.429; P = 0.003), and ALT (OR = 1.042, 95%CI: 1.007–1.079; P = 0.018), serum asprosin levels (OR = 1.006, 95%CI: 1.001–1.010; P = 0.014) were independently associated with MAFLD in T2DM.

Table 2 Multivariable analysis of factors associated with type 2 diabetes mellitus accompanied by MAFLD.
Full size table

In correlation analyses, serum asprosin levels amounts had positive correlations with BMI (r = 0.288, P < 0.001), TG (r = 0.227, P = 0.001), GGT (r = 0.182, P = 0.007), Scr (r = 0.389, P < 0.001), FINS (r = 0.184, P = 0.006) and HOMA-IR (r = 0.142, P = 0.036), and a negative correlation with eGFR (r=-0.314, P < 0.001) (Table 3).

Table 3 Associations of serum asprosin levels with other clinical factors
Full size table

Discussion

In the present study, elderly adults with T2DM and MAFLD showed higher serum asprosin levels than those with T2DM but not MAFLD. Moreover, serum asprosin levels was independently associated with MAFLD in older diabetic adults. Therefore, simple blood draws to measure asprosin levels could be used to screen for MAFLD among patients with T2DM. Still, ultrasound is also an inexpensive, accurate, and readily available method for the screening of MAFLD. Maybe the two methods could be combined concurrently or sequentially in a strategy to improve the screening of MAFLD in the future.

In T2DM, asprosin levels are high and positively correlated with insulin resistance and could serve as a biomarker to predict T2DM onset and monitor treatment effects [17]. Additionally, high asprosin levels have been reported in T2DM [17], and asprosin levels correlated with FINS and HOMA-IR in the present study. Individuals with asprosin deficiency are extremely lean and maintain euglycemia despite low plasma insulin levels [26]. On the other hand, insulin resistance in patients and animal models is associated with high asprosin levels, and a single injection of recombinant asprosin in mice was sufficient to increase glycemia [26]. Asprosin also impairs insulin signaling [27] and causes inflammation, endoplasmic reticulum stress, and insulin resistance [28]. Regarding the markers of glucose and insulin metabolism, asprosin has a positive correlation with HOMA-IR and a negative association with HOMA-β [29]. Furthermore, asprosin levels are independently associated with T2DM [29,30,31,32]. Of note, You et al. [33] recently reported that asprosin is not necessarily elevated in all T2DM patients but mainly in those with peripheral artery disease, which warrants future investigation. In this work, asprosin levels were associated with BMI, TG, FINS, and HOMA-IR and inversely correlated with eGFR, indicating that high serum asprosin correlates with T2DM features, nephropathy, and metabolic syndrome.

In this study, asprosin levels were higher in older patients. Asprosin levels appear to increase with maternal age in pregnant women [34]. However, a study showed no correlation between age and asprosin levels [29]. This discrepancy could be due to different study populations. Nevertheless, obesity, T2DM, and MAFLD are conditions associated with age. The potential relationship between age and asprosin levels should be further investigated.

Asprosin has also been suggested to be associated with MAFLD [18, 19] and is considered a diagnostic marker of MAFLD [19]. Asprosin is independently associated with obesity [35,36,37] and blood TG levels [29, 37], which are two risk factors for MAFLD [14,15,16]. Asprosin is elevated in obese children and even more in counterparts with MAFLD [18]. The link between asprosin and MAFLD could be insulin resistance and inflammation [26, 38], as well as the endothelial-to-mesenchymal transition [33], but the exact mechanisms remain undefined. In the present work, individuals with T2DM and MAFLD had significantly elevated asprosin levels in comparison with T2DM cases without MAFLD.

Since early MAFLD is benign and reversible [39], timely diagnosis of MAFLD is important. In the present work, asprosin levels correlated with GGT levels, suggesting asprosin as a blood biomarker for diagnosing MAFLD. It would be easier to detect blood asprosin levels, which may be more accepted by the patients, compared with liver biopsy or more expensive imaging examinations. Asprosin could even be a treatment target since targeting asprosin with a specific antibody has been shown to improve hyperinsulinemia in metabolic syndrome [26, 40].

Asprosin also appears to be associated with T2DM complications such as diabetic nephropathy [41]. In addition to the association of asprosin with obesity [35,36,37], which is in turn associated with T2DM, high asprosin levels were also observed in polycystic ovarian syndrome (PCOS), a condition often diagnosed in association with obesity and T2DM [17]. Asprosin is also involved in the development of cardiovascular diseases (CVD) [17], and T2DM is a risk factor for CVD. Nevertheless, the exact causal relationships among the above factors and conditions remain to be investigated.

The current study had limitations. Firstly, because all patients were from only two health centers in the same city, a limited number of cases were analyzed, indicating low generalizability of the present findings. In addition, only older adults were included; consequently, more patients of different ages should be included. Secondly, in recent years, the same concept of disease rapidly evolved from non-alcoholic fatty liver disease [39] to MAFLD [24] to metabolic-associated steatotic liver disease (MASLD) [42], shedding some confusion in definitions and data analysis. Still, Hagstrom et al. [43] showed that 99.5% of the patients diagnosed with NAFLD met the criteria for MASLD, concluding that “previous natural history data can be used”. Thirdly, due to the cross-sectional design, no causal conclusions could be drawn, and whether higher asprosin causes or results from MAFLD deserves further attention. Fourthly, because liver biopsy is not popular among patients, the diagnosis of MAFLD was mainly made by ultrasound, which could miss some cases of mild hepatic MAFLD since the sensitivity of ultrasound is lower for mild MAFLD compared with more advanced diseases [21]. Fifthly, the relationship between serum asprosin and MAFLD severity could not be evaluated because of the diagnostic method used. Therefore, well-designed prospective and longitudinal trials are required to determine asprosin’s value in MAFLD screening and diagnosis in patients with T2DM. Sixthly, although the present study identified the asprosin as being independent from time from T2MD diagnosis, it has to be noted that the time from diagnosis is an imperfect metric to determine the duration of diabetes since some patients can have T2DM for some time before diagnosis. Still, it was the only metric available. Finally, the sample size was too small to perform a reliable analysis of asprosin’s diagnostic value.

Conclusions

High serum asprosin levels are associated with MAFLD in patients with T2DM, after adjusted for age, time from T2DM diagnosis, WHR, TG, HDL-C, ALT, GGT, FINS, and HOMA-IR.

Data availability

All data generated or analyzed during this study are included in this published article.

References

  1. Rinella ME. Nonalcoholic fatty liver disease: a systematic review. JAMA. 2015;313:2263–73.

    Article  CAS  PubMed  Google Scholar 

  2. Chalasani N, Younossi Z, Lavine JE, Diehl AM, Brunt EM, Cusi K, Charlton M, Sanyal AJ, American Gastroenterological A, American Association for the Study of Liver D. American College of G: the diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology. 2012;142:1592–609.

    Article  PubMed  Google Scholar 

  3. European Association for the Study of the L. European Association for the Study of D, European Association for the study of O: EASL-EASD-EASO Clinical Practice guidelines for the management of non-alcoholic fatty liver disease. J Hepatol. 2016;64:1388–402.

    Article  Google Scholar 

  4. Adams LA, Sanderson S, Lindor KD, Angulo P. The histological course of nonalcoholic fatty liver disease: a longitudinal study of 103 patients with sequential liver biopsies. J Hepatol. 2005;42:132–8.

    Article  PubMed  Google Scholar 

  5. Ekstedt M, Franzen LE, Mathiesen UL, Thorelius L, Holmqvist M, Bodemar G, Kechagias S. Long-term follow-up of patients with NAFLD and elevated liver enzymes. Hepatology. 2006;44:865–73.

    Article  CAS  PubMed  Google Scholar 

  6. Collaboration NCDRF. Worldwide trends in diabetes since 1980: a pooled analysis of 751 population-based studies with 4.4 million participants. Lancet. 2016;387:1513–30.

    Article  Google Scholar 

  7. Wang L, Li X, Wang Z, Bancks MP, Carnethon MR, Greenland P, Feng YQ, Wang H, Zhong VW. Trends in Prevalence of diabetes and control of risk factors in diabetes among US Adults, 1999–2018. JAMA 2021.

  8. Wang L, Peng W, Zhao Z, Zhang M, Shi Z, Song Z, Zhang X, Li C, Huang Z, Sun X, et al. Prevalence and treatment of diabetes in China, 2013–2018. JAMA. 2021;326:2498–506.

    Article  PubMed  PubMed Central  Google Scholar 

  9. American Diabetes Association. Introduction: standards of Medical Care in Diabetes-2022. Diabetes Care. 2022;45:1–S2.

    Article  Google Scholar 

  10. Chatterjee S, Khunti K, Davies MJ. Type 2 diabetes. Lancet. 2017;389:2239–51.

    Article  CAS  PubMed  Google Scholar 

  11. Rao Kondapally Seshasai S, Kaptoge S, Thompson A, Di Angelantonio E, Gao P, Sarwar N, Whincup PH, Mukamal KJ, Gillum RF, Holme I, et al. Diabetes mellitus, fasting glucose, and risk of cause-specific death. N Engl J Med. 2011;364:829–41.

    Article  PubMed  PubMed Central  Google Scholar 

  12. Bragg F, Holmes MV, Iona A, Guo Y, Du H, Chen Y, Bian Z, Yang L, Herrington W, Bennett D, et al. Association between Diabetes and cause-Specific Mortality in Rural and Urban areas of China. JAMA. 2017;317:280–9.

    Article  PubMed  PubMed Central  Google Scholar 

  13. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2014;37(Suppl 1):81–90.

    Article  Google Scholar 

  14. Dharmalingam M, Yamasandhi PG. Nonalcoholic fatty liver disease and type 2 diabetes Mellitus. Indian J Endocrinol Metab. 2018;22:421–8.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Parry SA, Hodson L. Managing NAFLD in Type 2 diabetes: the Effect of Lifestyle interventions, a Narrative Review. Adv Ther. 2020;37:1381–406.

    Article  PubMed  PubMed Central  Google Scholar 

  16. Tomah S, Alkhouri N, Hamdy O. Nonalcoholic fatty liver disease and type 2 diabetes: where do diabetologists stand? Clin Diabetes Endocrinol. 2020;6:9.

    Article  PubMed  PubMed Central  Google Scholar 

  17. Yuan M, Li W, Zhu Y, Yu B, Wu J. Asprosin: a Novel Player in Metabolic diseases. Front Endocrinol (Lausanne). 2020;11:64.

    Article  PubMed  Google Scholar 

  18. Liu LJ, Kang YR, Xiao YF. Increased asprosin is associated with non-alcoholic fatty liver disease in children with obesity. World J Pediatr. 2021;17:394–9.

    Article  CAS  PubMed  Google Scholar 

  19. Ke F, Xue G, Jiang X, Li F, Lai X, Zhang M, Shen Y, Gao L. Combination of asprosin and adiponectin as a novel marker for diagnosing non-alcoholic fatty liver disease. Cytokine. 2020;134:155184.

    Article  CAS  PubMed  Google Scholar 

  20. Berger D, Desai V, Janardhan S. Con: liver biopsy remains the Gold Standard to evaluate fibrosis in patients with nonalcoholic fatty liver disease. Clin Liver Dis (Hoboken). 2019;13:114–6.

    Article  PubMed  Google Scholar 

  21. Shen FF, Lu LG. Advances in noninvasive methods for diagnosing nonalcoholic fatty liver disease. J Dig Dis. 2016;17:565–71.

    Article  PubMed  Google Scholar 

  22. National Institute for Health and Care Excellence.: National Institute for Health and Care Excellence guideline on non-alcoholic fatty liver disease, assessment and managementhttps://www.nice.org.uk/guidance/ng49 Accessed March 6 2022. London: National Institute for Health and Care Excellence; 2016

  23. Alberti KG, Zimmet PZ. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation. Diabet Med. 1998;15:539–53.

    Article  CAS  PubMed  Google Scholar 

  24. Huang J, Ou W, Wang M, Singh M, Liu Y, Liu S, Wu Y, Zhu Y, Kumar R, Lin S. MAFLD Criteria Guide the Subtyping of patients with fatty liver disease. Risk Manag Healthc Policy. 2021;14:491–501.

    Article  PubMed  PubMed Central  Google Scholar 

  25. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28:412–9.

    Article  CAS  PubMed  Google Scholar 

  26. Romere C, Duerrschmid C, Bournat J, Constable P, Jain M, Xia F, Saha PK, Del Solar M, Zhu B, York B, et al. Asprosin, a Fasting-Induced glucogenic protein hormone. Cell. 2016;165:566–79.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  27. Jung TW, Kim HC, Kim HU, Park T, Park J, Kim U, Kim MK, Jeong JH. Asprosin attenuates insulin signaling pathway through PKCdelta-activated ER stress and inflammation in skeletal muscle. J Cell Physiol. 2019;234:20888–99.

    Article  CAS  PubMed  Google Scholar 

  28. Lee T, Yun S, Jeong JH, Jung TW. Asprosin impairs insulin secretion in response to glucose and viability through TLR4/JNK-mediated inflammation. Mol Cell Endocrinol. 2019;486:96–104.

    Article  CAS  PubMed  Google Scholar 

  29. Wang Y, Qu H, Xiong X, Qiu Y, Liao Y, Chen Y, Zheng Y, Zheng H. Plasma Asprosin Concentrations Are Increased in Individuals with Glucose Dysregulation and Correlated with Insulin Resistance and First-Phase Insulin Secretion. Mediators Inflamm 2018, 2018:9471583.

  30. Zhang L, Chen C, Zhou N, Fu Y, Cheng X. Circulating asprosin concentrations are increased in type 2 diabetes mellitus and independently associated with fasting glucose and triglyceride. Clin Chim Acta. 2019;489:183–8.

    Article  CAS  PubMed  Google Scholar 

  31. Zhang X, Jiang H, Ma X, Wu H. Increased serum level and impaired response to glucose fluctuation of asprosin is associated with type 2 diabetes mellitus. J Diabetes Investig. 2020;11:349–55.

    Article  PubMed  Google Scholar 

  32. Li X, Liao M, Shen R, Zhang L, Hu H, Wu J, Wang X, Qu H, Guo S, Long M, Zheng H. Plasma Asprosin Levels Are Associated with Glucose Metabolism, Lipid, and Sex Hormone Profiles in Females with Metabolic-Related Diseases. Mediators Inflamm 2018, 2018:7375294.

  33. You M, Liu Y, Wang B, Li L, Zhang H, He H, Zhou Q, Cao T, Wang L, Zhao Z, et al. Asprosin induces vascular endothelial-to-mesenchymal transition in diabetic lower extremity peripheral artery disease. Cardiovasc Diabetol. 2022;21:25.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  34. Janoschek R, Hoffmann T, Morcos YAT, Sengle G, Dotsch J, Hucklenbruch-Rother E. Asprosin in pregnancy and childhood. Mol Cell Pediatr. 2020;7:18.

    Article  PubMed  PubMed Central  Google Scholar 

  35. Duerrschmid C, He Y, Wang C, Li C, Bournat JC, Romere C, Saha PK, Lee ME, Phillips KJ, Jain M, et al. Asprosin is a centrally acting orexigenic hormone. Nat Med. 2017;23:1444–53.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  36. Wang CY, Lin TA, Liu KH, Liao CH, Liu YY, Wu VC, Wen MS, Yeh TS. Serum asprosin levels and bariatric surgery outcomes in obese adults. Int J Obes (Lond). 2019;43:1019–25.

    Article  CAS  PubMed  Google Scholar 

  37. Wang M, Yin C, Wang L, Liu Y, Li H, Li M, Yi X, Xiao Y. Serum asprosin concentrations are increased and Associated with insulin resistance in children with obesity. Ann Nutr Metab. 2019;75:205–12.

    Article  CAS  PubMed  Google Scholar 

  38. Alan M, Gurlek B, Yilmaz A, Aksit M, Aslanipour B, Gulhan I, Mehmet C, Taner CE. Asprosin: a novel peptide hormone related to insulin resistance in women with polycystic ovary syndrome. Gynecol Endocrinol. 2019;35:220–3.

    Article  CAS  PubMed  Google Scholar 

  39. Iqbal U, Perumpail BJ, Akhtar D, Kim D, Ahmed A. The Epidemiology, Risk Profiling and Diagnostic challenges of nonalcoholic fatty liver disease. Med (Basel) 2019, 6.

  40. Mishra I, Duerrschmid C, Ku Z, He Y, Xie W, Silva ES, Hoffman J, Xin W, Zhang N, Xu Y et al. Asprosin-neutralizing antibodies as a treatment for metabolic syndrome. Elife 2021, 10.

  41. Goodarzi G, Setayesh L, Fadaei R, Khamseh ME, Aliakbari F, Hosseini J, Moradi N. Circulating levels of asprosin and its association with insulin resistance and renal function in patients with type 2 diabetes mellitus and diabetic nephropathy. Mol Biol Rep. 2021;48:5443–50.

    Article  CAS  PubMed  Google Scholar 

  42. Rinella ME, Lazarus JV, Ratziu V, Francque SM, Sanyal AJ, Kanwal F, Romero D, Abdelmalek MF, Anstee QM, Arab JP, et al. A multisociety Delphi consensus statement on new fatty liver disease nomenclature. Ann Hepatol. 2024;29:101133.

    Article  PubMed  Google Scholar 

  43. Hagstrom H, Vessby J, Ekstedt M, Shang Y. 99% of patients with NAFLD meet MASLD criteria and natural history is therefore identical. J Hepatol 2023.

Download references

Acknowledgements

None.

Funding

This study was funded by the Shanxi Provincial Health Commission (Project No. 2021050).

Author information

Authors and Affiliations

  1. Department of Geriatrics, The First Hospital of Shanxi Medical University, Taiyuan, China

    Junfang Cui

  2. Department of Endocrinology, The First Hospital of Shanxi Medical University, Taiyuan, China

    Yunfeng Liu, Mina Li, Jianhong Yin, Jing Yang & Linxin Xu

  3. Shanxi Medical University, Taiyuan, China

    Jing Yang

Authors
  1. Junfang Cui
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Yunfeng Liu
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Mina Li
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Jianhong Yin
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Jing Yang
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Linxin Xu
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

Junfang Cui and Linxin Xu carried out the study, participated in data collection, and drafted the manuscript. Jing Yang, Junfang Cui, Linxin Xu, and Yunfeng Liu performed the statistical analysis and participated in the study design. Jianhong Yin and Mina Li participated in data acquisition, analysis, and interpretation and drafted the manuscript. All authors read and approved the final manuscript.

Corresponding authors

Correspondence to Jing Yang or Linxin Xu.

Ethics declarations

Ethics approval and consent to participate

We confirm that all methods were carried out in accordance with relevant guidelines and regulations. This work has been carried out in accordance with the Declaration of Helsinki (2000) of the World Medical Association. This study was approved by the Ethics Committee of the First Hospital of Shanxi Medical University (2019 [K056]). This article is a retrospective study. Therefore, the Ethics Committee of the First Hospital of Shanxi Medical University waived the requirement to obtain distinct written informed consent from the patients.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Cui, J., Liu, Y., Li, M. et al. Association of serum asprosin with metabolic dysfunction-associated fatty liver disease in older adult type 2 diabetic patients: a cross-sectional study. BMC Endocr Disord 24, 27 (2024). https://doi.org/10.1186/s12902-024-01560-1

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12902-024-01560-1

Keywords

BMC Endocrine Disorders

ISSN: 1472-6823

Contact us