Skip to main content

Association between plasma omentin-1 levels in type 2 diabetic patients and peripheral artery disease



Type-2 diabetes mellitus is one of the major risk factors of atherosclerosis, particularly in peripheral artery disease (PAD). Several studies have documented a correlation between omentin-1 serum levels, atherosclerosis, and cardiovascular diseases. However, a clear link between circulating omentin-1 and PAD in diabetic patients has yet to be established. The aim of this study was to investigate the potential role of omentin-1 in PAD in type-2 diabetic patients.


In this cross-sectional study, we analyzed omentin-1 serum levels by ELISA in 600 type-2 diabetic patients with (n = 300) and without (n = 300) PAD at Fontaine’s stage II, III, or IV.


We found that omentin-1 serum levels were significantly lower in diabetic patients with PAD than in diabetic controls (29.46 vs 49.24 ng/mL, P < 0.001) and that the levels gradually decreased in proportion to disease severity (P < 0.05). The association between omentin-1 levels and PAD remained significant after adjusting for major risk factors in a multivariate analysis.


Our results suggest that omentin-1 is reduced in type 2 diabetic patients with PAD and that omentin-1 levels are related to disease severity.


Peripheral artery disease (PAD) represents a frequent manifestation of atherosclerosis disease. Approximately 202 million people worldwide are suffering from lower extremity artery disease [1]. The prevalence of PAD increases with the prevalence of type-2 diabetes mellitus (T2DM), one of the major risk factors of atherosclerosis. Furthermore, PAD has special features and poorer prognosis in diabetic patients than in non-diabetic patients. Patients with T2DM are a high-risk group for developing extensive vascular disease, which adversely affects quality of life. PAD, in these patients, represents an important public health problem, with a significant impact on healthcare and a heavy economic burden [2]. Consequently, early diagnosis and management of PAD in T2DM patients are critical for reducing the risk of major adverse cardiovascular events (MACE) and major adverse limb events (MALE), minimizing the risk of long-term disability [3]. International guidelines [4] addressing diagnosis, treatment, and overall management of patients with PAD suggest the ankle–brachial index (ABI) as an initial diagnostic test for PAD. However, ABI evaluation has a low sensitivity for detecting the initial stages of PAD, and it may not be applicable in patients with diabetes because of calcification of the artery walls, which can increase vessel stiffness [5].

Therefore, to be able to make an early diagnosis, we need to identify novel biomarkers that can detect PAD among diabetic patients.

In the past few years, attention has been focused on adipokines, cytokines produced and secreted by visceral adipose tissue and involved in the development of atherosclerotic disease. Studies have shown that some of these cytokines take part in the regulation of adipose tissue with a pro- or anti-inflammatory effect, and several researchers are investigating their possible role as biomarkers for metabolic disorders [6]. In this context, findings have documented a possible role of omentin serum levels in cardiovascular diseases. Omentin, a type of adipokine, is a hydrophilic protein with a molecular weight of 40 kDa; it is composed of 313 amino acids and is encoded by a gene present in chromosomal region 1q22–q23, which is related to T2DM [7]. This protein’s mRNA is expressed mainly in the fraction of the vascular stroma of the visceral adipose tissue, and poorly in subcutaneous adipose tissue and mature adipocytes. Omentin mRNA has also been identified in other tissues, such as endothelial cells, epicardial adipose tissue [8], thymus, small intestine, colon, reticulocytes, ovary, lung, and placenta. There are two main homologous isoforms: omentin-1, the most common form in human plasma; and omentin-2, which shares 83% of amino acids with isoform 1 [9]. Currently, the omentin-binding receptors are unknown [10]. Basic and clinical research has documented an anti-inflammatory action of omentin-1 and a mainly negative correlation between its plasma levels and insulin resistance, diabetes, obesity, and metabolic syndrome. Yoo and coworkers and Liu and colleagues, in cross-sectional studies, have documented that omentin-1 levels are reduced in patients with T2DM and metabolic syndrome, especially in patients with carotid plaques, compared to healthy subjects, diabetic subjects, or patients with metabolic syndrome without carotid atheromasia [11, 12]. More recent data have shown that, in general, the reduction of plasma levels of omentin increases the risk of diabetes and of atherosclerotic complications [13]. These observations have suggested a possible role of omentin-1 in atherosclerotic disease.

Other studies have investigated the relationship between omentin-1 and coronary artery disease [14, 15], stroke, and complications of T2DM [13, 16]. Based on these findings, some controversial data emerged about a negative, positive, or independent correlation between omentin-1 levels and cardiovascular risk factors. The analysis of these results revealed a different behavior of omentin-1 in healthy subjects compared to subjects with pre-existing metabolic disease [17, 18].

Only few, non-conclusive data exist regarding omentin-1 and PAD in non-diabetic patients [19] and a definitive link between circulating omentin-1 and PAD in diabetic patients has not yet been established.

The aim of this study was to investigate the potential role of omentin-1 in PAD of type-2 diabetic patients.


Study population

We performed a cross-sectional study of diabetic patients consecutively admitted to the Department of Vascular Diseases of the Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy, from 1 October 2015 to 31 June 2018. To be enrolled in the present study, each patient had to fulfill the inclusion criteria shown in Table 1. We enrolled diabetic patients with or without PAD. Type-2 diabetes mellitus was defined as a fasting plasma glucose level ≥ 126 mg/dl and/or a HbA1c level ≥ 6.5% or as a medical history of diabetes plus treatment with diabetes medication. Each patient enrolled in the study was assessed by a history of PAD symptoms or a confirmed PAD diagnosis, according to previous criteria established by the Ad Hoc Committee on Reporting Standards of the Society for Vascular Surgery and the International Society for Cardiovascular Surgery [20, 21]. Patients with clinical findings consistent with PAD underwent ABI measurement, and both lower limbs were assessed using arterial Doppler-enhanced ultrasonography, computed tomography angiography, lower limb angiography, at the attending physician’s judgment. Patients with an ABI > 0.90 and without symptoms of PAD did not undergo further testing and were deemed to be without PAD.

Table 1 Inclusion and exclusion criteria

The extent of PAD was determined by using the Fontaine classification, which defines four stages: stage I, asymptomatic; stage II, intermittent claudication; stage III, rest pain; stage IV, ischemic ulcers or gangrene [22].

Patients enrolled were also assessed by a history of heart failure symptoms or a confirmed diagnosis, as previously described [23].

The study was approved by the Ethics Committee of the Fondazione Policlinico Universitario A. Gemelli IRCCS and adhered to the principles of the Declaration of Helsinki. All patients enrolled gave their informed consent.

Biochemical measurements

All patients enrolled underwent a blood test after an overnight fasting period of 8 h. For every patient, fasting glucose, triglycerides, total cholesterol, and low- and high-density lipoprotein were determined. Renal function was assessed using estimated glomerular filtration rate (eGFR), which was calculated using the modification of diet in renal disease (MDRD) formula. Serum obtained and separated by centrifugation of blood samples was stored at − 80 °C before every measurement. Serum omentin-1 levels were determined by a commercially available ELISA kit (E-EL-H2028, Elabscience) according to its protocol. The intra- and inter-assay coefficients of variation were 3.5% and 10.5%, respectively. The sensitivity, defined as the mean ± 3 SD of the 0 standard, was calculated to be 0.15 pmol/ml. For each patient, the serum levels were measured twice, and the results were averaged.

Statistical analysis

Demographic and clinical data of the groups were compared using a Chi squared test and a t-test. Omentin-1 serum levels were compared with a Mann–Whitney, Kruskal–Wallis and Dunn’s Multiple Comparison, when appropriate. A log transformation was applied to the not normally distributed variables (fasting glucose, glycated hemoglobin, triglyceride, and omentin-1 levels) prior to performing further analysis. A multivariate stepwise logistic regression analysis was performed, adjusted for traditional risk factors and omentin-1 levels. The area under the receiver operating characteristics (ROC) curve was calculated to test the predictive discrimination of PAD. All analyses were performed using STATA version 11.0 for Windows (Statistics/Data Analysis, Stata Corporation, College Station, TX, USA). Statistical significance was established at P < 0.05.


The demographic and clinical characteristics of diabetic patients with PAD (indicated as PAD in Table 2) and without PAD (WPAD) are summarized in Table 2. Among the 600 diabetic patients enrolled in the study, 300 were included as PAD, and 300 as WPAD. PAD patients were more often smokers (P = 0.011), had higher blood pressure values (P = 0.010), had more frequent coronary artery disease (defined as a history of ischemic heart disease and/or previous coronary revascularization) (P = 0.022), and had higher LDL-cholesterol values (P = 0.02) than WPAD patients. There were no significant differences between groups regarding sex (P = 0.66), age (P = 0.19), body mass index (BMI) (P = 0.83), heart failure (P = 0.82), mean duration of diabetes (P = 0.48), fasting glucose (P = 0.76), glycated hemoglobin (P = 0.76), eGFR (P = 0.32), total cholesterol (TC) (P = 0.78), HDL-cholesterol (P = 0.59), and triglyceride (P = 0.78). No statistical difference in terms of diabetic therapy was observed between the two patient groups. According to the Fontaine’s classification, 168 patients were defined as stage II, 72 as stage III, and 60 as stage IV.

Table 2 Demographic and clinical data of diabetic subjects with and without PAD

Omentin-1 levels were lower among patients with PAD (29.46 ± 2.32 ng/ml) than among those without PAD (49.24 ± 6.44 ng/ml), as highlighted in Fig. 1. Moreover, when evaluating omentin-1 concentration according to patients’ functional status, we observed a distinct trend, with lower levels of circulating omentin-1 in patients with more severe disease (Fig. 2).

Fig. 1
figure 1

Omentin-1 levels according to PAD diagnosis. On the box plots, central lines represent the median, the length of the box represents the interquartile range and the lines extend to minimum and maximum values. Omentin-1 levels were lower among patients with PAD than among those without PAD (**P < 0.001)

Fig. 2
figure 2

Omentin-1 levels according to PAD severity. On the box plots, central lines represent the median, the length of the box represents the interquartile range and the lines extend to minimum and maximum values. According to patients’ functional status, represented by the Leriche-Fontaine classification, lower levels of circulating omentin-1 in patients with more severe disease were detected (LF II vs LF III, *P < 0.05; LF III vs LF IV, *P < 0.05)

The multivariate logistic regression analysis showed that, after adjustments for the cardiovascular risk factors age, male sex, BMI, eGFR, smoking, hypertension, ABI, CAD, heart failure, LDL-cholesterol, and omentin-1 levels, only ABI (OR 7.12, P = 0.011) and LDL-cholesterol (OR 2.37, P = 0.025) were independent determinants for the presence of PAD in patients with T2DM. Interestingly, there was an inverse relationship between omentin-1 levels and PAD in our diabetic population (OR 0.90, P < 0.001) (Table 3).

Table 3 Multivariable stepwise logistic regression model for presence of PAD adjusted for common risk factors and for omentin-1

The ability of the area under the ROC curve based on omentin-1 levels to predict the presence of PAD in diabetic patients was 0.968 (Fig. 3) and the best cut-off value of omentin-1 for prediction of the occurrence of PAD in our population was < 37.57 ng/ml (Sensitivity 97%, Specificity 96.33%).

Fig. 3
figure 3

ROC curve analysis of the ability of omentin-1 to predict the presence of PAD in diabetic patients. The ability of the area under the ROC curve was 0.968


Peripheral arterial disease is an endemic problem, with high direct and indirect social costs. Patients with PAD are often unable to work, require frequent hospitalizations, and often undergo major amputations [20, 24,25,26]. Considering the relevance of the disease, the ability to make an early diagnosis of PAD in diabetic patients is becoming increasingly important. Of the various diagnostic tests available, none of them is currently sensitive and specific enough to make an early diagnosis, and often the patient consults the specialist when the disease is already well advanced.

Inflammation plays a fundamental role in the formation of atherosclerotic plaque, particularly in the diabetic patient. A state of latent chronic inflammation can result from the initiation and progression of atherosclerotic disease. This inflammation is linked to different pathways, is mediated by hyperglycemia, and altered by the oxidation–reduction status and the release of inflammatory cytokines [27,28,29]. Adipose tissue is a very important source of inflammation, through the secretion of cytokines that directly or indirectly promote inflammatory pathways [30]. Among the various cytokines produced by adipose tissue, adipokines represent a pool responsible for various detrimental or protective processes [6, 30, 31]. For this reason, we wanted to evaluate the role of an easy-to-measure adipokine in diabetic patients. We found that omentin-1 is reduced in diabetic patients with PAD and that omentin-1 serum levels are statistically significantly lower in T2DM patients with PAD than in diabetic patients without PAD. This result is very interesting because the relationship between omentin and PAD in T2DM has never been documented before. In fact, Onur and colleagues have evaluated, in a cross-sectional and observational study, the association between the levels of omentin-1 and PAD of the lower limbs, demonstrating how the serum levels of this adipokine are lower in patients affected by PAD compared to healthy controls [19]. This study confirms that this adipokine is not only part of the energy balance but has a protective effect in diabetic patients, being involved in the lipid metabolism and inflammation that cause the vascular complications of diabetes. As already mentioned, omentin-1 levels are negatively associated with diabetes and metabolic syndrome and are reduced in diabetic patients with carotid atherosclerosis [11, 12]. The protective effect of omentin-1 could be explained by the suppression of inflammation and apoptosis of endothelial cells [6, 32]. To our knowledge, this is the first time that reduced omentin-1 serum levels were assessed as a potential biomarker for PAD in a diabetic population. Furthermore, we also demonstrated that omentin-1 serum levels decrease according to disease severity. This is a further important finding because, within the diabetic population affected by PAD, the values of omentin-1 could help to stratify patients to facilitate a more appropriate diagnostic and therapeutic process. Finally, we have documented that the relationship between lower omentin-1 levels and PAD in T2DM remains significant also after adjustment for potential confounding variables such as age, smoking status, hypertension, CAD, heart failure and serum lipid profile. If such a result is confirmed, the determination of omentin-1 serum levels could prove to be a new biomarker for early diagnosis and an effective follow-up of PAD in diabetic patients.

A limitation of our study is that its cross-sectional nature is not able to establish causal relationships between the findings. We need prospective data to confirm these results and to examine whether lower omentin-1 levels may also suffice as an effective biomarker for PAD in patients with type-2 diabetes. A further limitation is that we did not use a healthy control population to determine normal levels of omentin-1. In fact, there is no unequivocal evidence regarding the normal levels of omentin-1 [33,34,35]. Another limitation of the study is that we have not considered the distribution of adipose tissue in patients, and it is conceivable that a different distribution of fat, other than the one measured by the simple body mass index, could influence the levels of omentin-1. A further confounding factor is that we have not considered therapy among the significant variables, and it is possible that statins and hypoglycemic agents can play a role in the homeostasis of this adipokine. An additional limitation of our study is that we have not made a distinction between the type of antidiabetic therapy and the levels of omentin-1. Furthermore, it was not possible to study a relationship between aerobic exercise and the levels of this adipokine. Indeed, Menzel and coworkers suggest how different metabolic conditions can influence omentin levels, and this might also have happened in our model [17]. Finally, genetic analysis could help to better define the relationship between omentin-1 and PAD in diabetic patients. In fact, Jamshidi and colleagues evaluated the correlation between the polymorphism of the omentin Val109Asp gene—a missense variant of exon 4—and the risk of coronary artery disease [36]. Such a study of polymorphisms in our population could potentially provide interesting data.


In conclusion, we have shown that a relationship exists between omentin-1 levels and the presence of PAD in a diabetic population, that omentin-1 levels are reduced in T2DM affected by PAD, and that omentin-1 levels correlate with disease severity. Although further confirmations are necessary, these findings could foster earlier diagnosis and better management of this widespread disease.

Availability of data and materials

Not applicable.



ankle–brachial index


body mass index


computed tomography


coronary artery disease


estimated glomerular filtration rate


high-density lipoprotein


low-density lipoprotein


major adverse cardiovascular events


major adverse limb events


peripheral artery disease


receiver-operating characteristics


type 2 diabetes mellitus


very low-density lipoprotein


without PAD


  1. Fowkes FG, Rudan D, Rudan I, Aboyans V, Denenberg JO, McDermott MM, Norman PE, Sampson UK, Williams LJ, Mensah GA, et al. Comparison of global estimates of prevalence and risk factors for peripheral artery disease in 2000 and 2010: a systematic review and analysis. Lancet. 2013;382(9901):1329–40.

    PubMed  Article  Google Scholar 

  2. Malyar N, Fürstenberg T, Wellmann J, Meyborg M, Lüders F, Gebauer K, Bunzemeier H, Roeder N, Reinecke H. Recent trends in morbidity and in-hospital outcomes of in-patients with peripheral arterial disease: a nationwide population-based analysis. Eur Heart J. 2013;34(34):2706–14.

    PubMed  Article  Google Scholar 

  3. Marso SP, Hiatt WR. Peripheral arterial disease in patients with diabetes. J Am Coll Cardiol. 2006;47(5):921–9.

    PubMed  Article  Google Scholar 

  4. Aboyans V, Ricco J-B, Bartelink M-LEL, Björck M, Brodmann M, Cohnert T, Collet J-P, Czerny M, De Carlo M, Debus S, et al. 2017 ESC Guidelines on the Diagnosis and Treatment of Peripheral Arterial Diseases, in collaboration with the European Society for Vascular Surgery (ESVS): Document covering atherosclerotic disease of extracranial carotid and vertebral, mesenteric, renal. Eur Heart J. 2018;39(9):763–816.

    PubMed  Article  Google Scholar 

  5. Potier L, Abi Khalil C, Mohammedi K, Roussel R. Use and utility of ankle brachial index in patients with diabetes. Eur J Vasc Endovasc Surg. 2011;41(1):110–6.

    CAS  PubMed  Article  Google Scholar 

  6. Ohashi K, Shibata R, Murohara T, Ouchi N. Role of anti-inflammatory adipokines in obesity-related diseases. Trends Endocrinol Metab. 2014;25(7):348–55.

    CAS  PubMed  Article  Google Scholar 

  7. Xiang K, Wang Y, Zheng T, Jia W, Li J, Chen L, Shen K, Wu S, Lin X, Zhang G, et al. Genome-wide search for type 2 diabetes/impaired glucose homeostasis susceptibility genes in the Chinese: significant linkage to chromosome 6q21-q23 and chromosome 1q21-q24. Diabetes. 2004;53(1):228–34.

    CAS  PubMed  Article  Google Scholar 

  8. Qi XY, Qu SL, Xiong WH, Rom O, Chang L, Jiang ZS. Perivascular adipose tissue (PVAT) in atherosclerosis: a double-edged sword. Cardiovasc Diabetol. 2018;17(1):134.

    PubMed  PubMed Central  Article  Google Scholar 

  9. de Souza Batista CM, Yang RZ, Lee MJ, Glynn NM, Yu DZ, Pray J, Ndubuizu K, Patil S, Schwartz A, Kligman M, et al. Omentin plasma levels and gene expression are decreased in obesity. Diabetes. 2007;56(6):1655–61.

    PubMed  Article  Google Scholar 

  10. Watanabe T, Watanabe-Kominato K, Takahashi Y, Kojima M, Watanabe R. Adipose tissue-derived omentin-1 function and regulation. Compr Physiol. 2017;7(3):765–81.

    PubMed  Article  Google Scholar 

  11. Yoo HJ, Hwang SY, Hong HC, Choi HY, Yang SJ, Seo JA, Kim SG, Kim NH, Choi KM, Choi DS, et al. Association of circulating omentin-1 level with arterial stiffness and carotid plaque in type 2 diabetes. Cardiovasc Diabetol. 2011;10:103.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  12. Liu R, Wang X, Bu P. Omentin-1 is associated with carotid atherosclerosis in patients with metabolic syndrome. Diabetes Res Clin Pract. 2011;93(1):21–5.

    CAS  PubMed  Article  Google Scholar 

  13. Rathwa N, Patel R, Pramanik Palit S, Jadeja SD, Narwaria M, Ramachandran AV, Begum R. Circulatory Omentin-1 levels but not genetic variants influence the pathophysiology of Type 2 diabetes. Cytokine. 2019;119:144–51.

    CAS  PubMed  Article  Google Scholar 

  14. Ji Q, Zhang J, Du Y, Zhu E, Wang Z, Que B, Miao H, Shi S, Qin X, Zhao Y, et al. Human epicardial adipose tissue-derived and circulating secreted frizzled-related protein 4 (SFRP4) levels are increased in patients with coronary artery disease. Cardiovasc Diabetol. 2017;16(1):133.

    PubMed  PubMed Central  Article  Google Scholar 

  15. Saddic LA, Nicoloro SM, Gupta OT, Czech MP, Gorham J, Shernan SK, Seidman CE, Seidman JG, Aranki SF, Body SC, et al. Joint analysis of left ventricular expression and circulating plasma levels of Omentin after myocardial ischemia. Cardiovasc Diabetol. 2017;16(1):87.

    PubMed  PubMed Central  Article  Google Scholar 

  16. Hayashi M, Morioka T, Hatamori M, Kakutani Y, Yamazaki Y, Kurajoh M, Motoyama K, Mori K, Fukumoto S, Shioi A, et al. Plasma omentin levels are associated with vascular endothelial function in patients with type 2 diabetes at elevated cardiovascular risk. Diabetes Res Clin Pract. 2019;148:160–8.

    CAS  PubMed  Article  Google Scholar 

  17. Menzel J, di Giuseppe R, Biemann R, Wittenbecher C, Aleksandrova K, Pischon T, Fritsche A, Schulze MB, Boeing H, Isermann B, et al. Omentin-1 and risk of myocardial infarction and stroke: results from the EPIC-Potsdam cohort study. Atherosclerosis. 2016;251:415–21.

    CAS  PubMed  Article  Google Scholar 

  18. Elsaid NH, Sadik NA, Ahmed NR, Fayez SE, Mohammed NAE. Serum omentin-1 levels in type 2 diabetic obese women in relation to glycemic control, insulin resistance and metabolic parameters. J Clin Transl Endocrinol. 2018;13:14–9.

    PubMed  PubMed Central  Google Scholar 

  19. Onur I, Oz F, Yildiz S, Kuplay H, Yucel C, Sigirci S, Elitok A, Pilten S, Kasali K, Yasar Cizgici A, et al. A decreased serum omentin-1 level may be an independent risk factor for peripheral arterial disease. Int Angiol. 2014;33(5):455–60.

    CAS  PubMed  Google Scholar 

  20. Aboyans V, Ricco JB, Bartelink MEL, Björck M, Brodmann M, Cohnert T, Collet JP, Czerny M, De Carlo M, Debus S, et al. 2017 ESC Guidelines on the Diagnosis and Treatment of Peripheral Arterial Diseases, in collaboration with the European Society for Vascular Surgery (ESVS): Document covering atherosclerotic disease of extracranial carotid and vertebral, mesenteric, renal, upper and lower extremity arteriesEndorsed by: the European Stroke Organization (ESO) The Task Force for the Diagnosis and Treatment of Peripheral Arterial Diseases of the European Society of Cardiology (ESC) and of the European Society for Vascular Surgery (ESVS). Eur Heart J. 2017;39:763–816.

    Article  Google Scholar 

  21. Gerhard-Herman MD, Gornik HL, Barrett C, Barshes NR, Corriere MA, Drachman DE, Fleisher LA, Fowkes FG, Hamburg NM, Kinlay S, et al. 2016 AHA/ACC guideline on the management of patients with lower extremity peripheral artery disease: a report of the american college of cardiology/american heart association task force on clinical practice guidelines. Circulation. 2017;135(12):e726–79.

    PubMed  Google Scholar 

  22. Becker F. Exploration of arterial function with noninvasive technics. Results in chronic arterial occlusive disease of the lower limbs according to Leriche and Fontaine classification. Int Angiol. 1985;4(3):311–22.

    CAS  PubMed  Google Scholar 

  23. Narumi T, Watanabe T, Kadowaki S, Kinoshita D, Yokoyama M, Honda Y, Otaki Y, Nishiyama S, Takahashi H, Arimoto T, et al. Impact of serum omentin-1 levels on cardiac prognosis in patients with heart failure. Cardiovasc Diabetol. 2014;13:84.

    PubMed  PubMed Central  Article  Google Scholar 

  24. American Diabetes Association. Peripheral arterial disease in people with diabetes. Diabetes Care. 2003;26(12):3333–41.

    Article  Google Scholar 

  25. Anand SS, Caron F, Eikelboom JW, Bosch J, Dyal L, Aboyans V, Abola MT, Branch KRH, Keltai K, Bhatt DL, et al. Major adverse limb events and mortality in patients with peripheral artery disease: the COMPASS trial. J Am Coll Cardiol. 2018;71(20):2306–15.

    PubMed  Article  Google Scholar 

  26. Cornejo Del Río V, Mostaza J, Lahoz C, Sánchez-Arroyo V, Sabín C, López S, Patrón P, Fernández-García P, Fernández-Puntero B, Vicent D, et al. Prevalence of peripheral artery disease (PAD) and factors associated: an epidemiological analysis from the population-based Screening PRE-diabetes and type 2 DIAbetes (SPREDIA-2) study. PLoS ONE. 2017;12(10):e0186220.

    PubMed  PubMed Central  Article  Google Scholar 

  27. Bergmann K, Sypniewska G. Diabetes as a complication of adipose tissue dysfunction Is there a role for potential new biomarkers? Clin Chem Lab Med. 2013;51(1):177–85.

    CAS  PubMed  Article  Google Scholar 

  28. Domingueti CP, Dusse LM, Carvalho M, de Sousa LP, Gomes KB, Fernandes AP. Diabetes mellitus: the linkage between oxidative stress, inflammation, hypercoagulability and vascular complications. J Diabetes Complications. 2016;30(4):738–45.

    PubMed  Article  Google Scholar 

  29. Signorelli SS, Katsiki N. Oxidative stress and inflammation: their role in the pathogenesis of peripheral artery disease with or without type 2 diabetes mellitus. Curr Vasc Pharmacol. 2017;16:547–54.

    Article  Google Scholar 

  30. Wang Z, Nakayama T. Inflammation, a link between obesity and cardiovascular disease. Mediators Inflamm. 2010;2010:535918.

    PubMed  PubMed Central  Article  Google Scholar 

  31. Yamawaki H. Vascular effects of novel adipocytokines: focus on vascular contractility and inflammatory responses. Biol Pharm Bull. 2011;34(3):307–10.

    CAS  PubMed  Article  Google Scholar 

  32. De Jager SC, Pasterkamp G. Atheroprotective properties of human Omentin-1 in experimental atherosclerosis. Cardiovasc Res. 2016;110(1):1–3.

    PubMed  Article  Google Scholar 

  33. Ouerghi N, Ben Fradj MK, Bezrati I, Feki M, Kaabachi N, Bouassida A. Effect of high-intensity interval training on plasma omentin-1 concentration in overweight/obese and normal-weight youth. Obes Facts. 2017;10(4):323–31.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  34. Akbarzadeh S, Ghasemi S, Kalantarhormozi M, Nabipour I, Abbasi F, Aminfar A, Jaffari SM, Motamed N, Movahed A, Mirzaei M, et al. Relationship among plasma adipokines, insulin and androgens level as well as biochemical glycemic and lipidemic markers with incidence of PCOS in women with normal BMI. Gynecol Endocrinol. 2012;28(7):521–4.

    CAS  PubMed  Article  Google Scholar 

  35. Zhang Q, Zhu L, Zheng M, Fan C, Li Y, Zhang D, He Y, Yang H. Changes of serum omentin-1 levels in normal subjects, type 2 diabetes and type 2 diabetes with overweight and obesity in Chinese adults. Ann Endocrinol (Paris). 2014;75(3):171–5.

    Article  Google Scholar 

  36. Jamshidi J, Ghanbari M, Asnaashari A, Jafari N, Valizadeh GA. Omentin Val109Asp polymorphism and risk of coronary artery disease. Asian Cardiovasc Thorac Ann. 2017;25(3):199–203.

    CAS  PubMed  Article  Google Scholar 

Download references


Not applicable.


The authors are financially supported by the Fondazione Policlinico Universitario A. Gemelli IRCCS, Roma, Italy.

Author information

Authors and Affiliations



FB, EN participated in the design of the study, performed data analysis and reviewed the manuscript. FA and GP carried out the immunoassays. NB, DP and MF participated in the design of the study and performed statistical analyses. FB, RL and AF conceived the study, participated in its design and coordination and helped draft the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Federico Biscetti.

Ethics declarations

Ethics approval and consent to participate

The study was approved by the Ethics Committee of the Fondazione Policlinico Universitario A. Gemelli IRCCS and adhered to the principles of the Declaration of Helsinki. All the individuals agreed to participate in the study and gave informed consent.

Consent for publication

All authors have read the paper and agree that it can be published.

Competing interests

The authors declare that they have no competing interests.

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 distributed under the terms of the Creative Commons Attribution 4.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Biscetti, F., Nardella, E., Bonadia, N. et al. Association between plasma omentin-1 levels in type 2 diabetic patients and peripheral artery disease. Cardiovasc Diabetol 18, 74 (2019).

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI:


  • Omentin-1
  • Peripheral artery disease (PAD)
  • Type 2 diabetes
  • Atherosclerosis