Omentin serum concentration and hepatic expression in chronic hepatitis C patients – together or apart?

Kukla, Michał; Waluga, Marek; Adamek, Brygida; Zalewska‐Ziob, Marzena; Kasperczyk, Janusz; Gabriel, Andrzej; Bułdak, Rafał Jakub; Sobala-Szczygieł, Barbara; L, Kepa; Ziora, Katarzyna; Żwirska-Korczala, K; Surma, Edward; Sawczyn, Tomasz; Hartleb, Marek

doi:10.5114/pjp.2015.54956

Cited by 13 publications

(17 citation statements)

References 38 publications

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“…Our previous study of non-obese CHC patients, 16% of whom were cirrhotic, showed significantly higher omentin serum levels compared to healthy controls. However, omentin serum levels were not associated with any histopathological findings[14]. Similar results were found by Nassif et al[18]’ s study, which showed significantly higher serum omentin levels in CHC subjects; however, no information was provided regarding histopathological examination.…”

Section: Discussionsupporting

confidence: 72%

“…The data regarding hepatic omentin expression is equivocal. Our previous study confirmed omentin expression in the liver tissue from chronic hepatitis C (CHC) patients[14]. However, an earlier study by Yang et al[15] found higher omentin expression in the stroma-vascular cells of omental fat and lower expression in the intestine and lung; no expression was observed in the liver, kidney and pancreas.…”

Section: Introductionsupporting

confidence: 73%

“…As mentioned above, there are conflicting results regarding omentin synthesis in the liver[14,15]. Our previous study of non-obese CHC patients, 16% of whom were cirrhotic, showed significantly higher omentin serum levels compared to healthy controls.…”

Section: Discussionmentioning

confidence: 96%

“…However, hepatic gene expression was not associated with its serum levels or any histopathological feature. Moreover, omentin was not up-regulated in cirrhosis[14]. …”

Section: Discussionmentioning

confidence: 99%

“…However, the role of omentin in CLD is unclear. A small number of studies have shown that omentin serum are levels increased in CHC, NAFLD and cirrhosis[14,18,19]. …”

Section: Introductionmentioning

confidence: 99%

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Serum omentin and vaspin levels in cirrhotic patients with and without portal vein thrombosis

Kukla

Waluga

Żorniak

et al. 2017

WJG

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AIMTo investigate serum omentin and vaspin levels in cirrhotic patients; and to assess the relationship of these levels with hemostatic parameters, metabolic abnormalities, cirrhosis severity and etiology.METHODSFifty-one cirrhotic patients (17 with portal vein thrombosis) were analyzed. Serum omentin and vaspin levels were measured with commercially available direct enzyme-linked immunosorbent assays (ELISAs). To assess platelet activity, the following tests were performed using a MULTIPLATE®PLATELET FUNCTION ANALYZER: (1) an ADP-induced platelet activation test; (2) a cyclooxygenase dependent aggregation test (ASPI test); (3) a von Willebrand factor and glycoprotein Ib-dependent aggregation (using ristocetin) test (RISTO test); and (4) a test for thrombin receptor-activating peptide-6 induced activation of the thrombin receptor, which is sensitive to IIb/IIIa receptor antagonists.RESULTSOmentin, but not vaspin, serum concentrations were significantly decreased in patients with portal vein thrombosis (PVT) (P = 0.01). Prothrombin levels were significantly increased in patients with PVT (P = 0.01). The thrombin receptor activating peptide (TRAP) test results were significantly lower in the PVT group (P = 0.03). No significant differences in adipokines serum levels were found regarding the etiology or severity of liver cirrhosis assessed according to the Child-Pugh or Model of End-Stage Liver Disease (MELD) scores. There was a significant increase in the TRAP (P = 0.03), ASPI (P = 0.001) and RISTO high-test (P = 0.02) results in patients with lower MELD scores. Serum omentin and vaspin levels were significantly down-regulated in patients without insulin resistance (P = 0.03, P = 0.02, respectively). A positive relationship between omentin and vaspin levels were found both when all of the patients were analyzed (r = 0.41, P = 0.01) and among those with PVT (r = 0.94, P < 0.001).CONCLUSIONSerum omentin levels are increased in patients without PVT. Cirrhosis origin and grade do not affect omentin and vaspin levels. The analyzed adipokines do not influence platelet activity.

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Section: Discussionsupporting

confidence: 72%

Section: Introductionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 96%

“…However, hepatic gene expression was not associated with its serum levels or any histopathological feature. Moreover, omentin was not up-regulated in cirrhosis[14]. …”

Section: Discussionmentioning

confidence: 99%

“…However, the role of omentin in CLD is unclear. A small number of studies have shown that omentin serum are levels increased in CHC, NAFLD and cirrhosis[14,18,19]. …”

Section: Introductionmentioning

confidence: 99%

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Serum omentin and vaspin levels in cirrhotic patients with and without portal vein thrombosis

Kukla

Waluga

Żorniak

et al. 2017

WJG

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Adipose Tissue‐Derived Omentin‐1 Function and Regulation

Watanabe

Watanabe‐Kominato

Takahashi

et al. 2017

Comprehensive Physiology

186

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Omentin-1, also known as intelectin-1, is a recently identified novel adipocytokine of 313 amino acids, which is expressed in visceral (omental and epicardial) fat as well as mesothelial cells, vascular cells, airway goblet cells, small intestine, colon, ovary, and plasma. The level of omentin-1 expression in (pre)adipocytes is decreased by glucose/insulin and stimulated by fibroblast growth factor-21 and dexamethasone. Several lines of experimental evidence have shown that omentin-1 plays crucial roles in the maintenance of body metabolism and insulin sensitivity, and has anti-inflammatory, anti-atherosclerotic, and cardiovascular protective effects via AMP-activated protein kinase/Akt/nuclear factor-κB/mitogen-activated protein kinase (ERK, JNK, and p38) signaling. Clinical studies have indicated the usage of circulating omentin-1 as a biomarker of obesity, metabolic disorders including insulin resistance, diabetes, and metabolic syndrome, and atherosclerotic cardiovascular diseases. It is also possible to use circulating omentin-1 as a biomarker of bone metabolism, inflammatory diseases, cancers, sleep apnea syndrome, preeclampsia, and polycystic ovary syndrome. Decreased omentin-1 levels are generally associated with these diseases. However, omentin-1 increases to counteract the acute phase after onset of these diseases. These findings indicate that omentin-1 may be a negative risk factor for these diseases, and also act as an acute-phase reactant by its anti-inflammatory and atheroprotective effects. Therapeutic strategies to restore omentin-1 levels may be valuable for the prevention or treatment of these diseases. Weight loss, olive oil-rich diet, aerobic training, and treatment with atorvastatin and antidiabetic drugs (metformin, pioglitazone, and exenatide) are effective means of increasing circulating omentin-1 levels. This review provides insights into the potential use of omentin-1 as a biomarker and therapeutic target for these diseases. © 2017 American Physiological Society. Compr Physiol 7:765-781, 2017.

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