ABSTRACT PURPOSE: To investigate the effect of curcumin on visfatin and zinc-α2-glycoprotein (ZAG) expression levels in rats with non-alcoholic fatty liver disease (NAFLD). METHODS: Fifty-six male rats were randomly divided into a control group (n=16) and model group (n=40) and were fed on a normal diet or a high-fat diet, respectively. Equal volumes of sodium carboxymethyl cellulose (CMC) were intragastrically administered to the control group for 4 weeks. At the end of the 12th week, visfatin and ZAG protein expression levels were examined by immunohistochemistry. Visfatin mRNA levels were measured by semi-quantitative reverse transcription polymerase chain reaction. RESULTS: Compared with the control group, the model group showed significantly increased expression of visfatin in liver tissue (P < 0.01) and significantly decreased expression of ZAG (P < 0.01). These effects were ameliorated by curcumin treatment. CONCLUSIONS: Visfatin and zinc-α2-glycoprotein may be involved in the pathogenesis of NAFLD. Treatment of NAFLD in rats by curcumin may be mediated by the decrease of visfatin and the increase of non-alcoholic fatty liver disease.

Abstract Background: Migraines are headaches caused by changes in the trigeminovascular metabolic pathway. Migraine headache attacks are associated with neurovascular inflammation, but their pathophysiological mechanisms have not been fully explained. Objective: To investigate the relationship between serum vaspin, visfatin, chemerin and interleukin-18 (IL-18) levels and the frequency of attacks in migraine headache. Methods: Three groups were established: migraine with aura (n = 50), migraine without aura (n = 50) and control group (n = 50). The migraine diagnosis was made in accordance with the International Classification of Headache Disorders-III beta diagnostic criteria. The analyses on serum vaspin, visfatin, chemerin and IL-18 levels were performed using the enzyme-linked immunosorbent assay method. Results: The serum vaspin, visfatin, chemerin and IL-18 levels were found to be significantly higher in the migraine patients than in the control group (p < 0.01). No statistically significant differences in serum vaspin, visfatin, chemerin and IL-18 levels were found among the migraine patients during attacks or in the interictal period (p>0.05). The serum visfatin and chemerin levels of the migraine patients were positively correlated with their serum IL-18 levels (p < 0.01), while their serum chemerin and visfatin levels were positively correlated with their serum vaspin levels (p < 0.05). Conclusions: This study showed that these biomarkers may be related to migraine pathogenesis. Nonetheless, we believe that more comprehensive studies are needed in order to further understand the role of vaspin, visfatin, chemerin and IL-18 levels in the pathophysiology of migraine headaches.

Introduction: Nicotinamide Phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for NAD biosynthesis. Its extracellular form (eNAMPT), mainly secreted by visceral fat, has been shown to have bimodal, concentration- and structure-functional-dependent effects in important metabolic pathways and has been connected to a wide variety of diseases. Data suggests that as serum eNAMPT concentration rises to pathophysiological levels, as in obesity and type 2 diabetes (T2D), eNAMPT adopts a monomeric form capable of proinflammatory NAD-independent effects. Strategies to block the actions of the eNAMPT monomer could represent promising therapeutic approaches for obesity-related metabolic disorders. Consumption of anthocyanin rich foods appears to prevent or treat obesity-related consequences, such as T2D, inflammation and oxidative stress, but the mechanism behind this is unknown. Moreover, anthocyanins have been shown to inhibit the secretion of eNAMPT in animal models. With this study, we aim to understand if treating a rat model of obesity with anthocyanins could abrogate the impact of a high fat diet in the expression of monomeric eNAMPT. Methods: Mesenteric adipose tissue (mAT) was obtained from four groups of male Wistar rats, treated with different diets: (C) standard diet; (BE) standard diet + blackberry extract; (HFD) high fat diet; (HFDBE) high-fat diet + blackberry extract. eNAMPT monomer’s protein expression was measured by Western Blotting, after protein extraction and quantification from mAT, to access the differences between the animals fed a standard diet and those of increased metabolic risk – HFD, with and without treatment with anthocyanins. Results: The mAT from HFD rats displayed a higher expression of eNAMPT monomer, compared to C rats (138,6% ± 11,4% HFBE vs 100% C, p=0,01). The anthocyanin’s treatment influence on mAT eNAMPT monomer expression was also assessed. mAT eNAMPT monomer expression was significantly decreased in the HFDBE group compared to HFD (-54,1 ± 15,3 % [-89.4, -18.8], p<0,01). Conclusions: Anthocyanin consumption might be an interesting dietary approach to abrogate the impact of a high fat diet on the rise of monomeric eNAMPT in mesenteric adipose tissue. Ultimately, our results suggest that long-term anthocyanin treatment/supplementation might be effective for sustaining lower levels of monomeric eNAMPT in the context of diet-induced obesity, potentially preventing or delaying the consequent metabolic impairments such as the alarming epidemic of T2D.