دانلود مقاله ISI انگلیسی شماره 33813
عنوان فارسی مقاله

غلظت ویسفاتین سرم در بیماران سوء حاد و بازیابی وزن با بیماری بی اشتهایی عصبی

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
33813 2015 9 صفحه PDF سفارش دهید محاسبه نشده
خرید مقاله
پس از پرداخت، فوراً می توانید مقاله را دانلود فرمایید.
عنوان انگلیسی
Serum visfatin concentration in acutely ill and weight-recovered patients with anorexia nervosa
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Psychoneuroendocrinology, Volume 53, March 2015, Pages 127–135

کلمات کلیدی
بی اشتهایی عصبی - بازیابی وزن بیماری بی اشتهایی عصبی - لپتین -
پیش نمایش مقاله
پیش نمایش مقاله غلظت ویسفاتین سرم در بیماران سوء حاد و بازیابی وزن با بیماری بی اشتهایی عصبی

چکیده انگلیسی

Visfatin is a recently described protein that is thought to regulate the process of adipocyte differentiation. Findings suggest that visfatin may be actively involved in the control of weight regulatory networks. However, to what extent and which role it plays in eating disorders is still poorly understood, as mixed results have been reported. The aim of the current study was to investigate serum visfatin concentrations on a cross sectional sample between acute anorexia nervosa patients (n = 44), weight recovered patients (n = 13) and healthy controls (n = 46) and a longitudinal sample of acute patients (n = 57) during weight recovery at three different time-points. Results did not show significant differences in visfatin between the three groups; however, acute patients showed a higher visfatin/BMI-SDS ratio than controls and recovered patients. Longitudinal results revealed an increase of visfatin levels during therapy. Our results suggest that high ratios of visfatin/BMI-SDS could be a state marker in acute anorexia nervosa, displaying a compensatory mechanism of the individual to maintain normal visfatin levels under malnourished conditions.

مقدمه انگلیسی

Adipokines play a central role in the control of energy metabolism. They provide signals about the nutrient status of an organism, such as energy intake and expenditure as well as insulin sensitivity (Badman and Flier, 2007) and have therefore become a matter of central interest in the field of eating disorder research. Over the last years, particular attention has been paid to the role of leptin (Ehrlich et al., 2009, Föcker et al., 2011 and Hebebrand et al., 2007). In contrast, our knowledge of the novel adipokine visfatin is still sparse. Visfatin appears to be a multifunctional protein, acting as hormone, cytokine, and enzyme (for a review, see Sonoli et al., 2011). It was firstly identified as a Pre-B Cell Colony-Enhancing Factor (PBEF; Samal et al., 1994), which facilitated the maturation of early B-lymphocytes. It was also found to act as an enzyme called nicotinamide phosphoribosyl transferase (NAMPT), which is involved in the nicotine adenine dinucleotide (NAD+) salvage pathway. In 2005, Fukuhara et al. demonstrated that the adipokine visfatin, which amino acid sequence was identical to NAMPT/PBEF, acted as a protein mediator secreted by fat cells. It appears that visfatin secretion increases in the course of adipocyte differentiation and its synthesis is regulated by several factors including glucocorticoids, tumor necrosis factor alpha, interleukin 6, and growth factor hormone (Jia et al., 2004). Although the role of visfatin in energy homeostasis or weight regulation is of particular interest with respect to eating disorders and diabetes, reported results have been very heterogeneous, as highlighted in Table 1. Several studies have demonstrated elevated visfatin levels both in obese adults (Auguet et al., 2013, Jin et al., 2008, Manco et al., 2007, Pagano et al., 2006, Terra et al., 2012 and Wen et al., 2012) and children (Davutoglu et al., 2009, Dogru et al., 2007, Pagano et al., 2006, Revollo et al., 2004 and Sandeep et al., 2007) as well as in patients with diabetes mellitus (Chen et al., 2006, Dogru et al., 2007, Pagano et al., 2006, Revollo et al., 2004 and Sandeep et al., 2007), suggesting a possible link to insulin and glucose homeostasis. Further investigations found visfatin to be closely correlated with white adipose tissue (WAT) accumulation (Curat et al., 2006 and Jia et al., 2004). However, initial reports that visfatin is preferentially expressed by visceral adipose tissue (VAT; Araki et al., 2008, Barth et al., 2010 and Fukuhara et al., 2005) could not be confirmed by other studies (Berndt et al., 2005, Haider et al., 2006a and Körner et al., 2007). Similarly heterogeneous results were reported from studies testing for associations between visfatin levels and BMI in healthy individuals. Some authors found positive correlations while others found no relationship at all (see Table 1). Equally mixed results were observed in obese samples (Pagano et al., 2006 and Ziora et al., 2012). Important for eating disorder research are also notions of visfatin sharing associations with thyroid hormones (Caixàs et al., 2009 and Ozkaya et al., 2009) as well as bone formation (Xie et al., 2007), steroid hormone synthesis and ovarian functioning (Chan et al., 2007, Reverchon et al., 2013, Tsouma et al., 2014 and Zhang et al., 2014), however, results are again quite heterogeneous. Table 1. Visfatin research on weight related disorders. The table shows differences in visfatin between studied groups, whether visfatin in the sample showed a correlation with BMI, the used immunoassay, and type of blood sample. Author, year Group comparison Correlation with BMI Assay Serum/plasma Araki et al., 2008 HC < OB No ELISA a, b Plasma Auguet et al., 2013 HC < OB Not reported ELISA c Serum Dogru et al., 2007 HC < D No ELISA b Plasma Dostálová et al., 2009 HC = AN Not reported EIA Serum Davutoglu et al., 2009 HC < OB No in HC Yes (+) in Ob ELISA d Plasma Körner et al., 2007 HC = OB No ELISA c Serum Martos-Moreno et al., 2011 HC < OB Yes (+) EIA Serum Miazgowski et al., 2013 HC = normal weight OB No EIA Serum Olszanecka-Glinianowicz et al., 2012 HC = OB No ELISA b Plasma Pagano et al., 2006 HC > OB Yes (−) EIA Plasma Terra et al., 2012 HC < OB No before weight loss Yes after weight loss ELISA c Serum Wen et al., 2012 HC > OB NO ELISA e Plasma Zahorska-Markiewicz et al., 2007 HC < OB NO EIA Serum Ziora et al., 2012 HC > AN/NOS HC < OB Yes (+) in HC Yes (−) in OB EIA Serum HC = healthy control group; OB = obesity; AN = anorexia nervosa; D = diabetes mellitius; EIA = enzyme immune assay; ELISA = enzyme linked immunosorbent assay. ELISA a = RD Systems, Minneapolis, MN; ELISA b = Phoenix Pharmaceuticals, Belmont, CA/USA; ELISA c = AdipoGen Inc., Seoul, Korea; ELISA d = Alpco Diagnostics, Salem, NH; ELISA e = HuameiBio Inc., Wuhan, China. (–) = negative assocation; (+) = positive association. Table options These inconsistent findings may be partly due to the fact that researchers have not applied standard laboratory procedures, i.e. studies have used either serum or plasma samples and employed different immunoassays (see Table 1). According to a recent study (Körner et al., 2007) some of these immunoassays may deliver erroneous results due to unspecific binding. Research investigating visfatin under catabolic conditions has been rare. Reduced dietary intake (De Luis et al., 2008, Haider et al., 2006b, Manco et al., 2007 and Martos-Moreno et al., 2011) as well as exercise (Choi et al., 2007) have been associated with reduced visfatin concentrations in some but not all studies (Kang et al., 2011). Insights into the role of visfatin as an adipokine in weight disorders and its function in metabolic processes might be gained by investigating visfatin levels in anorexia nervosa (AN), a severe illness characterized by markedly reduced calorie intake and fear of weight gain leading to a significant decrease in overall adipose tissue (Treasure and Schmidt, 2005). To date, only two studies have investigated visfatin levels in AN – again with mixed results (see Table 1). Both used a cross-sectional design and applied an Enzyme Immunoassay (EIA; Phoenix Pharmaceuticals Inc., USA), which according to Körner et al. (2007) may have limited performance due to non-specific binding. Longitudinal data and data from recovered AN patients are still missing. The aim of the current study was to investigate visfatin levels in patients with acute AN, recovered from AN as well as longitudinally, using the only immunoassay (ELISA) that has been shown to measure serum visfatin with an acceptable specificity (Körner et al., 2007), with the overarching goal of establishing the potential clinical utility of visfatin as an endocrine biomarker in AN.

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