scholarly journals Measurement of Plasma Resistin Concentrations in Horses with Metabolic and Inflammatory Disorders

Animals ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 77
Author(s):  
Beatriz Fuentes-Romero ◽  
Alberto Muñoz-Prieto ◽  
José J. Cerón ◽  
María Martín-Cuervo ◽  
Manuel Iglesias-García ◽  
...  

Obesity and its associated complications, such as metabolic syndrome, are an increasing problem in both humans and horses in the developed world. The expression patterns of resistin differ considerably between species. In rodents, resistin is expressed by adipocytes and is related to obesity and ID. In humans, resistin is predominantly produced by inflammatory cells, and resistin concentrations do not reflect the degree of obesity, although they may predict cardiovascular outcomes. The aim of this study was to investigate the usefulness of resistin and its relationship with ID and selected indicators of inflammation in horses. Seventy-two horses, included in one of the four following groups, were studied: healthy controls (C, n = 14), horses with inflammatory conditions (I, n = 21), horses with mild ID (ID1, n = 18), and horses with severe ID (ID2, n = 19). Plasma resistin concentrations were significantly different between groups and the higher values were recorded in the I and ID2 groups (C: 2.38 ± 1.69 ng/mL; I: 6.85 ± 8.38 ng/mL; ID1: 2.41 ± 2.70 ng/mL; ID2: 4.49 ± 3.08 ng/mL). Plasma resistin was not correlated with basal insulin concentrations. A significant (r = 0.336, p = 0.002) correlation was found between resistin and serum amyloid A. Our results show that, as is the case in humans, plasma resistin concentrations in horses are predominantly related to inflammatory conditions and not to ID. Horses with severe ID showed an elevation in resistin that may be secondary to the inflammatory status associated with metabolic syndrome.

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Giulia Savioli ◽  
Joy Archer ◽  
Emanuele Brianti ◽  
Giovanni Benelli ◽  
Manuela Schnyder ◽  
...  

Abstract Background Dogs are the main reservoir hosts of Leishmania infantum; nevertheless, recent investigations indicate a likely role for cats in the epidemiology of Leishmania infection. Feline leishmaniosis (FeL) remains poorly characterised, partly due to the lack of suitable diagnostic tools. This study aimed to compare serum amyloid A (SAA) levels and serum protein electrophoresis (SPE) profiles (specifically, alpha 2 and gamma globulins) in cats naturally exposed to or infected by L. infantum from southern Italy versus those of healthy controls and versus cats with neoplastic or inflammatory conditions from non-endemic areas. Methods Serum or plasma samples from four cohorts of cats were analysed for SAA levels and by SPE: (i) G1: healthy controls from Leishmania-non-endemic regions of Switzerland; (ii) G2: cats pre-diagnosed with neoplastic or inflammatory conditions available from the University of Cambridge sample archive; (iii) G3: L. infantum-seropositive, quantitative (q)PCR-negative cats from southern Italy; (iv) G4: L. infantum-seropositive and qPCR-positive cats from southern Italy. SAA data were assessed for normality and homoscedasticity using the Shapiro–Wilk and Levene’s tests, respectively; the Kruskall–Wallis test, followed by Dunn’s test with Bonferroni correction were subsequently used to compare SAA serum levels between groups. A weighted generalised linear model with a binomial distribution was used to assess statistically significant differences in the numbers of animals displaying elevated gamma globulins and increased alpha 2 globulins between groups. Results Overall, 68 samples were analysed (G1: n = 16, G2: n = 20, G3: n = 20, G4: n = 12). Cats suffering from neoplastic and inflammatory conditions (G2 ) showed significantly higher SAA levels than healthy controls (G1) (median values [interquartile range]: G1: 0.00 [0.00–0.00] mg/l versus G2: 0.85 [0.00–49.55] mg/l). G2, G3 and G4 cats showed higher percentages of individuals with increased alpha 2 globulins (percentages ± standard error: G1 = 20.0% ± 10.3, G2 = 80.0% ± 8.9, G3 = 70.0% ± 10.2, G4 = 75.0% ± 12.5) and gamma globulins (G1 = 0.0% ± 0, G2 = 65.0% ± 10.7, G3 = 50.0% ± 11.2, G4 = 58.3% ± 14.2) than healthy control cats (G1). For all three markers, no significant difference between cats within G2, G3 and G4 was recorded. Conclusions This study indicates that the proportions of animals with elevated levels of alpha 2 and gamma globulins are significantly higher in cats exposed to and infected with L. infantum. Levels of SAA and alpha 2 and gamma globulins may not be used to differentiate between L. infantum infection or exposure, and neoplastic and/or inflammatory conditions. Graphic Abstract


2020 ◽  
Author(s):  
Giulia Savioli ◽  
Joy Archer ◽  
Emanuele Brianti ◽  
Manuela Schnyder ◽  
Roberta Iatta ◽  
...  

Abstract Background: Although dogs are the main reservoir host of Leishmania infantum, recent investigations indicate a role for cats in its epidemiology. Feline leishmaniosis (FeL) remains poorly characterised, partly due to the lack of diagnostic tools. This study aimed to compare Serum Amyloid A (SAA) levels and serum protein electrophoresis (SPE) profiles (specifically, α2- and gamma globulins) in cats naturally exposed to or infected by L. infantum from southern Italy with those of healthy controls and of cats with neoplastic or inflammatory conditions from non-endemic areas.Methods: Serum or plasma samples from four cohorts of cats were analysed for SAA and by SPE, i.e G1: healthy controls from Leishmania-non-endemic regions of Switzerland, G2: cats pre-diagnosed with neoplastic or inflammatory conditions from the University of Cambridge’s sample archive, G3: L. infantum seropositive, qPCR-negative cats from southern Italy, G4: L. infantum seropositive and qPCR-positive cats from southern Italy. SAA data was assessed for normality using the Kolmogorov-Smirnoff and Shapiro-Wilk normality tests, then compared using a homogeneity of variance test for non-parametric data; the Kruskall-Wallis test, followed by Dunn’s multiple comparison test were used to compare SAA serum levels between groups. The Fisher’s Exact test was used to assess statistically significant differences in the numbers of animals displaying elevated gamma globulins and increased α2-globulins between groups.Results: Overall, 68 samples were analysed (G1 n=16, G2 n=20, G3 n=20, G4 n=12). Cats previously exposed to and/or infected with L. infantum, as well as cats suffering from neoplastic and inflammatory conditions showed significantly higher SAA levels (median values G1=0.00 (0.00-0.00) mg/L, G2=0.85 (0.00-49.55) mg/L, G3=0.00 (0.00-4.53) mg/L, G4= 0.00 (0.00-7.5) mg/L), and higher percentages of cats with increased α2-globulins (G1=20.0% ±10.3, G2=80.0% ±8.9, G3=70.0% ±10.2, G4=75.0% ±12.5) and gamma globulins (G1=0.0% ±0, G2=65.0% ±10.7, G3=50.0% ±11.2, G4=58.3% ±14.2) than healthy control cats. For all three markers, there was no significant difference between G2, G3 and G4.Conclusions: This study indicates that, whilst levels of gamma and α2-globulins and SAA are significantly elevated in cats infected by L. infantum, they cannot be used to differentiate between L. infantum infection or exposure and neoplastic or inflammatory conditions. Nevertheless, these indicators might assist monitoring of ongoing FeL if further studies indicate reduction during or following successful treatment.


2009 ◽  
Vol 1 (1) ◽  
pp. 53
Author(s):  
Marita Kaniawati ◽  
Andi Wijaya ◽  
Anwar Susanto

BACKGROUND: Low-HDL cholesterol is a risk factor of CAD. Although levels of HDLC are within normal limit in some patients, they suffer CAD. These normal HDL-C levels might become pro-inflammatoric. This study is to measure the correlations between myeloperoxidase (MPO), serum amyloid-A (SAA) protein, and secretoryphospholipase-A2 (sPLA2) with inflammatory status of HDL-C.METHODS: This was a cross-sectional study recruited 49 subjects with high HDL-C (> 40 mg/dL) and 31 subjects with low HDL-C (< 40 mg/dL). HDL-C was determined into antiinflammatory and proinflammatory based on levels of Apo A-1 and hs-CRP. Concentrations of MPO, SAA and s-PLA2 were measured by ELISA method. Levels of Apo A-1 was determined by immunoturbidimetric method. Multiple logistic regression analysis was done using inflammatory status of HDL-C as dependent variables and levels of MPO, SAA, sPLA2, ages, total cholesterol and triglycerides as independent variables.RESULTS: Patient’s age was 43.4 + 8.3 year, HDL-C was 43.1 + 9.5 mg/dL, Apo A-1 was 128.3 + 21.5 mg/dL, hs-CRP was 1.92 + 3.0 mg/dL. Concentrations of MPO, SAA and sPLA2 successively were 63.2 + 16.9 ng/mL, 7015.6 + 5021.1 ng/mL and 1340.2 + 406.3 pg/mL. Multiple logistic regression analysis showed that SAA is an independent predictor of pro-inflammatory status of HDL-C in high HDL-C group with prevalence ratio of 11.74 (95% CI : 2.51 – 54.84; P = 0.002). In contrast, MPO and sPLA2 were not independent predictor with PR of 1.26 (95% CI : 0.30 – 5.23; P = 0.75) and of 0.94 (95% CI : 0.23 – 3.91; P = 0.93).CONCLUSIONS: SAA is an independent predictor of pro-inflammatory HDL-C even in subjects with high HDL-C.KEYWORDS: Atherosclerosis, Apo A-I, serum amyloid A protein, secretory phospholipase A2, myeloperoxidase


2021 ◽  
Author(s):  
Shreya Ghosh ◽  
Akansha Garg ◽  
Chayanika Kala ◽  
Ashwani Kumar Thakur

AbstractThe formation of granuloma is one of the characteristic feature of tuberculosis. Besides, rise in the concentration of acute phase response proteins mainly serum amyloid A is the indicator for chronic inflammation associated with tuberculosis. Serum amyloid A drives secondary amyloidosis in tuberculosis and other chronic inflammatory conditions. The linkage between serum amyloid A (SAA) protein and amyloid deposition site is not well understood in tuberculosis and other chronic inflammatory conditions. We hypothesized that granuloma could be a potential site for amyloid deposition because of the presence of serum amyloid A protein and proteases that cleave SAA and trigger amyloid formation. Based on this hypothesis, for the first time we have shown the presence of amyloid deposits in the granuloma of tuberculosis patients using the gold standard, Congo red dye staining.


2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Claire K Mulvey ◽  
Timothy W Churchill ◽  
Karen Terembula ◽  
Jane F Ferguson ◽  
Nehal N Mehta ◽  
...  

Introduction Although high-density lipoprotein (HDL) is inversely correlated with cardiovascular risk, HDL loses its protective role in pathologic inflammatory states like type 2 diabetes (T2DM). HDL dysfunction contributes to accelerated atherosclerosis in T2DM, but the mechanism is incompletely defined. The acute phase reactant serum amyloid A (SAA) displaces apolipoprotein A-I and may impair HDL-mediated reverse cholesterol efflux. We hypothesized that SAA alters the inverse association between HDL and coronary artery calcium (CAC) in the Penn Diabetes Heart Study, a cross-sectional study of T2DM patients free of overt cardiovascular or renal disease. Methods We measured SAA in serum samples by immunonephelometry (N=975; mean age 58 ± 9 years; 63% male, 57% Caucasian; mean BMI 33 ± 6 kg/m 2 ). HDL was measured enzymatically in lipoprotein fractions after ultracentrifugation. Agatston CAC scores were quantified from electron beam tomography at the same visit. Spearman correlation and logistic regression were used to test associations of SAA with clinical factors and metabolic syndrome. We used Tobit regression to analyze associations between CAC and HDL, both overall and stratified by 3 categories of SAA: undetectable, lower half detectable, and upper half detectable. Results Spearman correlations revealed moderate association of SAA with C-reactive protein (r=0.52) and weak associations of SAA with BMI (r=0.25) and HDL (r=0.17; all p<0.001). In logistic regression, the group with highest SAA levels had increased odds of metabolic syndrome compared to those with undetectable levels (OR 1.56, 95% CI 1.03 to 2.38, p=0.036). In adjusted Tobit regression, HDL was inversely associated with CAC (Tobit coefficient for 1-SD increase in HDL: -0.30; 95% CI -0.54 to -0.06; p=0.013). Across the categories of SAA, however, there was no difference in the association of HDL with CAC (Tobit coefficient for 1-SD increase in HDL: -0.17 [95% CI -0.49 to 0.16] for undetectable vs. -0.31 [95% CI -0.79 to 0.17] for lower half detectable vs. -0.49 [95% CI -1.01 to 0.03] for upper half detectable). Conclusions Despite the association of SAA with metabolic syndrome, these data suggest that elevated SAA may not change the inverse relationship of HDL with CAC in T2DM.


2008 ◽  
Vol 158 (3) ◽  
pp. 333-341 ◽  
Author(s):  
T Lappalainen ◽  
M Kolehmainen ◽  
U Schwab ◽  
L Pulkkinen ◽  
D E Laaksonen ◽  
...  

ObjectiveSerum amyloid A (SAA) is a novel link between increased adipose tissue mass and low-grade inflammation in obesity. Little is known about the factors regulating its serum concentration and mRNA levels. We investigated the association between SAA and leptin in obese and normal weight subjects and analyzed the effect of weight reduction on serum SAA concentration and gene expression in adipose tissue of the obese subjects.MethodsSeventy-five obese subjects (60±7 years, body mass index (BMI) 32.9±2.8 kg/m2, mean±s.d.) with impaired fasting plasma glucose or impaired glucose tolerance and other features of metabolic syndrome, and 11 normal weight control subjects (48±9 years, BMI 23.7±1.9 kg/m2) were studied at the baseline. Twenty-eight obese subjects underwent a 12-week intensive weight reduction program followed by 5 months of weight maintenance. Blood samples and abdominal s.c. adipose tissue biopsies were taken at the baseline and after the follow-up. Gene expression was studied using real-time quantitative PCR.ResultsThe gene expressions in women and serum concentrations of leptin and SAA were interrelated independently of body fat mass in the obese subjects (r=0.54, P=0.001; r=0.24, P=0.039 respectively). In multiple linear regression analyses, leptin mRNA explained 38% of the variance in SAA mRNA (P=0.002) in the obese women. Weight loss of at least 5% increased SAA mRNA expression by 48 and 36% in men and women, but serum SAA concentrations did not change.ConclusionsThe association between SAA and leptin suggests an interaction between these two adipokines, which may have implications in inflammatory processes related to obesity and the metabolic syndrome.


Obesity ◽  
2013 ◽  
Vol 21 (2) ◽  
pp. 361-366 ◽  
Author(s):  
Robin P. F. Dullaart ◽  
Jan Freark de Boer ◽  
Wijtske Annema ◽  
Uwe J.F. Tietge

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shazli Azmi ◽  
Maryam Ferdousi ◽  
Yifen Liu ◽  
Safwaan Adam ◽  
Tarza Siahmansur ◽  
...  

AbstractObesity and associated dyslipidemia may contribute to increased cardiovascular disease. Obesity has also been associated with neuropathy. We have investigated presence of peripheral nerve damage in patients with severe obesity without type 2 diabetes and the status of metabolic syndrome and lipoprotein abnormalities. 47participants with severe obesity and 30 age-matched healthy controls underwent detailed phenotyping of neuropathy and an assessment of lipoproteins and HDL-functionality. Participants with severe obesity had a higher neuropathy symptom profile, lower sural and peroneal nerve amplitudes, abnormal thermal thresholds, heart rate variability with deep breathing and corneal nerve parameters compared to healthy controls. Circulating apolipoprotein A1 (P = 0.009), HDL cholesterol (HDL-C) (P < 0.0001), cholesterol efflux (P = 0.002) and paroxonase-1 (PON-1) activity (P < 0.0001) were lower, and serum amyloid A (SAA) (P < 0.0001) was higher in participants with obesity compared to controls. Obese participants with small nerve fibre damage had higher serum triglycerides (P = 0.02), lower PON-1 activity (P = 0.002) and higher prevalence of metabolic syndrome (58% vs. 23%, P = 0.02) compared to those without. However, HDL-C (P = 0.8), cholesterol efflux (P = 0.08), apoA1 (P = 0.8) and SAA (P = 0.8) did not differ significantly between obese participants with and without small nerve fibre damage. Small nerve fibre damage occurs in people with severe obesity. Patients with obesity have deranged lipoproteins and compromised HDL functionality compared to controls. Obese patients with evidence of small nerve fibre damage, compared to those without, had significantly higher serum triglycerides, lower PON-1 activity and a higher prevalence of metabolic syndrome.


2014 ◽  
Vol 84 (1-2) ◽  
pp. 35-44 ◽  
Author(s):  
Kanjana Suriyaprom ◽  
Benjaluck Phonrat ◽  
Pratana Satitvipawee ◽  
Anchalee Tungtrongchitr ◽  
Rungsunn Tungtrongchitr

This study aims to investigate serum amyloid A, homocysteine, and biochemical-anthropometric measurements in post-menopausal women with and without metabolic syndrome (MS), and determine whether serum amyloid A and homocysteine are linked to MS among this group. This study was performed with 405 post-menopausal Thai volunteers with a mean age of 57.95 ± 5.90 years (135 subjects with MS and 270 subjects without MS). The levels of serum amyloid A, homocysteine, vitamins, glucose, and lipids were measured. Homocysteine levels were significantly higher in the group with MS than in that without MS (p < 0.001), whereas for serum amyloid A, vitamin A, vitamin E and vitamin B12, there were no significant differences. There were significant differences between the groups in folate, HDL-C, and anthropometric measurements (p < 0.001). Thirty seven percent of the group with MS and 14.1 % of the group without MS were classified as having hyperhomocysteinemia (p < 0.001). Furthermore, logistic regression analysis revealed that hyperhomocysteinemia (odds ratio (OR): 2.67, 95 % confidence interval (95 %CI): 1.57 - 4.58), low folate (OR: 1.79, 95 %CI: 1.11 - 2.89), and BMI (OR: 1.25, 95 %CI: 1.16 - 1.33) were significantly related to MS. These findings suggest that increased homocysteine levels and decreased folate concentrations may influence susceptibility to MS and this effect may be an early event in the development of cardiovascular diseases among post-menopausal women. Therefore, there is a need to evaluate homocysteine levels, especially among post-menopausal Thai women.


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