METHODS: This is a cross-sectional study using multiple logistic regression to identify predictors of elevated CRP among pre-treatment, newly diagnosed BCa patients. Studied variables were socio-demographic and medical characteristics, anthropometric measurements [body weight, Body Mass Index, body fat percentage, fat mass/fat free mass ratio, muscle mass, visceral fat], biochemical parameters [albumin, hemoglobin, white blood cell (WBC), neutrophil, lymphocyte], energy-adjusted Dietary Inflammatory Index, handgrip strength (HGS), scored Patient Generated-Subjective Global Assessment, physical activity level and perceived stress scale (PSS).
RESULTS: A total of 105 participants took part in this study. Significant predictors of elevated CRP were body fat percentage (OR 1.222; 95 % CI 1.099-1.358; p < 0.001), PSS (OR 1.120; 95 % CI 1.026-1.223; p = 0.011), low vs normal HGS (OR 41.928; 95 % CI 2.155-815.728; p = 0.014), albumin (OR 0.779; 95 % CI 0.632-0.960; p = 0.019), and WBC (OR 1.418; 95% CI 1.024-1.963; p = 0.036).
CONCLUSION: Overall, predictors of elevated CRP in pre-treatment, newly diagnosed BCa population were body fat percentage, PSS, HGS category, albumin and WBC.
METHODS: Information regarding the consumption of coffee, tea, and alcohol was collected from the UK Biobank, with sample sizes of 428,860, 447,485, and 462,346 individuals, respectively. Data on 41 inflammatory cytokines were obtained from summary statistics of 8293 healthy participants from Finnish cohorts.
RESULTS: The consumption of coffee was found to be potentially associated with decreased levels of Macrophage colony-stimulating factor (β = -0.57, 95% CI -1.06 ~ -0.08; p = 0.022) and Stem cell growth factor beta (β = -0.64, 95% CI -1.16 ~ -0.12; p = 0.016), as well as an increase in TNF-related apoptosis-inducing ligand (β = 0.43, 95% CI 0.06 ~ 0.8; p = 0.023) levels. Conversely, tea intake was potentially correlated with a reduction in Interleukin-8 (β = -0.45, 95% CI -0.9 ~ 0; p = 0.045) levels. Moreover, our results indicated an association between alcohol consumption and decreased levels of Regulated on Activation, Normal T Cell Expressed and Secreted (β = -0.24, 95% CI -0.48 ~ 0; p = 0.047), as well as an increase in Stem cell factor (β = 0.17, 95% CI 0.02 ~ 0.31; p = 0.023) and Stromal cell-derived factor-1 alpha (β = 0.20, 95% CI 0.04 ~ 0.36; p = 0.013).
CONCLUSION: Revealing the interactions between beverage consumption and various inflammatory cytokines may lead to the discovery of novel therapeutic targets, thereby facilitating dietary interventions to complement clinical disease treatments.
METHODS: Using a randomised double-blind crossover design, 21 (men = 6, women = 15) T2D subjects consumed test meals (3.65 MJ) consisting of a high fat muffin (containing 50 g test fats provided as PO, IPO or HOS) and a milkshake. Postprandial changes in gut hormones, glucose homeostasis, satiety, lipid and inflammatory parameters after meals were analysed. Some of the solid fractions of the IPO were removed and thus the fatty acid composition of the PO and IPO was not entirely equal (PO vs IPO: palmitate 39.8 vs 38.7; oleate 43.6 vs 45.1). PO, IPO and HOS contained 9.7, 38.9 and 0.2 g/100 g total fatty acids of palmitic acid at the sn-2 position, respectively. At 37 °C, IPO contained 4.2% SFC whereas PO and HOS were completely melted.
RESULTS: Our novel observation shows that the incremental area under curve (iAUC) 0-6 h of plasma GIP concentration was on average 16% lower following IPO meal compared with PO and HOS (P
PURPOSE: The present work aimed to assess the antidiabetic potential of arjunolic acid (AA) isolated from Terminalia arjuna in type 2 diabetic rats.
STUDY DESIGN: After extraction, isolation and purification, AA was orally administered to type 2 diabetic Sprague Dawley rats to investigate antidiabetic effect of AA.
METHOD: T2DM was induced via single intraperitoneal injection of streptozotocin-nicotinamide (STZ-NIC) in adult male rats. After 10 days, fasting and random blood glucose (FBG and RBG), body weight (BW), food and water intake, serum C-peptide, insulin and glycated hemoglobin (HbA1c) was measured to confirm T2DM development. Dose dependent effects of orally administered AA (25 and 50 mg/kg/day) for 4 weeks was investigated by measuring BW variation, fasting and postprandial hyperglycemia, oral glucose tolerance test (OGTT), and levels of serum HbA1c, serum total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL), high density lipoprotein (HDL), serum and pancreatic C-peptide, insulin, growth differentiation factor 15 (GDF-15), serum and pancreatic inflammatory cytokines.
RESULTS: The oral administration of AA in preclinical model of T2DM significantly normalized FBG and RBG, restored BW, controlled polyphagia, polydipsia and glucose tolerance. In addition, AA notably reduced serum HbA1c, TC, TG, LDL with non-significant increase in HDL. On the other hand, significant increase in serum and pancreatic C-peptide and insulin was observed with AA treatment, while serum and pancreatic GDF-15 were non-significantly altered in AA treated diabetic rats. Moreover, AA showed dose dependent reduction in serum and pancreatic proinflammatory cytokines including TNF-α, IL-1β and IL-6.
CONCLUSION: For the first time our findings highlighted AA as a potential candidate in type 2 diabetic conditions.
METHODS AND STUDY DESIGN: A cross-sectional study was conducted on 112 healthy men and women from 3 main ethnic group (Malay, Chinese, and Indian) who were aged 18-60 years. The participants were categorized into normal body mass index (BMI), overweight and obese groups according to WHO criteria for BMI in Asian populations (18.5 kg/m2
METHOD: Blood samples were obtained from 20 healthy blood donors, 30 RA patients who presented with anaemia and 30 patients who had pure iron deficiency anaemia (IDA). The samples were analysed for full blood count, iron, ferritin, transferrin, soluble transferrin receptor and prohepcidin.
RESULTS: The mean prohepcidin level in the control subjects was 256 microg/L. The prohepcidin level was significantly lower in IDA patients (100 microg/L; p < 0.0001) but not significantly different from that of control in RA patients (250 microg/L; p > 0.05). Higher serum soluble transferrin receptor (sTfR) levels were observed in IDA (p < 0.0001) but not in RA compared with that of control (p > 0.05). RA patients were divided into iron depleted and iron repleted subgroups based on the ferritin level. Prohepcidin in the iron depleted group was significantly lower than the iron repleted group and the control (p < 0.0001) and higher levels were observed in the iron repleted group (p < 0.01). sTfR levels in the iron depleted group were significantly higher than the control and the iron repleted patients (p < 0.001). In the iron repleted group, sTfR level was not statistically different from that of control (p > 0.05).
CONCLUSION: Serum prohepcidin is clearly reduced in uncomplicated iron deficiency anaemia. The reduced prohepcidin levels in the iron depleted RA patients suggests that there may be conflicting signals regulating hepcidin production in RA patients. In RA patients who have reduced hepcidin in the iron depleted group (ferritin <60 microg/L) where sTfR levels are increased suggests that these patients are iron deficient. Further studies with a larger cohort of patients are required to substantiate this point.