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Background: Metabolic syndrome is a known risk factor for various diseases including coronary artery disease and is associated with subclinical-inflammation. Various inflammatory markers have been evaluated in metabolic syndrome. However, the data evaluating serum ferritin in metabolic syndrome is sparse. The current study aims to evaluate the correlation between serum ferritin and metabolic syndrome. Materials and methods:This cross-sectional study included 100 subjects with metabolic syndrome and 50 gender matched healthy controls. Results:The mean age (SD) in study and control groups was 52.34 (7.64) and 48.36 (9.16) years, respectively. Majority were females in both groups (60% vs 52%). The mean (SD) HbA1c amongst study vs control was 8.26 (2.33) vs 5.10 (0.51); <0.0001. Mean (SD) serum iron and hsCRP were significantly higher in the study group (115.50 ±42.6 vs 65.741±9.16; p<0.001) and (6.33±4.87 vs 3.45±3.5; p<0.007) respectively. Mean serum ferritin level was significantly higher in the study group (123.9 vs 59.02; p<0.0001). A statistically significant correlation was found between serum ferritin and waist hip ratio, triglyceride, BMI and HOMA IR (r=0.49, p<0.0001; r=0.50, p<0.0001; r=0.47, p<0.0001 and r=0.54, p<0.0001 respectively). An inverse correlation was found between serum ferritin and serum HDL levels (r=-0.46, p<0.0001). Even after adjusting for age, serum ferritin levels were found to be significantly associated with metabolic syndrome Coeff (95% CI) -65.6 (-84.23, -46.98); p<0.0001. Conclusion:Significantly higher levels of serum ferritin were found in metabolic syndrome, and a significant correlation with its components was seen. Therefore, serum ferritin may be used as a marker of inflammation for an early intervention.
RESUMO
Heat Stress (HS) induces diverse pathophysiological changes, which include brain ischemia, oxidative stress and neuronal damage. The present study was undertaken with the objective to ascertain whether neuroinflammation in Hypothalamus (HTH) caused under HS affects monoamine levels and hence, its physiological role in thermoregulation. Rats were exposed to HS in a heat simulation environmental chamber (Ambient temperature, Ta=45±0.5°C and Relative Humidity, RH=30±10%) with real-time measurement of core temperature (Tc) and skin temperature (Ts). Animals were divided into two subgroups: Moderate HS (MHS) (Tc=40°C) and Severe HS (SHS)/Heat stroke (Tc=42°C). Rats with MHS showed an increase in Mean Arterial Pressure (MAP) and Heart Rate (HR) while fall in MAP and rise in HR was observed in rats with SHS. In addition, oxidative stress and an increase in pyknotic neurons were observed in HTH. High levels of Adrenocorticotropic-hormone (ACTH), Epinephrine (EPI), Norepinephrine (NE) and Dopamine (DA) in the systemic circulation and progressive increase in EPI and DA levels in HTH were recorded after the thermal insult. Moreover, a substantial increase in Glutamate (Glu) level was observed in HTH as well as in systemic circulation of heat stroke rats. We found a rise in NE whereas a fall in Serotonin (5-HT) level in HTH at MHS, without perturbing inflammatory mediators. However, rats with SHS exhibited significant elevations in NF-kB, IL-1ß, COX2, GFAP and Iba1 protein expression in HTH. In conclusion, the data suggest that SHS induces neuroinflammation in HTH, which is associated with monoamines and Glu imbalances, leading to thermoregulatory disruption.
