Visfatin, an adipocytokine with insulin-mimetic activity, has been previously reported to associate with obesity. Herein, we aimed to investigate the serum level of visfatin and association with proinflammatory markers and insulin resistance in obese type 2 diabetic patients. A case control study was carried out among 80 diabetics and 40 non-diabetic healthy controls, after obtaining Anthropometric measurements and blood pressure. Serum level of visfatin and C-reactive protein (CRP) were measured by Enzyme Immunoassay. Interleukin 6 (IL6), tumor necrosis factor α (TNF-) were measured by ELISA and the homeostasis model assessment for insulin resistance was calculated as a marker of insulin resistance. Compared to healthy controls, diabetic patients showed a significant high serum levels of visfatin (40.33±9.98 vs 19.03±8.22), (P= 0.001), IL6 (12.06±2.69 vs 6.02±3.03), (P0.0001), TNF- (13.53±2.54 vs 8.70±3.40), P0.0001) and CRP (7.77±1.61 vs 6.01±1.99), (P=0.003). Also there was a strong positive correlation between serum level of visfatin, IL6, TNF- and CRP and some anthropometric characteristics including (WC,BMI and insulin resistance). Furthermore, among 80 diabetic patients, serum level of visfatin was positively correlated with IL6 (r=0.47, P0.0001), TNF- (r=0.62, P0.0001), CRP (r=0.4, P=0.002) respectively. In conclusion, there is a strong positive correlation between visfatin serum level and the inflammatory markers IL6, TNF- and CRP in type 2 diabetic patients. There is also a positive correlation with insulin resistance and BMI which indicates association of visfatin with obesity and type 2 diabetes mellitus.

Visfatin, an adipocytokine with insulin-mimetic activity, has been previously reported to associate with obesity. Herein, we aimed to investigate the serum level of visfatin and association with proinflammatory markers and insulin resistance in obese type 2 diabetic patients. A case control study was carried out among 80 diabetics and 40 non-diabetic healthy controls, after obtaining Anthropometric measurements and blood pressure. Serum level of visfatin and C-reactive protein (CRP) were measured by Enzyme Immunoassay. Interleukin 6 (IL6), tumor necrosis factor α (TNF-) were measured by ELISA and the homeostasis model assessment for insulin resistance was calculated as a marker of insulin resistance. Compared to healthy controls, diabetic patients showed a significant high serum levels of visfatin (40.33±9.98 vs 19.03±8.22), (P= 0.001), IL6 (12.06±2.69 vs 6.02±3.03), (P0.0001), TNF- (13.53±2.54 vs 8.70±3.40), P0.0001) and CRP (7.77±1.61 vs 6.01±1.99), (P=0.003). Also there was a strong positive correlation between serum level of visfatin, IL6, TNF- and CRP and some anthropometric characteristics including (WC,BMI and insulin resistance). Furthermore, among 80 diabetic patients, serum level of visfatin was positively correlated with IL6 (r=0.47, P0.0001), TNF- (r=0.62, P0.0001), CRP (r=0.4, P=0.002) respectively. In conclusion, there is a strong positive correlation between visfatin serum level and the inflammatory markers IL6, TNF- and CRP in type 2 diabetic patients. There is also a positive correlation with insulin resistance and BMI which indicates association of visfatin with obesity and type 2 diabetes mellitus.

Visfatin, an adipocytokine with insulin-mimetic activity, has been previously reported to associate with obesity. Herein, we aimed to investigate the serum level of visfatin and association with proinflammatory markers and insulin resistance in obese type 2 diabetic patients. A case control study was carried out among 80 diabetics and 40 non-diabetic healthy controls, after obtaining Anthropometric measurements and blood pressure. Serum level of visfatin and C-reactive protein (CRP) were measured by Enzyme Immunoassay. Interleukin 6 (IL6), tumor necrosis factor α (TNF-) were measured by ELISA and the homeostasis model assessment for insulin resistance was calculated as a marker of insulin resistance. Compared to healthy controls, diabetic patients showed a significant high serum levels of visfatin (40.33±9.98 vs 19.03±8.22), (P= 0.001), IL6 (12.06±2.69 vs 6.02±3.03), (P0.0001), TNF- (13.53±2.54 vs 8.70±3.40), P0.0001) and CRP (7.77±1.61 vs 6.01±1.99), (P=0.003). Also there was a strong positive correlation between serum level of visfatin, IL6, TNF- and CRP and some anthropometric characteristics including (WC,BMI and insulin resistance). Furthermore, among 80 diabetic patients, serum level of visfatin was positively correlated with IL6 (r=0.47, P0.0001), TNF- (r=0.62, P0.0001), CRP (r=0.4, P=0.002) respectively. In conclusion, there is a strong positive correlation between visfatin serum level and the inflammatory markers IL6, TNF- and CRP in type 2 diabetic patients. There is also a positive correlation with insulin resistance and BMI which indicates association of visfatin with obesity and type 2 diabetes mellitus.

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Purpose Recent studies suggested that the non-familiar form of Alzheimer's disease (AD) could be consequence of metabolic syndrome and neuroinflammation. Elettaria cardamomum extract (EC) has exhibited antidiabetic, antioxidant and anti-inflammatory properties. This research was conducted to evaluate the effects of EC on AD-like alterations in rats induced by high fructose and high fat diet coupled with a single small dose of STZ (25 mg/kg) (T2DM rats). Methods Phytochemical analysis was carried out. Behavioral tests, immunohistochemical examination, biochemical analysis and gene expression determination were performed in treated and controls rats. Results The majority of EC compounds were terpenoids. EC extract administration for 8 weeks attenuated AD-like alterations. It reversed a T2DM-induced decline in cognitive functions in passive avoidance task and Morris water maze test. It significantly lowered the elevated hippocampal level of AChE activity and caspase-3 activity, an indicator of degeneration in T2DM rats Also, it reduced the accumulation of Aβ and p-tau in the brain of T2DM rats. Furthermore, it elevated the suppressed glutamate receptor expression (AMPA GluR1 subunit and NMDA receptor subunits NR1, NR2A, NR2B). EC treatment reduced hippocampal lipid peroxidation marker malondialdehyde (MDA) and augmented antioxidant defensive system, including superoxide dismutase (SOD) and reduced glutathione (GSH). Meanwhile, it lowered hippocampal TNFα, IL β1but not IL6 and reduced GSK-3β in brainT2D rats. Conclusion EC treatment could ameliorate AD-like alterations in T2DM rats through activation of blunted insulin signal transduction in the brain, attenuation of associated oxidative stress and neuroinflammation.