摘要
Background As two novel adipocytokines, chemerin and apelin play a key role in the pathological process of insulin resistance （IR）, glucose metabolism and obesity, researchers have found that the levels of chemerin and apelin changed significantly in type 2 diabetic patients with obesity, however, the underlying mechanism involved remains unclear. The aim of this study was to investigate whether chemerin and apelin play an important role in the pathophysiologic proceeding of diabetes. Methods This study enrolled 81 newly diagnosed obese type 2 diabetes mellitus （T2DM） patients （T2DM group, n=81）. All the patients were randomly assigned to DM1 group treated with metformin （n=41） and DM2 group treated with pioglitazone （n=40）. After hypoglycemic agents treatment, patients under better blood glucose control were chosen to be given antioxidant treatment. Another 79 subjects without T2DM were recruited as normal control group （NC group）, including 40 subjects （NC1 group） with normal body mass index （BMI） and 39 obese subjects （NC2 group）. Levels of chemerin, apelin, BMI, tumor necrosis factor-α（TNF-α）, homeostasis model assessment of IR （HOMA-IR） and 8-isoprotaglandim F2α（8-iso-PGF2α） were examined at baseline and post-treatment. The relationship between chemerin, apelin and BMI, TNF-α, HOMA-IR, 8-iso-PGF2α was analyzed. Results The baseline levels of chemerin, apelin, TNF-α, HOMA-IR and 8-iso-PGF2α in T2DM group were significantly higher than normal control group （P 〈0.001）. All indices mentioned above were significantly decreased after treatment （P 〈0.05）. In T2DM patients treated with pioglitazone, indices mentioned above except for HOMA-IR, were decreased significantly compared with patients treated with mefformin （P〈0.05）. After antioxidant treatment using lipoic acid, levels of chemerin, apelin, TNF-α and 8-iso-PGF2α were further significantly decreased （P 〈0.05）. Correlation analysis showed that the levels of chemerin and apelin correlated positively with BMI, TNF-α, HOMA-IR and 8-iso-PGF2α before and after treatment with hypoglycemic agents （P〈0.01）. The levels of chemerin and apelin also had positive correlation with TNF-a and 8-iso-PGF2α after antioxidant treatment （P〈0.05）. Conclusions The levels of chemerin and apelin in obese T2DM patients are closely related to IR. The increased levels may be a result of compensatory response to IR, and also may be the causative factor of IR. The levels of chemerin and apelin correlate closely with oxidative stress and inflammation. The two adipokines may be inflammatory factors playing important roles in the initiation and development of obese T2DM. Chemerin and apelin are related to the pathophysiology of IR, oxidative stress and inflammation.
Background As two novel adipocytokines, chemerin and apelin play a key role in the pathological process of insulin resistance （IR）, glucose metabolism and obesity, researchers have found that the levels of chemerin and apelin changed significantly in type 2 diabetic patients with obesity, however, the underlying mechanism involved remains unclear. The aim of this study was to investigate whether chemerin and apelin play an important role in the pathophysiologic proceeding of diabetes. Methods This study enrolled 81 newly diagnosed obese type 2 diabetes mellitus （T2DM） patients （T2DM group, n=81）. All the patients were randomly assigned to DM1 group treated with metformin （n=41） and DM2 group treated with pioglitazone （n=40）. After hypoglycemic agents treatment, patients under better blood glucose control were chosen to be given antioxidant treatment. Another 79 subjects without T2DM were recruited as normal control group （NC group）, including 40 subjects （NC1 group） with normal body mass index （BMI） and 39 obese subjects （NC2 group）. Levels of chemerin, apelin, BMI, tumor necrosis factor-α（TNF-α）, homeostasis model assessment of IR （HOMA-IR） and 8-isoprotaglandim F2α（8-iso-PGF2α） were examined at baseline and post-treatment. The relationship between chemerin, apelin and BMI, TNF-α, HOMA-IR, 8-iso-PGF2α was analyzed. Results The baseline levels of chemerin, apelin, TNF-α, HOMA-IR and 8-iso-PGF2α in T2DM group were significantly higher than normal control group （P 〈0.001）. All indices mentioned above were significantly decreased after treatment （P 〈0.05）. In T2DM patients treated with pioglitazone, indices mentioned above except for HOMA-IR, were decreased significantly compared with patients treated with mefformin （P〈0.05）. After antioxidant treatment using lipoic acid, levels of chemerin, apelin, TNF-α and 8-iso-PGF2α were further significantly decreased （P 〈0.05）. Correlation analysis showed that the levels of chemerin and apelin correlated positively with BMI, TNF-α, HOMA-IR and 8-iso-PGF2α before and after treatment with hypoglycemic agents （P〈0.01）. The levels of chemerin and apelin also had positive correlation with TNF-a and 8-iso-PGF2α after antioxidant treatment （P〈0.05）. Conclusions The levels of chemerin and apelin in obese T2DM patients are closely related to IR. The increased levels may be a result of compensatory response to IR, and also may be the causative factor of IR. The levels of chemerin and apelin correlate closely with oxidative stress and inflammation. The two adipokines may be inflammatory factors playing important roles in the initiation and development of obese T2DM. Chemerin and apelin are related to the pathophysiology of IR, oxidative stress and inflammation.
