1.Correlation Study between Adiponectin and Type 2 Diabetes Process
Chuyuan WANG ; Lingfang KONG ; Yongsheng HOU ; Yue LIU ; Yang ZHANG
Journal of China Medical University 2014;(5):429-431,436
Objective To investigate the serum concentration of adiponectin(apM1)in patients of Han population with type 2 diabetes(T2DM), impaired glucose tolerance(IGT)and normal glucose tolerance(NGT)in Liaoning Province,and explore its correlation with T2DM process. Meth-ods Unrelated 278 subjects in Liaoning Province were enrolled for the study,including 97 newly diagnosed T2DM subjects,88 IGT subjects,and 93 cases with NGT. Serum apM1,fasting and post-glucose load glucose and insulin,blood lipids,blood pressure,calculate HOMA-IR and HOMA-B,height,weight,waist,hips were measured;body mass index(BMI)and waist hip ratio(WHR)were calculated. Three groups were divided into obese overweight and non-obese overweight subgroups with BMI≥25 kg/m2 as the boundary point. Then central and peripheral obesity was distin-guished using WHR(male≥0.90,female≥0.85 as the boundary point). Results Reduced apM1 levels was first observed in obese NGT stage. Accompanied by elevated levels of insulin resistance,apM1 levels showed a gradual decline trend paralleled with the NGT-IGT-T2DM model. Se-rum apM1 in T2DM was significantly lower than that in NGT(P<0.001). Negative correlations were found between apM1 and WHR,fasting plas-ma glucose,HOMA-IR and triglyceride. Stepwise multiple regression analysis indicated that,HOMA-IR and triglyceride were independent factors for serum apM1 levels. Conclusion Reduced apM1 levels were first appeared in obese NGT stage;apM1 is closely related to insulin resistance and T2DM process. Low level of apM1 can be used as a predictor of early intervention of IGT outcome and T2DM process.
2.Effect of aerobic exercise on enteric nervous injury in rats exposed to malathion
Haishan LI ; Lingfang KONG ; Songtao WANG ; Erlei ZHANG ; Wenchao AI ; Wenping XIE ; Huiming CHEN
Chinese Journal of Pharmacology and Toxicology 2014;(2):238-242
OBJECTIVE To investigate the effects of aerobic exercise on enteric nervous injury in rats exposed to malathion.METHODS Adult male Wistar rats were treated with non-load swi mming every other day,three ti mes a week,each one hour,for six weeks.Before exercise,the rats were trea-ted with malathion 100 mg·kg -1·d -1 by oral gavage,six days a week,for six weeks.The activities of seru m acetylcholinesterase(AChE)and butyrocholinesterase(BuChE)were determined.In addition,the s mall intestinal propulsion indexes were measured.Also,the distribution of nerve plexus in ileu m was observed.The i mmunohistoche mical method was used to measure the levels of protein gene-related petide 9.5 (PGP9.5),substance P (SP),and vasoactive intestinal peptide (VIP).RESULTS Co m-pared with normal control,malathion exposure decreased the activities of seru m AChE and BuChE (P<0.01 ),increased the s mall intestinal propulsion indexes (P <0.05).In addition,the levels of PGP9.5 decreased (P<0.05).At the sa me ti me,the levels of SP increased,and the levels of VIP decreased (P<0.05).Aerobic exercise did not change the activites of cholinesterases,but decreased s mall intes-tinal propulsion indexes,increased the levels of PGP9.5,decreased the levels of SP,and increased the levels of VIP.Co mpared with the malathion exposure only,the rats in malathion ad ministration co mbined with aerobic exercise group de monstrated much lower activites of cholinesterase (P <0.01 ),and the s mall intestinal propulsion indexes decreased fro m (89 ±4)% to (79 ±5)%(P <0.01 ).Moreover,the levels of PGP9.5 increased fro m 0.012 ±0.003 to 0.029 ±0.015 (P <0.01 ).At the sa me ti me,the levels of SP decreased fro m0.174 ±0.067 to 0.1 10 ±0.057(P<0.05),and the levels of VIP increased fro m 0.0076 ±0.0029 to 0.01 1 1 ±0.0047 (P <0.05).The levels of above para meters were sa me or close to those of the normal control.CONCLUSION Malathion exposure induced disorders of enteric nervous syste m in rats,and the aerobic exercise abated the toxic response in enteric nervous syste m of malathion exposure rats.However,these effects were not mediated through recovery of cholinesterases inhibition.