| Objective To investigate the effects of exercise intervention during IR formation of high-fat-induced SD rats as well as some mechanisms.Methods Normal male SD rats were divided into four groups: normal dietary control group(C group), normal dietary exercise group(E group), high fat dietary control group(H group)and high fat dietary exercise group(HE group)after one week's adaptive feeding. H and HE groups were fed 10-weeks'high-fat(23.5% protein,44.1% fat and 32.4% carbohydrate, supply energy about 408Kcal/100g)in order to induce IR, while E and HE groups began to swim without loading. Comprehensive using body weight, FINS, FBG, HOMA-IR, ISI and insulin tolerant test(ITT) to evaluate the building of animal model and effects of exercise intervention. Observing the impacts of high-fat feeding and exercise on blood lipids, visceral fat reserves, liver weight, liver function(ALT and AST), as well as tissue lipids(liver and skeletal muscle)ectopic deposition. Adopting ELISA and real-time PCR to observe adiponectin and its receptors(R1 and R2)mRNA expression systematically and comprehensive, including serum adiponectin, visceral fat tissue adiponectin mRNA expression, skeletal muscle and liver adiponectin receptors mRNA expression and their distributions in SD rats. Using western blotting to determinate AMPKαexpression and its phosphorylation level of liver and red quadriceps(considering the reaction to aerobic exercise is more sensitive on slow muscle fiber)after high-fat-induced and regular exercise.Results (1) There were no difference of weight before experiment while that of H was higher than C group, E was lower than C group, HE was lower than H group, HE was higher than E group after experiment(P<0.01).The average weight gain was the fastest on H group while E group was the slowest. There were no difference on FBG and HOMA-IR(P>0.05); H was higher than C group, E was lower than C group, HE was lower than H group on FINS index(P<0.05); on the contrary, H was lower than C group, E was higher than C group, HE was higher than H group on ISI index(P<0.05). (2) In ITT, there were no difference of FBG at zero point. After intraperitoneal injection of insulin, FBG of H group was higher significantly than C group at 15min, 30min and 60min points(P<0.05); HE group was lower than H group at the same points(P<0.05); E group was lower significantly than C group at 15min and 30min points(P<0.05).(3) H group was higher than C group, E group was lower than C group, and HE group was lower than H group on visceral fat reserves, liver weight and AW/BW(P<0.01orP<0.05).(4) H group was higher than C group on TC, TG, LDL-C, TC/HDL(P<0.05), and there were no difference of HDL-C and FFA(P>0.05); there were no difference between E and C group of TC, HDL-C, TC/HDL(P>0.05), H group were lower than C group on TG, LDL-C, FFA(P<0.01or P<0.05); there were no difference between HE and H group of HDL-C, LDL-C, FFA(P>0.05), HE group were lower than H group on TC, TG, TC/LDL(P<0.05or<0.01); there were no difference between HE and E group of TC,TG(P>0.05), HE group was lower than E group on HDL-C(P<0.05), while higher than E group on LDL-C,TC/LDL and FFA(P<0.01or<0.05).(5) There were no difference between H group and C group of liver TC and skeletal muscle TG(P>0.05), liver TG and FFA were higher than C group significantly(P<0.01or<0.05); There were no difference between E group and C group on liver TC and skeletal muscle TG(P>0.05), liver TG and FFA were lower than C groupsignificantly(P<0.01or<0.05); There were no difference between HE group and H group on skeletal muscle TG(P>0.05), liver TC, TG and FFA were lower than H group significantly(P<0.05or<0.01); There were no difference between four groups on serum ALT and AST(P>0.05).(6) In spite of no significant difference(P>0.05), serum adiponectin was negative correlation with FINS and ALT(R=-0.069,R=-0.179)while positive correlation with HDL(R=0.043).There were no difference between four groups of serum adiponectin(P>0.05). H group was lower than C group on adiponectin mRNA expression of visceral fat tissue(P<0.05), E group was slightly lower than C group and HE group was slightly lower than H group, but the difference were unsignificantly(P>0.05).(7) Adiponectin R1mRNA expression was abundant on quadriceps and R2mRNA expression was abundant on liver tissue(P<0.05). H group were lower than C group significantly on adiponectin R1/R2mRNA expression(P<0.05), while the two exercise groups were as much as the two sedentary groups(P>0.05).(8) There were no significant difference between four groups on AMPKαexpression of quadriceps(P>0.05). HE group was 43.2% higher than H group(P<0.05)and E group was 83.7% higher than C group on AMPKα(Thr172) phosphorylation level(P<0.01).(9) There were no significant difference between four groups of AMPKαexpression of liver tissue(P>0.05). HE group was 51.1% higher than H group on AMPKα(Thr172) phosphorylation level(P<0.05)and there were no difference betweenthe others(P>0.05).conclusions (1) High-fat-feeding for 10 weeks may induce normal SD rats into IR. When evaluating IR indirectly, ISI index was more sensitive than HOMA-IR index. Exercise improved rats insulin sensitivity. (2) Lipid metabolism abnormal may occur before glucose metabolism abnormal during IR formation of high-fat-induced rats. Exercise intervention delayed blood lipids metabolism abnormal, visceral fat accumulation, and liver lipids ectopic deposition significantly. The relationship between skeletal muscle lipids and IR still remained unclear when exercise was for improving insulin sensitivity. (3) Reduction on adiponectin mRNA expression of visceral fat tissue may one of the mechanisms of IR formation of high-fat-induced rats. Cycle adiponectin level may not be the main contribution factor and mechanism of delaying IR formation of high-fat-induced rats by exercise. Energy negative balance caused by exercise may paly the main role.(4) Adiponectin R1/R2 mRNA expressed in both liver and quadriceps of normal SD rats.R1 was high expressed in quadriceps and R2 was in liver. Reduction on adiponectin R1/R2 mRNA expression of skeletal muscle and liver may one of the mechanisms of IR formation of high-fat-induced rats. The study had not observed the significant effects of exercise intervention.(5) Exercise improved skeletal muscle AMPKα(Thr172) phosphorylation level of C group rats, which suggesting that rats skeletal muscle adapted to regular endurance exercise may be caused by continuous activation of skeletal muscle AMPKα. Exercise improved liver and skeletal muscle AMPKα(Thr172) phosphorylation level of H group rats, which suggesting that continuous activation of liver and skeletal muscle AMPKαmay be one of the key mechanisms of delaying IR formation of high-fat-induced rats by exercise. |
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