Effects Of Adiponectin On Fatty Deposition And Types Of Skeletal Muscle Fibers Of Mice

Adiponectin, a bioactive compound mainly secreted by adipose tissue, is also theonly adipocytokine discovered to date whose blood levels will drop with the increaseof adipose tissue. The adiponectin level in blood and body fat rate is inverselycorrelated; it can regulate the metabolic activities of the skeletal muscle, including toincrease the glucose intake, the oxidation of fatty acid and to enhance the insulinsensitivity; it can influence the growth of skeletal muscle with the result of changingthe muscle fiber composition, thus to improve muscle quality. The experiment usedthe mice as the model by intraperitoneal injection with recombinate mouseadiponectin (rmAdp), aiming at exploring the effects and mechanism of rmAdp onmesentery fatty deposition, the gastrocnemius muscle growth and muscle fiber typesof mice.1The effects of rmAdp on the mice slaughter index and growth indexForty21-day-old mice were randomly divided into two groups respectively, inhalf male and half female. The test group was injected with rmAdp (10μg/kg d),while the control group was injected with PBS at the same dosage for three weeks.Mice were slaughted2days after the final injection. Slaughter index and growth indexwere determined.The results showed that the food intake, body weight, mesentery fat weight, andgastrocnemius muscle weight of mice had no obvious difference between the testgroup and the control group.The results indicated that the rmAdp had no significant effects on the micegrowth and the utilization ratio of forage.2The effects of rmAdp on the mice haematological indexesBlood samples were taken from the orbital vein before slaughter. The mice bloodglucose and blood fat level of the test group and the control group were tested. Theresults showed that the triglyceride (TG) content of rmAdp treatment group wasremarkable lower than that of the control group (P<0.05).There was no significantdifference of glucose (GLU), low density lipoprotein cholesterol (LDL-C) and highdensity lipoprotein cholesterol (HDL-C) between the test group and the control group.The results indicated that the rmAdp decreased serum triglyceride level of miceby increasing fatty acid oxidation. 3The effects of rmAdp on the mice mesentery adipose tissue and its mechanismAfter the mice of the above-mentioned test group and the control group wereslaughtered, the samples of mice mesentery adipose tissue were collected immediately.The expression of mRNA of adiponectin (Adp), adiponectin receptor1and2(AdpR1,AdpR2), PPARα and AMPK were determined by Real-time fluorescence quantitativeRT-PCR.The results showed that:(1) Expression of AdpR1and AdpR2in rmAdptreatment group were higher than the control group significantly (P<0.05), while thereis no significant difference between the two groups in expression of Adp.(2) Theexpression of AMPK and PPARa in rmAdp treatment group were higher than thecontrol group at extremely remarkable level and remarkable level respectively(P<0.01, P<0.05).The results indicated that the certain dosage of rmAdp can act on the adiposetissue to up-regulate the AdpR1, AdpR2in mesentery adipose tissue which mayactivate the AMPK and PPARa signal pathways, thus to regulate the fat metabolismand deposition of adipose tissue.4The effects of rmAdp on the mice gastrocnemius muscle growth and musclefiber types and its mechanismAfter the mice of the above-mentioned test group and the control groupslaughtered, the samples of mice gastrocnemius muscle tissue were collectedimmediately. Adp, AdpR1, AdpR2, four isoforms of myosin heavy chain (MyHCI,MyHC2a, MyHC2b and MyHC2x), PPARa and AMPK mRNA levels of the muscletissue were determined by Real-time fluorescence quantitative RT-PCR. The resultsshowed that:(1) Expression of Adp and AdpR2in rmAdp treatment group weresignificantly higher than those in the control group (P<0.01), while there is nosignificant difference between the two groups in expression of AdpR1.(2) Theexpression of MyHC2x, MyHC2b in rmAdp treatment group were significantly lowerthan the control group (P<0.05), while there is no significant difference between thetwo groups in expression of MyHC1and MyHC2a.(3) rmAdp increased theexpression of AMPK (P<0.01) and PPARα significantly(P<0.05).The results indicated that the certain dosage of rmAdp can act on the skeletalmuscle by binding AdpR2and activate AMPK and PPARα signal pathways, thus todown-regulate the expression of the MyHC2x and MyHC2b in skeletal muscle, thenchange the composition of muscle fibers and improve muscle quality consequently.