Corticosterone suppresses insulin- and NO-stimulated muscle glucose uptake in broiler chickens (Gallus gallus domesticus).
We evaluated the effects of stress as mimicked by corticosterone (CORT) administration on the uptake of glucose by skeletal muscles (M. fibularis longus) in broiler chickens (Gallus gallus domesticus). The results showed that both chronic (7 d) and short-term (3 h) CORT administration resulted in hyperglycemia and hyperinsulinemia. Plasma level of nitric oxide (NO) and the activity of NO synthase (NOS) were both suppressed by either chronic or acute stress. In vivo CORT treatment could stimulate the in vitro uptake of 2-deoxy-D-[1,2-3H]-glucose (2-DG). Sodium nitroprusside (SNP) administration improved the in vitro uptake of 2-DG in both CORT and control groups. In CORT treatment, however, the stimulating effect of NO on 2-DG uptake was relatively lower compared to control group, whereas it was restored by insulin. Insulin stimulated muscle in vitro 2-DG uptake in either control or CORT group, with the improvement being significantly higher in control chickens. The results indicated that the reduced circulating and muscle level of NO level via the suppression of NOS by corticosterone treatment was involved in the stress-induced insulin resistance. It appears that CORT could suppress the insulin stimulated glucose uptake in skeletal muscle, inducing insulin resistance in broiler chickens. We conclude that NO could stimulate glucose transport in chicken skeletal muscle and that the reduced circulating and muscle level of NO is involved in the insulin resistance induced by corticosterone treatment.
Zhao
J P
JP
Department of Animal Science, Shandong Agricultural University, Taian, Shandong 271018, PR China.
Lin
H
H
Jiao
H C
HC
Song
Z G
ZG
D000818:Animals; D001692:Biological Transport; D001786:Blood Glucose / Q000378:metabolism*; D002645:Chickens; D003345:Corticosterone / Q000008:administration & dosage* / Q000009:adverse effects; D003847:Deoxyglucose / Q000378:metabolism; D004032:Diet; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006003:Glycogen / Q000378:metabolism; D006943:Hyperglycemia / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D006946:Hyperinsulinism / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D007333:Insulin Resistance; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000097:blood / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D009599:Nitroprusside / Q000494:pharmacology; D013997:Time Factors
D001786:Blood Glucose; D004791:Enzyme Inhibitors; D007328:Insulin; D020030:Nitric Oxide Donors; D009599:Nitroprusside; D009569:Nitric Oxide; D006003:Glycogen; D003847:Deoxyglucose; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester; D003345:Corticosterone