title: Insulin stimulates laser Doppler signal by rat muscle in vivo, consistent with nutritive flow recruitment.
abstract: Insulin-mediated increases in limb blood flow are thought to enhance glucose uptake by skeletal muscle. Using the perfused rat hindlimb, we report that macro laser Doppler flowmetry (LDF) probes positioned on the surface of muscle detect changes in muscle capillary (nutritive) flow. With this as background, we examined the effects of insulin and adrenaline (epinephrine), which are both known to increase total leg blood flow, on the LDF signals from scanning and stationary probes on the muscle surface in vivo. The aim is to assess the relationship between capillary recruitment, total limb blood flow and glucose metabolism. Glucose infusion rate, femoral arterial blood flow (FBF) and muscle LDF, using either scanning or a stationary probe positioned over the biceps femoris muscle, were measured. With scanning LDF, animals received insulin (10 m-units x min(-1) x kg(-1)), adrenaline (0.125 microg.min(-1) x kg(-1)) or saline. By 1 h, insulin had increased the glucose infusion rate from 0 to 128 micromol.min(-1) x kg(-1) and the scanning LDF had increased by 62+/-8% (P<0.05), but FBF was unaffected. Adrenaline increased FBF by 49% at 15 min, but LDF was unchanged. With saline at 1 h, neither FBF nor LDF had changed. With the stationary LDF surface probe, insulin at 1 h had increased FBF by 47% (P<0.05) and LDF by 47% (P<0.05) relative to saline controls. Adrenaline increased FBF (39%), but LDF was unaltered. The stimulation of LDF by insulin is consistent with capillary recruitment (nutritive flow) as part of the action of this hormone in vivo. The recruitment may be independent of changes in total flow, as adrenaline, which also increased FBF, did not increase LDF. The time of onset suggests that LDF closely parallels glucose uptake. Thus, depending on probe design, measurement of muscle haemodynamic effects mediated by insulin in normally responsive and insulin-resistant patients should be possible.
authors.affiliation: Division of Biochemistry, Medical School, University of Tasmania, GPO Box 252-58, 7001 Hobart, Australia.
authors.forename: A D
authors.initials: AD
authors.lastname: Clark
authors.forename: E J
authors.initials: EJ
authors.lastname: Barrett
authors.forename: S
authors.initials: S
authors.lastname: Rattigan
authors.forename: M G
authors.initials: MG
authors.lastname: Wallis
authors.forename: M G
authors.initials: MG
authors.lastname: Clark
mesh_terms: D000322:Adrenergic Agonists / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D001786:Blood Glucose / Q000032:analysis / Q000187:drug effects / Q000378:metabolism; D004837:Epinephrine / Q000494:pharmacology; D005263:Femoral Artery / Q000502:physiology; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D017078:Laser-Doppler Flowmetry / Q000379:methods*; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000187:drug effects; D051381:Rats; D012039:Regional Blood Flow
chemical_list: D000322:Adrenergic Agonists; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D004837:Epinephrine