PMID- 11350781 OWN - NLM STAT- MEDLINE DCOM- 20010614 LR - 20171213 IS - 0193-1849 (Print) IS - 0193-1849 (Linking) VI - 280 IP - 6 DP - 2001 Jun TI - Functional limitations to glucose uptake in muscles comprised of different fiber types. PG - E994-9 AB - Skeletal muscle glucose uptake requires delivery of glucose to the sarcolemma, transport across the sarcolemma, and the irreversible phosphorylation of glucose by hexokinase (HK) inside the cell. Here, a novel method was used in the conscious rat to address the roles of these three steps in controlling the rate of glucose uptake in soleus, a muscle comprised of type I fibers, and two muscles comprised of type II fibers. Experiments were performed on conscious rats under basal conditions or during hyperinsulinemic euglycemic clamps. Rats received primed, constant infusions of 3-O-methyl-[3H]glucose (3-O-MG) and [1-14C]mannitol. Total muscle glucose concentration and the steady-state ratio of intracellular to extracellular 3-O-MG concentration, which distributes based on the transsarcolemmal glucose gradient (TSGG), were used to calculate glucose concentrations at the inner and outer sarcolemmal surfaces ([G](im) and [G](om), respectively) in muscle. Muscle glucose uptake was much lower in muscle comprised of type II fibers than in soleus under both basal and insulin-stimulated conditions. Under all conditions, the TSGG in type II muscle exceeded that in soleus, indicating that glucose transport plays a more important role to limit glucose uptake in type II muscle. Although hyperinsulinemia increased [G](im) in soleus, indicating that phosphorylation was a limiting factor, type II muscle was limited primarily by glucose delivery and glucose transport. In conclusion, the relative importance of glucose delivery, transport, and phosphorylation in controlling the rate of insulin-stimulated muscle glucose uptake varies between muscle fiber types, with glucose delivery and transport being the primary limiting factors in type II muscle. FAU - Halseth, A E AU - Halseth AE AD - Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. amy.e.halseth@pharmacia.com FAU - Bracy, D P AU - Bracy DP FAU - Wasserman, D H AU - Wasserman DH LA - eng GR - R01 DK-54902/DK/NIDDK NIH HHS/United States PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Am J Physiol Endocrinol Metab JT - American journal of physiology. Endocrinology and metabolism JID - 100901226 RN - 0 (Carbon Radioisotopes) RN - 0 (Diuretics, Osmotic) RN - 0 (Hypoglycemic Agents) RN - 0 (Insulin) RN - 10028-17-8 (Tritium) RN - 146-72-5 (3-O-Methylglucose) RN - 3OWL53L36A (Mannitol) RN - 9G2MP84A8W (Deoxyglucose) SB - IM MH - 3-O-Methylglucose/*pharmacokinetics MH - Animals MH - Carbon Radioisotopes MH - Deoxyglucose/pharmacokinetics MH - Diuretics, Osmotic/pharmacokinetics MH - Energy Metabolism/drug effects/physiology MH - Glucose Clamp Technique MH - Hypoglycemic Agents/pharmacology MH - Insulin/pharmacology MH - Male MH - Mannitol/pharmacokinetics MH - Muscle Fibers, Fast-Twitch/*metabolism MH - Muscle Fibers, Slow-Twitch/*metabolism MH - Muscle, Skeletal/cytology/*metabolism MH - Phosphorylation MH - Rats MH - Rats, Sprague-Dawley MH - Tritium EDAT- 2001/05/15 10:00 MHDA- 2001/06/23 10:01 CRDT- 2001/05/15 10:00 PHST- 2001/05/15 10:00 [pubmed] PHST- 2001/06/23 10:01 [medline] PHST- 2001/05/15 10:00 [entrez] AID - 10.1152/ajpendo.2001.280.6.E994 [doi] PST - ppublish SO - Am J Physiol Endocrinol Metab. 2001 Jun;280(6):E994-9. doi: 10.1152/ajpendo.2001.280.6.E994.