A substantial part of GLUT-1 in crude membranes from muscle originates from perineurial sheaths

1992 ◽  
Vol 262 (5) ◽  
pp. E721-E727 ◽  
Author(s):  
A. Handberg ◽  
L. Kayser ◽  
P. E. Hoyer ◽  
J. Vinten
Keyword(s):  
Soleus Muscle ◽  
Membrane Fraction ◽  
Skeletal Muscles ◽  
Femoral Nerve ◽  
Muscle Cells ◽  
Substantial Part ◽  
Glut 1 ◽  
Glut 4 ◽  
Intramuscular Nerves ◽  
Perineurial Sheath

The distribution of GLUT-1 and GLUT-4 in cryosections of rat skeletal muscles was investigated immunocytochemically. Intense labeling of GLUT-1 was found in the perineurial sheaths of intramuscular nerves, whereas only a very faint signal was associated with the sarcolemma, and labeling of extraneural vessels was not detectable. The majority of the GLUT-4 reactivity was located at the periphery of muscle cells in nonuniform patches, and GLUT-4 was absent in vessels and nerves. In sections of femoral nerve GLUT-1 was confined to the perineurial sheath and endoneurial vessels. The contribution of GLUT-1 from intramuscular perineurial sheaths to total GLUT-1 in a muscle was determined from immunoblots of crude membranes isolated from mixtures of homogenates of excised nerves and muscles. The recovery of GLUT-1 increased linearly with the amount of nerve added, and it was calculated that GLUT-1 from intramuscular perineurial sheaths accounted for approximately 60% of the GLUT-1 content in a membrane fraction from soleus muscle or red gastrocnemius. The remaining 40% of GLUT-1 is likely to originate from the sarcolemma.

scholarly journals Differential regulation of the GLUT-1 and GLUT-4 glucose transport systems by glucose and insulin in L6 muscle cells in culture

1991 ◽  
Vol 266 (4) ◽  
pp. 2615-2621 ◽  
Author(s):  
U M Koivisto ◽  
H Martinez-Valdez ◽  
P J Bilan ◽  
E Burdett ◽  
T Ramlal ◽  
...  
Keyword(s):  
Glucose Transport ◽  
Muscle Cells ◽  
Differential Regulation ◽  
Transport Systems ◽  
Glut 1 ◽  
Glut 4 ◽  
Cells In Culture ◽  
L6 Muscle Cells

Nutritional regulation of glucose transporter in muscle and adipose tissue of weaned rats

1991 ◽  
Vol 260 (4) ◽  
pp. E588-E593 ◽  
Author(s):  
A. Leturque ◽  
C. Postic ◽  
P. Ferre ◽  
J. Girard
Keyword(s):  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Skeletal Muscles ◽  
Glucose Transporter ◽  
Nutritional Regulation ◽  
Suckling Rats ◽  
Glut 1 ◽  
Glut 4 ◽  
Enhanced Expression ◽  
Nutritional Environment

The role of glucose transporters GLUT-1 and GLUT-4 in the development of insulin sensitivity at weaning in rat skeletal muscles and adipose tissue was studied in relation to the nutritional changes when suckling rats shift from a high-fat (HF) to a high-carbohydrate (HCHO) diet. Insulin stimulated the translocation of GLUT-4 protein from an intracellular pool to the plasma membrane in adipocytes from suckling and HCHO- or HF-weaned rats. The GLUT-4 protein and the insulin stimulation were threefold higher in adipocytes from HCHO-weaned rats than in suckling or HF-weaned rats. GLUT-4 mRNA and protein were low in adipose tissue and skeletal muscles of suckling rats and increased two- to threefold in HCHO-weaned rats. This increase was prevented in HF-weaned rats. GLUT-1 mRNA was not affected in both tissues by the developmental stage or the nutritional environment. After feeding HCHO to a suckling rat, GLUT-4 mRNA was threefold increased in 6 days and reached a peak after 4 days in both tissues. The insulin sensitivity of glucose transport in rats at weaning might be conferred by an enhanced expression of GLUT-4, which can be induced within a few hours after feeding a HCHO diet.

Glucose transporter expression in human skeletal muscle fibers

2000 ◽  
Vol 279 (3) ◽  
pp. E529-E538 ◽  
Author(s):  
M. Gaster ◽  
A. Handberg ◽  
H. Beck-Nielsen ◽  
H. D. Schrøder
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Glucose Transporter ◽  
Muscle Fibers ◽  
Muscle Cells ◽  
Glut 1 ◽  
Adult Muscle ◽  
Glut 4 ◽  
Skeletal Muscle Fibers ◽  
Transporter Expression

The present study was initiated to investigate GLUT-1 through -5 expression in developing and mature human skeletal muscle. To bypass the problems inherent in techniques using tissue homogenates, we applied an immunocytochemical approach, employing the sensitive enhanced tyramide signal amplification (TSA) technique to detect the localization of glucose transporter expression in human skeletal muscle. We found expression of GLUT-1, GLUT-3, and GLUT-4 in developing human muscle fibers showing a distinct expression pattern. 1) GLUT-1 is expressed in human skeletal muscle cells during gestation, but its expression is markedly reduced around birth and is further reduced to undetectable levels within the first year of life; 2) GLUT-3 protein expression appears at 18 wk of gestation and disappears after birth; and 3) GLUT-4 protein is diffusely expressed in muscle cells throughout gestation, whereas after birth, the characteristic subcellular localization is as seen in adult muscle fibers. Our results show that GLUT-1, GLUT-3, and GLUT-4 seem to be of importance during muscle fiber growth and development. GLUT-5 protein was undetectable in fetal and adult skeletal muscle fibers. In adult muscle fibers, only GLUT-4 was expressed at significant levels. GLUT-1 immunoreactivity was below the detection limit in muscle fibers, indicating that this glucose transporter is of minor importance for muscle glucose supply. Thus we hypothesize that GLUT-4 also mediates basal glucose transport in muscle fibers, possibly through constant exposure to tonal contraction and basal insulin levels.

Phosphatidylinositol 3-kinase and dynamics of insulin resistance in denervated slow and fast muscles in vivo

1997 ◽  
Vol 272 (4) ◽  
pp. E661-E670 ◽  
Author(s):  
J. S. Elmendorf ◽  
A. Damrau-Abney ◽  
T. R. Smith ◽  
T. S. David ◽  
J. Turinsky
Keyword(s):  
Insulin Receptor ◽  
Glucose Uptake ◽  
Soleus Muscle ◽  
Phosphatidylinositol 3 Kinase ◽  
Plantaris Muscle ◽  
Glut 1 ◽  
Glut 4 ◽  
Denervated Muscles ◽  
Phosphatidylinositol 3

Regulation of glucose uptake by 1- and 3-day denervated soleus (slow-twitch) and plantaris (fast-twitch) muscles in vivo was investigated. One day after denervation, soleus and plantaris muscles exhibited 62 and 65% decreases in insulin-stimulated 2-deoxyglucose uptake, respectively, compared with corresponding control muscles. At this interval, denervated muscles showed no alterations in insulin receptor binding and activity, amount and activity of phosphatidylinositol 3-kinase, and amounts of GLUT-1 and GLUT-4. Three days after denervation, there was no increase in 2-deoxyglucose uptake in response to insulin in soleus muscle, whereas plantaris muscle exhibited a 158% increase in basal and an almost normal absolute increment in insulin-stimulated uptake. Despite these differences, denervated soleus and plantaris muscles exhibited comparable decreases in insulin-stimulated activities of the insulin receptor (approximately 40%) and phosphatidylinositol 3-kinase (approximately 50%) and a pronounced decrease in GLUT-4. An increase in GLUT-1 in plantaris, but not soleus, muscle 3 days after denervation is consistent with augmented basal 2-deoxyglucose uptake in plantaris muscle at this interval. These results demonstrate that, in denervated muscles, there is a clear dissociation between insulin-stimulated 2-deoxyglucose uptake and upstream events involved in insulin-stimulated glucose uptake.

Effect of overexpressing GLUT-1 and GLUT-4 on insulin- and contraction-stimulated glucose transport in muscle

1996 ◽  
Vol 271 (3) ◽  
pp. E547-E555 ◽  
Author(s):  
E. Johannsson ◽  
K. J. McCullagh ◽  
X. X. Han ◽  
P. K. Fernando ◽  
J. Jensen ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Glucose Transport ◽  
Tibialis Anterior ◽  
Skeletal Muscles ◽  
Extensor Digitorum Longus ◽  
Muscle Contractions ◽  
Extensor Digitorum ◽  
Glut 1 ◽  
Glut 4 ◽  
Chronic Electrical Stimulation

To examine the effects of GLUT-1 on GLUT-4-dependent, insulin-stimulated, and contraction-stimulated 2-deoxy-D-glucose (2-DG) transport, we overexpressed GLUT-1 in metabolically heterogeneous skeletal muscles [red and white tibialis anterior (TA) and extensor digitorum longus (EDL)] via 7 days of chronic electrical stimulation. GLUT-1 was increased 1.6- to 16.4-fold (P < 0.05). Basal 2-DG transport was increased 1.7- to 3.0-fold (P < 0.05) and was equal to (red TA and EDL; P > 0.05) or exceeded insulin-stimulated 2-DG transport by 50% (white TA; P < 0.05) in the control muscles. GLUT-4 was concomitantly overexpressed (2.1- to 4.4-fold; P < 0.05). Insulin-stimulated 2-DG transport was increased 1.6- to 2.5-fold (P < 0.05). During muscle contractions, 2-DG transport increased 9- to 12-fold (P < 0.05) in control muscles, but this was reduced by approximately 25% (P < 0.05) in muscles overexpressing GLUT-1 and GLUT-4 (red TA and EDL). In contrast, in the experiment, white TA contraction-stimulated 2-DG transport was increased 1.7-fold (P < 0.05). Therefore, overexpression of GLUT-1, when GLUT-4 is also overexpressed, does not impair insulin-stimulated 2-DG transport, although contraction-stimulated transport may be reduced in some muscles.

scholarly journals Different role of insulin in GLUT-1 and -4 regulation in heart and skeletal muscle during perinatal hypothyroidism

2001 ◽  
Vol 281 (5) ◽  
pp. E1073-E1081 ◽  
Author(s):  
S. Ramos ◽  
L. Goya ◽  
C. Alvarez ◽  
M. A. Martín ◽  
M. Agote ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Skeletal Muscles ◽  
Serum Insulin ◽  
Glucose Transporters ◽  
Perinatal Period ◽  
Differential Sensitivity ◽  
Glut 1 ◽  
Glut 4 ◽  
Igf I ◽  
Specific Regulation

Two groups of hypothyroid rats were used; one group was given 2-mercapto-1-methylimidazole (MMI) treatment in the drinking water of the mothers and was killed at 2 and 4 days of life, and the other group was given similar MMI treatment and then was thyroidectomized at 5 days of life and killed at 8 or 20 days. Serum insulin, growth hormone (GH), and insulin-like growth factor I (IGF-I) were decreased in MMI-treated rats but increased in MMI-treated plus thyroidectomized rats. No significant reduction of thyroid hormones was observed in 2-day-old MMI rats. Protein and mRNA expression of GLUT-1 increased, and those of GLUT-4 decreased, in the heart in all populations independent of changes in insulin, GH, and IGF-I levels. However, GLUT-4 protein and mRNA expression in quadriceps and gastrocnemius skeletal muscles decreased at 4 days and increased at 8 and 20 days of life in parallel with insulin, GH, and IGF-I levels. GLUT-1 in the skeletal muscles seemed regulated posttranscriptionally and presented a decrease of mRNA expression in all stages studied. A differential sensitivity to insulin regulation of GLUT-1 and GLUT-4 glucose transporters seems to be one of the causes for the tissue-specific regulation of these glucose transporters in heart and skeletal muscles during the perinatal period.

Testosterone and DHEA activate the glucose metabolism-related signaling pathway in skeletal muscle

2008 ◽  
Vol 294 (5) ◽  
pp. E961-E968 ◽  
Author(s):  
Koji Sato ◽  
Motoyuki Iemitsu ◽  
Katsuji Aizawa ◽  
Ryuichi Ajisaka
Keyword(s):  
Skeletal Muscle ◽  
Glucose Metabolism ◽  
Signaling Pathway ◽  
Skeletal Muscles ◽  
Glucose Transporter ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Glut 4 ◽  
Kinase C ◽  
Pkc Ζ

Circulating dehydroepiandrosterone (DHEA) is converted to testosterone or estrogen in the target tissues. Recently, we demonstrated that skeletal muscles are capable of locally synthesizing circulating DHEA to testosterone and estrogen. Furthermore, testosterone is converted to 5α-dihydrotestosterone (DHT) by 5α-reductase and exerts biophysiological actions through binding to androgen receptors. However, it remains unclear whether skeletal muscle can synthesize DHT from testosterone and/or DHEA and whether these hormones affect glucose metabolism-related signaling pathway in skeletal muscles. We hypothesized that locally synthesized DHT from testosterone and/or DHEA activates glucose transporter-4 (GLUT-4)-regulating pathway in skeletal muscles. The aim of the present study was to clarify whether DHT is synthesized from testosterone and/or DHEA in cultured skeletal muscle cells and whether these hormones affect the GLUT-4-related signaling pathway in skeletal muscles. In the present study, the expression of 5α-reductase mRNA was detected in rat cultured skeletal muscle cells, and the addition of testosterone or DHEA increased intramuscular DHT concentrations. Addition of testosterone or DHEA increased GLUT-4 protein expression and its translocation. Furthermore, Akt and protein kinase C-ζ/λ (PKC-ζ/λ) phosphorylations, which are critical in GLUT-4-regulated signaling pathways, were enhanced by testosterone or DHEA addition. Testosterone- and DHEA-induced increases in both GLUT-4 expression and Akt and PKC-ζ/λ phosphorylations were blocked by a DHT inhibitor. Finally, the activities of phosphofructokinase and hexokinase, main glycolytic enzymes, were enhanced by testosterone or DHEA addition. These findings suggest that skeletal muscle is capable of synthesizing DHT from testosterone, and that DHT activates the glucose metabolism-related signaling pathway in skeletal muscle cells.

Effect of chronic hypoxia on glucose transporters in heart and skeletal muscle of immature and adult rats

1997 ◽  
Vol 273 (5) ◽  
pp. R1734-R1741 ◽  
Author(s):  
Ying Xia ◽  
Joseph B. Warshaw ◽  
Gabriel G. Haddad
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Chronic Hypoxia ◽  
Mrna Level ◽  
Tissue Type ◽  
Western Blots ◽  
Adult Skeletal Muscle ◽  
Appreciable Change ◽  
Glut 1 ◽  
Glut 4

Glucose transporter (GLUT) modulation can be an important mechanism that contributes to adaptation to hypoxic stress, but little is known about GLUT modulation in heart and skeletal muscle with prolonged hypoxia. In this work, the effect of chronic hypoxia on GLUT-4 and GLUT-1 mRNA and protein was studied in these two tissues in the adult and during development. Hypoxia (fractional inspired O2 = 9 ± 0.5%) was administered to two groups, i.e., an immature group exposed from 3 to 30 days of age and an adult group exposed from 90 to 120 days of age. Rats were then killed and their heart and skeletal muscles were sampled for measurements of GLUT mRNA and protein with Northern and Western blots. In the adult, chronic hypoxia significantly decreased cardiac GLUT mRNA level by >25% of control ( P < 0.05), but had little effect on GLUT protein. A very different hypoxic effect was seen in the immature rat heart with a major increase in protein and no appreciable change in mRNA density. Adult skeletal muscle had no change in GLUT mRNA level but GLUT protein increased (15–20%, P < 0.05) while both GLUT mRNA and protein were significantly increased in the immature skeletal muscles (60–90% over control). We conclude that during chronic O2 deprivation, GLUT-1 and GLUT-4 expressions show a similar pattern but greatly depend on tissue type and age. These differences in GLUT regulation may be due to different strategies for coping with prolonged O2 deprivation in both immature and adult animals.

Low-Flow Ischemia Leads to Translocation of Canine Heart GLUT-4 and GLUT-1 Glucose Transporters to the Sarcolemma In Vivo

Circulation ◽  
1997 ◽  
Vol 95 (2) ◽  
pp. 415-422 ◽  
Author(s):  
Lawrence H. Young ◽  
Yin Renfu ◽  
Raymond Russell ◽  
Xiaoyue Hu ◽  
Michael Caplan ◽  
...  
Keyword(s):  
Glucose Transporters ◽  
Low Flow ◽  
Canine Heart ◽  
Glut 1 ◽  
Glut 4

Effect of endurance training on glucose transport capacity and glucose transporter expression in rat skeletal muscle

1990 ◽  
Vol 259 (6) ◽  
pp. E778-E786 ◽  
Author(s):  
T. Ploug ◽  
B. M. Stallknecht ◽  
O. Pedersen ◽  
B. B. Kahn ◽  
T. Ohkuwa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transport ◽  
Glucose Transporter ◽  
Training Session ◽  
Residual Effect ◽  
Exercise Session ◽  
Transport Capacity ◽  
Glut 1 ◽  
Glut 4 ◽  
Fast Twitch

The effect of 10 wk endurance swim training on 3-O-methylglucose (3-MG) uptake (at 40 mM 3-MG) in skeletal muscle was studied in the perfused rat hindquarter. Training resulted in an increase of approximately 33% for maximum insulin-stimulated 3-MG transport in fast-twitch red fibers and an increase of approximately 33% for contraction-stimulated transport in slow-twitch red fibers compared with nonexercised sedentary muscle. A fully additive effect of insulin and contractions was observed both in trained and untrained muscle. Compared with transport in control rats subjected to an almost exhaustive single exercise session the day before experiment both maximum insulin- and contraction-stimulated transport rates were increased in all muscle types in trained rats. Accordingly, the increased glucose transport capacity in trained muscle was not due to a residual effect of the last training session. Half-times for reversal of contraction-induced glucose transport were similar in trained and untrained muscles. The concentrations of mRNA for GLUT-1 (the erythrocyte-brain-Hep G2 glucose transporter) and GLUT-4 (the adipocyte-muscle glucose transporter) were increased approximately twofold by training in fast-twitch red muscle fibers. In parallel to this, Western blot demonstrated a approximately 47% increase in GLUT-1 protein and a approximately 31% increase in GLUT-4 protein. This indicates that the increases in maximum velocity for 3-MG transport in trained muscle is due to an increased number of glucose transporters.

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