Insulin action on glucose uptake into skeletal muscle

Dietze, G.; Wicklmayr, M.; Böttger, I.; Mayer, L.

doi:10.1016/0014-5793(78)80773-x

Cited by 20 publications

(6 citation statements)

References 21 publications

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“…These workers have suggested that increased glucose utilization during exercise and after hypoxia (reactive hyperaemia) is due, in part, to the release from kininogen of kinins, which in turn cause an increase in the rate of production of prostaglandins that increase the sensitivity of some process in muscle to insulin. They have also shown that the administration of indomethacin to man results in resistance of glucose utilization to insulin (Dietze et al, 1978). However, the precise means by which prostaglandins could influence the effects of insulin were not considered.…”

Section: Discussionmentioning

confidence: 99%

“…There are several reports that prostaglandins either mimic or are involved in the effects of insulin on some of these processes (see, e.g., Willebrandt & Tasseron, 1968;Wieser & Fain, 1975;Dietze, 1982;Reeds & Palmer, 1983). The fact that administration of indomethacin, which is an inhibitor of prostaglandin synthesis, results in insulin resistance in man suggests that many of the reported effects of prostaglandins could be explained if prostaglandins increased the sensitivity of muscle to the effects of insulin (see Dietze et al, 1978;Dietze, 1982). We have shown previously that adenosine or adenosine-receptor agonists can dramatically decrease the sensitivity of glycolysis to insulin in isolated soleus muscle, but that they have no effect on the sensitivity of glycogen synthesis to insulin; adenosine antagonists or the presence of adenosine deaminase increase the sensitivity of glycolysis to insulin, but do not affect the sensitivity of glycogen synthesis (Espinal et al, 1983a;Budohoski et al, 1984).…”

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confidence: 99%

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The effect of prostaglandins E1, E2 and F2α and indomethacin on the sensitivity of glycolysis and glycogen synthesis to insulin in stripped soleus muscles of the rat

Leighton¹,

Budohoski²,

Lozeman³

et al. 1985

Biochemical Journal

100

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Prostaglandins E1 and E2 increased the sensitivity of glycolysis to insulin in the isolated stripped soleus muscle of the rat, but prostaglandin F2 alpha had no effect. Indomethacin, which inhibits prostaglandin formation, markedly decreased the sensitivity of glycolysis to insulin. These findings suggest that prostaglandins of the E series increase the sensitivity of muscle glycolysis to insulin in vivo.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

The effect of prostaglandins E1, E2 and F2α and indomethacin on the sensitivity of glycolysis and glycogen synthesis to insulin in stripped soleus muscles of the rat

Leighton¹,

Budohoski²,

Lozeman³

et al. 1985

Biochemical Journal

100

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“…Therefore, it cannot be excluded that the inhibition of PG synthesis might have resulted in decreased insulin sensitivity of resting muscle tissue, shifting the doseresponse curve to the right. The inhibitory effect of indomethacin on insulin-mediated glucose uptake of the forearm, as described by Dietze et al (1978b), was apparent at insulin concentrations ranging from 130 to 188 ,tunits/ml.…”

Section: Jurslf Ilii Nmentioning

confidence: 88%

“…In conclusion, we feel that the results of Zorzano et al (1986) do not exclude an involvement of PGs in insulinor exercise-mediated glucose uptake by skeletal muscle tissue. Studies in man by Dietze et al (1978b), Newman & Brodows (1983) and Bratusch-Marrain et al (1985) have shown that inhibition of PG synthesis in vivo impairs insulin-mediated glucose utilization significantly and, on the other hand, stimulation f PG synthesis by increased bradykinin availability was found to increase peripheral insulin sensitivity in post-surgical and diabetic patients (Jauch et al, 1986(Jauch et al, , 1987. Therefore, further studies with adequate design in a physiological system are necessary to elucidate completely the molecular basis of the observed changes.…”

Section: Jurslf Ilii Nmentioning

confidence: 99%

Prostaglandins and skeletal muscle glucose uptake

Hartl¹

1987

Biochemical Journal

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“…Yet at higher concentrations, many of these agents lose this specificity. For instance, at >50 ,uM, NDGA inhibits platelet (55) (60,61). Associations between arachidonic acid metabolism and hexose transport in diverse tissues are worthy of further study.…”

Section: Discussionmentioning

confidence: 99%

Role of arachidonic acid in stimulation of hexose transport by human polymorphonuclear leukocytes

Bass¹,

O’Flaherty²,

Szejda³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

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Whereas insulin does not stimulate hexose transport in polymorphonuclear leukocytes, we recently reported that C5a causes the leukocytes to take up 243Hldeoxy-glucose. We now find that fMet-Leu-Phe, in a concentrationrelated manner with an ECso (concentration producing 50% of stimulatory activity) of 1.2 nM, causes a 5.5-fold stimulation of deoxyglucose uptake. Moreover, arachidonic acid (5,8,11, acid) similarly stimulated deoxyglucose uptake with an EC50 of 0.6 gM. Stimulation by arachidonic acid exhibited structural specificity; five structural analogues of arachidonic acid, including arachidonyl alcohol, 8,11,14-eicosatrienoic acid, 11,14,17-eicosatrienoic acid, 5,8,11,14- Substances originally defined as stimulating chemotaxis of human polymorphonuclear leukocytes (PMNL), such as C5a and the synthetic oligopeptide N-formylmethionylleucylphenylalanine (fMet-Leu-Phe), interact with specific membrane receptors (1-3) that induce multifunctional cellular responses. In addition to stimulating motility, such chemotactic factors also stimulate adhesiveness (4, 5), aggregation (5-7), degranulation (3,8), and oxidative metabolism (9-12) of PMNL. PMNL require energy derived from glucose for each of these functions. It would be reasonable if chemotactic substances interacted with hexose transport systems of the PMNL membrane to facilitate the availability of glucose. We recently reported that C5a stimulated the uptake of 2-[3H]deoxyglucose (dGlc) (13). Similar concentrations of C5a were required to cause stimulation of chemotaxis and dGlc uptake. Whereas insulin had no effect on dGlc transport in PMNL, the 3-to 7-fold increase in uptake induced by C5a was comparable to that produced by insulin in human adipose tissue (14).Stimulation of membrane receptors by chemotactic factors produces a number of membrane responses which have been suggested as a sequence culminating in stimulation of cellular functions (15-17). These include (i) increase in levels of free calcium by influx of extracellular Ca2+ and (or) mobilization of intracellular or membrane-bound Ca2+ (18-22), (ii) activation of calcium-dependent phospholipase A2 (23), (iM) release of arachidonic acid from membrane phospholipids (24), and (iv) metabolism of arachidonic acid with generation of bioactive products (16,(25)(26)(27)(28)(29)(30)(31)(32)(33)(34), some of which are reincorporated into the membrane (30, 31) possibly causing increased membrane fluidity. Whether these events are involved in the stimulation of hexose transport is unknown.The synthetic oligopeptide fMet-Leu-Phe has been extensively used as an analogue of bacterical chemotactic factors and has proven invaluable as a probe for elucidating multifunctional effects and mechanisms of actions of chemotactic factors of PMNL. The present studies examined the ability of fMetLeu-Phe or arachidonic acid to stimulate dGlc uptake by PMNL, the effects of inhibitors of the cyclooxygenase and lipoxygenase pathways of arachidonic acid metabolism, and the nature of the hexose transport system. METHODS P...

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Insulin action on glucose uptake into skeletal muscle

Cited by 20 publications

References 21 publications

The effect of prostaglandins E1, E2 and F2α and indomethacin on the sensitivity of glycolysis and glycogen synthesis to insulin in stripped soleus muscles of the rat

The effect of prostaglandins E1, E2 and F2α and indomethacin on the sensitivity of glycolysis and glycogen synthesis to insulin in stripped soleus muscles of the rat

Prostaglandins and skeletal muscle glucose uptake

Role of arachidonic acid in stimulation of hexose transport by human polymorphonuclear leukocytes

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