I need this article to be summarized in simple terms as an article summary/notes

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I need this article to be summarized in simple terms as an article summary/notes.

Muscle glucose uptake, glycogen synt hase activity, and insulin signaling were invest igat ed in response to a physiological hyperinsulinemic (600 pmol1) -euglycemic clamp in young healthy subjects. Four hours before the clamp, the subjects perfor med one-legged ex er cise for 1 h. In the exercised leg, insulin more rapidly activat ed glucose uptake (half activation time [t,2l11 vs 34 min) and glycogen synthase activity (t/2- 8 vs. 17 min), and the magnitude of increase was two- to four- fold higher compared with the rested leg. However, vation by insulin has been observed >48 h after an exercise prior exerci se did not result in a gr eater or more rapid bout in human subjects (3-5). In rat skeletal muscle, it has increase in insulin-induced receptor tyrosine kinase been demonstrated that thereisa marked increase in insulin (IRTK) activity (t1/2 50 min), serine phosphorylation sensitivity for both glucose transport and glycogen synthase of Akt (11/2-1-2 min), or serine phosphorylation of activationater exercise(2,6). These changes facilitategyco- glycogen synthase kinase-3 (GSK-3) (l,/2-1-2 min) or gen resynthesis, and they may be the mechanism by which in a larger or more rapid GSK-3 activity (41/2 insulin infusion, glucose uptake, gl ycogen synthase activity, and signaling events were partially reversed in both the rest ed and the exercised leg. We the following: 1) physiological hyperinsulinemia induces We have previously hypothesized that an upregulation of sustained activation of insulin-signaling molecules in insulin signaling is involved in the increased insulin sensitiv- human skeletal muscle; 2) the more distal insulin- ity after exercise (9). However, if humans are subjected to signaling components (Akt, GSK-3) are activated much physiological hyperinsulinemia or if rat muscles are incu more rapidly than the proximal signaling molecules bated in the presence of insulin 3-4 h after exercise, insulin (IRTK as well as insulin recept or substrat e 1 and phos- receptor tyrosine kinase (IRTK) activity, insulin receptor phat idylinositol 3-kinase [Wojtaszewski et al., Diabetes substrate 1 (IRS-1) tyrosine phosphorylation, and ph 46:1775-1781, 1997; and 3) prior exercise increases phatidylinositol (Pi) 3-kinase activity are not enhanced in insulin stimulati on of both glucose uptake and glycogen synthase activity in the absence of an upregulation of signaling events in human skelet al muscle. Diabetes 49:325-331, 2000 uscle glucose transport and glycogen synthase activity are increased immediately after a single bout of exercise (1). In human skeletal muscle, the effects of exercise per se on mus- cle glucose transport are relatively short-lived (2-4 h), whereas the enhanced sensitivity for glucose transport acti ecrease in GSK-3 activity muscle glycogen storageis increased above pre-exerciseval ues, known as "supercompensation" (7,8). Whether prior exercise also increases the sensitivity for glycogen synthase min). Thirty minutes after cessation of lude theativation by insulin in human skeletal muscle is unknown skeletal muscle (9,10). This suggests that exercise may mod ulate insulin signaling further downstream or affect processes directly involved in glucose transporter translo- cation and activation

Explanation / Answer

Muscle glucose uptake and glycogen synthase activity increase with exercise, although the effect of exercise on glucose transport is short-lived. The increased sensitivity for glucose transport activation by insulin has been observed >48 hrs after exercise. Whether exercise also increases sensitivity for glycogen synthase activation has not been investigated yet.

In the present study, glucose uptake by muscle, activity of glycogen synthase and insulin signaling were investigated in response to hyperinsulinemic-euglycemic clamp. 4hrs before the clamp the young healthy volunteers were made to perform 1legged exercise for 1 he. It was observed that in exercised leg, insulin activated rapid glucose uptake (t1/2 = 11 vs 34 min), glycogen synthase activity (t1/2 = 8 vs 17 min). Thus , the magnitude of increase was 2 or 4 times compared to rested leg. However, no increase in Insulin induced receptor Kinase (IRTK) activity (t1/2 = 50 min) or decrease in Serine Phosphorylation of AKT (t1/2= 1-2min) or serine phosphorylation of glycogen synthase kinase 3 (t1/2 = 1-2min) could be observed.

After 30 min of cessation of insulin infusion, glucose uptake, glycogen synthase activity and insulin signaling were found to be partially reversed in both rested and exercised leg.

Hence, it was concluded that:

1. Physiological hyperinsulinemia induces activation of signaling molecules in human skeletal muscles

2. Distal signaling components (AKT, GSK3) are rapidly activated compared to proximal signaling molecules (IRTK, insulin receptor substrate 1)

3. excersice increases glucose uptake, glycogen synthase activity without upregulation of insulin signaling.

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