- Improvement of Leptin Resistance.
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Yong Woon Kim
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Yeungnam Univ J Med. 2013;30(1):4-9. Published online June 30, 2013
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DOI: https://doi.org/10.12701/yujm.2013.30.1.4
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- Leptin, a 16-kDa cytokine, is secreted by adipose tissue in response to the surplus of fat store. Thereby, the brain is informed about the body's energy status. In the hypothalamus, leptin triggers specific neuronal subpopulations (e.g., POMC and NPY neurons) and activates several intracellular signaling events, including the JAK/STAT, MAPK, PI3K, and mTOR pathway, which eventually translates into decreased food intake and increased energy expenditure. Leptin signal is inhibited by a feedback inhibitory pathway mediated by SOCS3. PTP1B involves another inhibitory pathway of leptin. Leptin potently promotes fat mass loss and body weight reduction in lean subjects. However, it is not widely used in the clinical field because of leptin resistance, which is a common feature of obesity characterized by hyperleptinemia and the failure of exogenous leptin administration to provide therapeutic benefit in rodents and humans. The potential mechanisms of leptin resistance include the following: 1) increases in circulating leptin-binding proteins, 2) reduced transport of leptin across the blood-brain barrier, 3) decreased leptin receptor-B (LRB), and/or 4) the provocation of processes that diminish cellular leptin signaling (inflammation, endoplasmic reticulum stress, feedback inhibition, etc.). Thus, interference of the cellular mechanisms that attenuate leptin signaling improves leptin action in cells and animal models, suggesting the potential utility of these processes as points of therapeutic intervention. Various experimental trials and compounds that improve leptin resistance are introduced in this paper.
- Effects of Regular Treadmill Running on GLUT4 Protein of Skeletal Muscle in STZ-diabetic Rats.
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Jong yeon Kim, Hyung il Bae, So young Park, Yong woon Kim, Suck kang Lee
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Yeungnam Univ J Med. 1998;15(2):341-349. Published online December 31, 1998
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DOI: https://doi.org/10.12701/yujm.1998.15.2.341
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- The purpose of this study was to investigate the effects of regular treadmill running on GLUT4 protein of skeletal muscle in STZ-diabetic rats. I used 19 male Sprague-Dawley rats weighing 140 to 160 grams. Rats were randomly assigned into normal, diabetes(DM) and DE(DE) groups. The exercise was loaded with treadmill running for 5 days per week during 4 weeks. All experimental procedures were carried out following overnight fasting 48 hours after last exercise. Gain(gm) in body weight in DM rats(82+/-2.4) was lowered compared to normal rats(109+/-2.8), and decreased by exercise. Plasma glucose concentration(mg/dl) in DM rats was 143+/-3.1 which is higher than that of normal group of 103+/-6.4. The concentration of DE group was lower than that of DM rats. Plasma insulin concentration(micronU/ml) of DM and DE rats was significantly lowerd compared to normal rats. There was no difference of plasma concentrations of FFA and HDL cholesterol among noraml, DM and DE groups. Plasma triglyceride concentration(mg/dl) was significantly highered in DM group compared to those of DM group, the concentration of DE group was lower. Glycogen concentration(mg/gm wet weight) of the plantaris muscle in DM and DE groups was significantly reduced compared to normal group. Glucose transporter 4(GLUT4) protein of soleus was analyzed by Western blot. In DM group, the GLUT4 protein level was markdly decreased compared to normal group, but the level was recovered to the level of normal group by 4 weeks treadmill running. In conclusion, the insulin resistance induced by STZ administration was partially improved by 4 weeks physical training in rats.
- Effect of Hyperglycemia and Hyperlipidemia on Cardiac Muscle Glycogen Usage during Exercise in Rats.
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Suck Kang Lee, Eun Jung Kim, Yong Woon Kim
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Yeungnam Univ J Med. 1998;15(1):29-35. Published online June 30, 1998
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DOI: https://doi.org/10.12701/yujm.1998.15.1.29
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- Rats were studied during 45 minutes treadmill exercise to determine the effects of hyperglycemia and hyperlipidemia on the utilization of cardiac muscle glycogen, and the utilization of diaphragm muscle glycogen was also studied for comparing to cardiac muscle. The hyperglycemia was produced by ingestion of 25% glucose solution(1ml/100gm, BW) and the hyperlipidemia by 10% intralipose ingestion(1ml/100gm, BW) with intraperitoneal injection of heparin(500 IU) 15 minutes before treadmill exercise. The mean blood glucose concentrations(mg/dL) in control and hyperglycemic rats were 110 and 145, respectively, and the mean plasma free fatty acid concentrations(micronEq/L) in control, control exercise(control-E) and hyperlipidemia exercise(HL-E) rats were 247, 260 and 444, respectively. In the hyperglycemic trial, the cardiac muscle glycogen concentration was not significantly decreased by the exercise but the concentration in control rats was decreased to 73.9%(p<0.05). The glycogen concentration of diaphragm was significantly decreased in both groups by the exercise, but the hyperglycemia decreased the glycogen utilization by approximately 10% compared to the control. The cardiac muscle glycogen concentration was not decreased by the exercise in control and hyperlipidemic rats but the utilization of glycogen in hyperlipidemic rats is lower than that of the control. These data illustrate the sparing effect of hyperglycemia on cardiac muscle glycogen usage during exercise, but the effect of hyperlipidemia was not conclusive. In the skeletal muscle, the usage of glycogen by exercise was spared by both hyperglycemia and hyperlipidemia.
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- The Effects of Treadmill Exercise on Blood components, Antioxidant enzymes and Reactive Oxygen in Hyperlipidemic Rats
Byeong-Ok Jung, Sang-Hun Jang, Hyun-Soo Bang Journal of the Korean Society of Physical Medicine.2013; 8(1): 71. CrossRef
- Effect of Acutely Increased Glucose Uptake on Insurin Sensitivity in Rats.
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Yong Woon Kim, Youl In Ma, Suck Kang Lee
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Yeungnam Univ J Med. 1997;14(1):53-66. Published online June 30, 1997
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DOI: https://doi.org/10.12701/yujm.1997.14.1.53
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- Insulin resistance is a prominent feature of diabetic state and has heterogeneous nature. However, the pathogenetic sequence of events leading to the emergence of the defect in insulin action remains controversial. It is well-known that prolonged hyperglycemia and hyperinsulinemia are one of the causes of development of insulin resistance, but both hyperglycemia and hyperinsulinemia stimulate glucose uptake in peripheral tissue. Therefore, it is hypothesized that insulin resistance may be generated by a kind of protective mechanism preventing cellular hypertrophy. In this study, to evaluate whether the acutely increased glucose uptake inhibits further glucose transport stimulated by insulin, insulin sensitivity was measured after preloaded glucose infusion for 2 hours at various conditions in rats. And also, to evaluate the mechanism of decreased insulin sensitivity, insulin receptor binding affinity and glucose transporter 4 (GLUT4) protein of plasma membrane of gastrocnemius muscle were assayed after hyperinsulinemic euglycemic clamp studies. Experimental animals were divided into five groups according to conditions of preloaded glucose infusion: group I, basal insulin (14+/-1.9 micronU/ml) and basal glucose (75+/-0.7 mg/dl), by normal saline infusion; group II, normal insulin (33+/-3.8 micronU/ml) and hyperglycemia (207+/-6.3 mg/dl), by somatostatin and glucose infusion; group III, hyperinsulinemia (134+/-34.8 micronU/ml) and hyperglycemia (204+/-4.6 mg/dl), by glucose infusion; IV, supramaximal insulin (100+/-2.2 mg/dl), by insulin and glucose infusion; group V, supramaximal insulin(4813+/-687.9 micronU/ml) and hyperglycemia (233+/-3.1 mg/dl), by insulin and glucose infusion. Insulin sensitivity was assessed with hyperinsulinemic euglycemic clamp technique. The amounts of preloaded glucose infusion(gm/kg) were 1.88+/-0.151 in group II, 2.69+/-0.239 in group III, 3.54+/-0.198 in groupIV, and 4.32+/-0.621 in group V. Disappearance rates of glucose (Rd, mg/kg/min) at steady state of hyperinsulinemic euglycemic clamp studies were 16.9+/-3.88 in group I, 13.5+/-1.05 in group II, 11.2+/-1.17 in group III, 13.2+/-2.05 in group IV, and 10.4+/-1.01 in group V. A negative correlation was observed between amount of preloaded glucose and Rd )r=-0.701, p<0.001) when all studies were combined. Insulin receptor binding affinity and content of GLUT4 were not significantly different in all experimental groups. These results suggest that increased glucose uptake may inhibit further glucose transport and lead to decreased insulin sensitivity.
- Insulin Resistance in Late Pregnant Rats.
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Myung Heup Chun, Yong Woon Kim, So Young Park, Jong Yeon Kim, Suck Kang Lee
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Yeungnam Univ J Med. 1995;12(2):319-330. Published online December 31, 1995
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DOI: https://doi.org/10.12701/yujm.1995.12.2.319
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- The influence of normal late pregnancy on insulin action and insulin secretion was studied in the Sprague-Dawley female rats. On 20th day after mating, intravenous glucose tolerance test(IVGTI) was performed in non pregnant control and pregnant rats. As results of IVGTT, glucose disappearance rate was not significantly different in both groups, but secretory response of insulin was significantly(p<0.05) increased in pregnant rat. And the ratio of insulin/ .glucose was significantly higher in pregnant rats, which means existence of insulin resistance. These insulin resistance was overcomed by increased secretory response of pancreatic insulin. Insulinogenic index( A insulin/glucose - 5 min) was highly significantly (r=0.62, p<0.01) correlated with progesterone concentration. Glycogen level and amounts of "C-glucose incorporated into glycogen after IVGTT were significantly(p<0. 05) decreased in the liver, but were not changed significantly in soleus. Glycogen synthase activity of soleus and liver was not differ significantly in the both groups. Insulin binding at varying concentrations of insulin to crude membrane of pregnant liver was not significantly different from control. In conclusions, although these pregnant rats were normal glucose tolerance due to increased secretory response of insulin, that was correlated with progesterone concentration, pregnant rat had insulin resistance. The mechanisms of insulin resistance were not related to defect of insulin binding phase and glycogen synthase, but suggest pre-receptor and/or postreceptor phase.
- Effect of Persistent Mild Hyperglycemic Hyperinsulinemia on Development of Insulin Resistance in Rats
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Yong Woon Kim, Jin Hyun Park, So Young Park, Jong Yeon Kim, Suck Kang Lee
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Yeungnam Univ J Med. 1995;12(2):269-281. Published online December 31, 1995
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DOI: https://doi.org/10.12701/yujm.1995.12.2.269
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- The effect of persistant mild hyperglycemic hyperinsulinemia on the development of the insulin resistance in rats was studied in vivo. Also, the characteristics of the insulin resistance compared with the insulin resistance of STZ diabetic rats. Persistant mild hyperglycemic hyperinsulinemic rat model was produced by ingestion of glucose polymer for 8 days. The glucose disappearance and infusion rate was measured by hyperinsulinemic euglycemic clamp to"Imique at steady state of blood glucose and insulin levels. The clamped level of blood glucose was 100 mg/dl, and the clamped levels of insulin were 70 pU/ml (physiologic condition) and 3000 pU/ml (supramaximal condition). Hepatic glucose producticon rate was calculated using measured data. And the glycogen synthetic capacity of skeletal muscle (soleus) and liver was measured after 2 hours of hyperinsulinemic euglycemic clamp study. The glucose disappearance and glucose infusion rate in glucose polymer group was decreased in the both physiological and supramaximal insulin level compared to the rate of the normal control group. The rate of STZ diabetic group was lowest at supramaximal insulin level among two another experimental groups. The hepatic glucose production rate of glucose polymer group was decreased compared to normal control but increased in STZ diabetic group. The glycogen synthetic capacity of skeletal muscle and liver of glucose polymer group was not significantly different from normal control group, but it was markedly decreased in STZ diabetic group. These results suggest that persistant mild hyperglycemic hyperinsulinemia may induce insulin resistance, but glycogen synthetic capacity is intact.
- The effect of regular physical exercise on glucose uptake in soleus and intravenous glucose tolerance in streptozotocin diabetic rats.
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Myung Heup Chun, Yong Woon Kim, Jong Yeon Kim, Young Man Lee, Suck Kang Lee
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Yeungnam Univ J Med. 1992;9(1):121-129. Published online June 30, 1992
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DOI: https://doi.org/10.12701/yujm.1992.9.1.121
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- The effect of exercise on plasma insulin, free fatty acid, and glucose uptake and glycogen concentration in soleus, and intravenous glucose tolerance of streptozotocin treated, diabetic Sprague-Dawley rats were studied. Diabetic-trained animals were subjected to a regular program of treadmill running for 4 weeks. Seventy-two hours after the last training session, basal and insulin-stimulated glucose uptake was studied in incubated strips (about 20 mg) of soleus muscle in vitro. Glucose tolerance was measured with intravenous infusion of 0.5 g glucose/kg body weight. In diabetic rats, training was associated with increase glucose uptake in basal and maximal insulin concentrations, decreased fasting glucose concentrations, and increased muscle glycogen levels, but there were no changes in glucose tolerance curve and plasma insulin concentrations. These results suggest that regular running program for 4 weeks improve responsiveness of insulin on soleus muscle, but fails to cause improvement of impaired intravenous glucose tolerance in mild degree streptozotocin induced diabetic rats.
- Glucose incorporation into glycogen molecules of hypertrophied slow and fast twitch muscles in vitro.
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Yong Woon Kim, Jong Yeon Kim, Suck Kang Lee
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Yeungnam Univ J Med. 1990;7(1):19-27. Published online June 30, 1990
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DOI: https://doi.org/10.12701/yujm.1990.7.1.19
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- This investigation was undertaken to clarify the in vitro effect of the various stimulations, such as exercise (E), insulin (I) direct electrical stimulation (EST) and the combinations of the above, on the glucose incorporation intro glycogen molecules (glycogen synthesis) of the normal slow (soleus) and fast twitch (plantaris) muscles, and the different responses of slow and fast twitch muscles to persistent overloads causing compensatory muscle hypertrophy. In resting state, slow twitch muscle has greater capacity for glycogen synthesis than fast twitch muscle, and responses of different muscle to various stimuli were differ as follows: In slow twitch muscle, the glycogen synthesis was increased by insulin, and electrical stimulation but not increased by exercise; exercise increased insulin sensitivity and the effect of electrical stimulation. Whereas the glycogen synthesis in fast twitch muscle was increased only by the stimuli combined with E and EST, and E, I, and EST. As the result of removal of synergistic muscle, both muscles were hypertrophied, and the degree of hypertrophy in response to persistent overload was higher in fast twitch muscle (182%) than slow twitch muscle (151%). In hypertrophied muscles, glycogen synthesis of soleus in any groups was lower than that of the control, but similar in plantaris. In conclusions, there were marked heterogeneity in different muscle fiber in the effects of exercise and insulin addition and electrical stimulation on muscle glycogen synthesis, and fast twitch muscle may be adapted more easily to that kind of persistent overload than slow twitch muscle.
- The Effect of Exercise on the Conversion Rate of Ingested Glucose to Glycogen in the Hindlimb Skeletal Muscles in Rats.
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Kyung Hwa Jung, Jong Yeon Kim, Yong Woon Kim, Suck Kang Lee
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Yeungnam Univ J Med. 1988;5(2):79-86. Published online December 31, 1988
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DOI: https://doi.org/10.12701/yujm.1988.5.2.79
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- In the present study the effect of exercise on the conversion rate of ingested glucose to glycogen in the different types of hindlimb skeletal muscles in Sprague-Dawley male rats was studied. The amounts of synthetized glycogen from ingested glucose of fast-twitch white (WV), fast-twitch red (RV), mixed type of fast-twitch white and red (EDL), and slow-twitch (SOL) muscles were determined at 30 and 90 min. after ingestion of 25% glucose solution which contained 14C-glucose(2 ml(luCi)/100gm B.W.) in control and exercise loaded rats. The result was summarized as follows: The about 55% at 30 min. and 70% at 90 min. after glucose ingestion were absorbed from gastrointestinal tract. This result shows no effects of exercise on absorption rate from gastrointestinal tract. The amount of synthetized glycogen of SOL from ingested glucose at 30 and 90 min. after glucose ingestion were highest, whether WV were lowest in hindlimb skeletal muscles in control and exercise loaded rats. In the exercise loaded rats, the amounts of synthetized glycogen of SOL, RV, and EDL at 90 min. after glucose ingestion was much higher than control rats, but not different in WV between exercise-loaded and control rats. At 30 min. after glucose ingestion, only SOL of exercise loaded rats was higher than control rats. In the control rat, the synthesis of glycogen was almost completed during initial 30 minutes. On the other hand, in the exercise loaded rat, except WV was opposite result of control rats, i.e., amounts of synthetized glycogen were major during late period. The amount of synthetized glycogen of liver at 30 and 90 min. after glucose ingestion in exercise loaded rats was higher than control rats. The rate of glycogen synthesis in control and exercise loaded rats were higher between 30-90 minute than initial 30 minutes.
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