Journal of Yeungnam Medical Science

Case Report

Generalized Chorea-Ballismus Associated with Nonketotic Hyperglycemia in Diabetes Mellitus: A Case Report.: Hyun Ran Shin, Ji Hoon Kim, Mee Young Park; Yeungnam Univ J Med. 2002;19(2):136-143. Published online December 31, 2002; DOI: https://doi.org/10.12701/yujm.2002.19.2.136

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Even though the nonketotic hyperglycemia is a metabolic disorder, it complicates hemic- horea-hemiballism rarely. Moreover, generalized chorea-ballism associated with nonketotic hyperglycemia in diabetes mellitus is very rare, so it has not been reported in Korean literature. Although the precise pathophysiologic mechanisms of these disorders are still poorly understood, deficiency of gamma aminobutyric acid (GABA) in nonketotic hyperglycemia or reduced GABAnergic inhibition by striatal lesion may increase inhibitory output to subthalamic nucleus. These result loss of pallidal inhibition and produce contralateral hemichorea-hemiballism. The striatal lesions, such as transient ischemia with reactive astrocytosis or small amount of petechial hemorrhage, are related with changes of magnetic resonance image (MRI) findings presumably. We report a diabetic old woman who developed generalized chorea-ballismus as a very rare complication of nonketotic hyperglycemia. Her brain MRI showed high signal intensity in left lentiform nucleus and right pallidum on T1 weighted images and low signal intensity in bilateral putamen on T2 weighted images with highly enhanced corresponding lesions on T1 weighted enhancement images.

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A Case of Type 2 Diabetes Mellitus Initially Presented as Monochorea Associated with Ketotic Hyperglycemia
Si Hyeong Lee, Dong Woo Lee, Yeong Min Lee, Tae Kyun Kim, Min Jeong Kwon, Soon Hee Lee, Jeong Hyun Park
The Journal of Korean Diabetes.2014; 15(4): 244. CrossRef

Original Articles

The Effects of Hyperglycemia and Hyperlipidemia on Muscle Glycogen Utilization during Exercise in rats.: Jong Chul Ahn, Dong Woo Lee, Oog Jin Shon, Seuk Kang Lee; Yeungnam Univ J Med. 1999;16(1):34-42. Published online June 30, 1999; DOI: https://doi.org/10.12701/yujm.1999.16.1.34

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Abstract PDF: The effects of hyperglycemia and hyperlipidemia on utilization of muscle glycogen during 45 minutes treadmill running(26 m/min, 8 % grade) were evaluated in Sprague Dawley rats, and the charateristic of the 4 different type of muscles, soleus, white and red gastrocnemius, and plantaris, on glycogen utilization were simultameously investigated. Hyperglycemia, 145-165 mg/dL, was induced by oral glucose ingestion, and hyperlipidemia, 444 uEq/L, was induced by combined treatment of intraperitoneal heparine injection and oral 10 % intralipose ingestion. During the hyperglycemic trial, the glycogen utilization of plantaris muscle was decreased by 13 % at 45 minutes duration of treadmill running comparing to the control trial(p<0.05), and the glycogen utilization of white gastrocnemius was also decreased. The sparing tendency of soleus and red gastrocnemius by 5-13 % was observed at 30 and 45 minutes of treadmill running in hyperglycemic trial. There was no glycogen sparing effect of hyperlipidemia in the soleus, red gastrocnemius and plantaris muscle subjected in this experiment during exercise. However, only a slight sparing tendency of white gastrocnemius muscle was observed. In summary, the glycogen sparing effect of hyperglycemia during exercise was observed in plantaris and white gastrocnemius muscles in rats. However, there was no glycogen sparing effect of hyperlipidemia in the 4 hindlimb muscles. It was observed that the glycogen sparing effect of hyperglycemia is more prominant in fast glycolytic muscle fiber.

Effect of Hyperglycemia and Hyperlipidemia on Cardiac Muscle Glycogen Usage during Exercise in Rats.: Suck Kang Lee, Eun Jung Kim, Yong Woon Kim; Yeungnam Univ J Med. 1998;15(1):29-35. Published online June 30, 1998; 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.: Yong Woon Kim, Youl In Ma, Suck Kang Lee; Yeungnam Univ J Med. 1997;14(1):53-66. Published online June 30, 1997; DOI: https://doi.org/10.12701/yujm.1997.14.1.53

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Abstract PDF: 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.

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