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Volume 24(2); April 2000
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Original Articles
Pancreas Islet Transplantation.
Bong Yun Cha, Hyun Shik Son
Korean Diabetes J. 2000;24(2):165-169.   Published online January 1, 2001
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No abstract available.
Critical Factors Determined Islet Graft Function In Canine Islet Autotransplantation.
Tae Young Yang, In Kyung Jeong, Seung Hoon Oh, Sang Hoon Lee, Dong Jun Kim, Jong Ryul Hahm, Byung Joon Kim, Kyu Jeung Ahn, Sung Joo Kim, Jae Hoon Chung, Yong Ki Min, Myung Shik Lee, Moon Kyu Lee, Kwang Won Kim
Korean Diabetes J. 2000;24(2):170-179.   Published online January 1, 2001
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BACKGROUND
Islet cell transplantation is an attractive alternative to whole organ pancreas transplantation, since it is clearly safer and simpler surgical procedure for the reciplents. However, several obstacles still remain, because the free islets appear to be more susceptible to non-specific inflammatory damage or immune mediated destruction than islets in an intact pancreas. Therefore, the purpose of this study is to examine the functional outcome of islet autograft and the factors related to the islets graft survival in mongrel dogs. METHODS: Twelve adult mongrel dogs weighting 12~16 kg were used for the experiment of total pancratectomy and islet autotransplantation. The islets were properly isolated by a modified Recordi method. The obtained islets were further purified by centrifugation on discontinuous gradients using cell separation system (Model 2991, Cobe, Lakewood Colo). After the heparization(50U/kg), the islets were injected slowly into the liver through the portal vain for 30 minutes. The post-transplantation intravenous glucose tolerence test (IVGTT) with glucose disappearance rate (K), liver function test (LFT), fasting plasma glucose (FPG) ware measured periodically. RESULTS: I) The median of Ks were 1.3%/min (range 0.3~2.1) and the lEq/kg (150 m equivalents/kg of recipient body weight) was 3520 (range 1350-6550). The Ks in recipients with high lEq/kg (> or =5,000) were significantly higher than those in recipients with low lEq/kg (<5,000)(r=0.78, p<0.05). 2) The islet cell viability were estimated to be 95% and the median of the required insulin dosage for the maintenance of normal FPG were 0.7 (range 0~1.6) U/kg/day, The insulin requirement correlated well with the level of lEq/kg (r=-0.90, p<0.01). 3) The median of the volume of the transplanted pancreatic islet cell were 2.1 mL (range 0.7~5.0) and the purity was 60k (range 10~95), The portal pressure gradients of during the transplant procedure were 4.0(range 0.5~12.0) cmH20. The portal pressure gradients in recipients with high purity were significantly lower than those in recipients with low purity (r=-0,80, p<0,05). CONCLUSIONS: In this study, we confirmed that autotransplantation of islet cell on the pancreatectomized dogs can render nearly normoglycemia, and transplanted islet mass was most critical factor to successful autotransplantation in canine model.
Distension and Collagenase Digestion Time of The Pancreas are Critical Factors in Islet Isolation of Canine Pancreas.
Tae Young Yang, In Kyung Jeong, Seung Hoon Oh, Sang Hoon Lee, Dong Jun Kim, Jong Ryul Hahm, Jung Hwan Park, Jong Sung Kim, Jin Soo Han, Sung Joo Kim, Jae Hoon Chung, Yong Ki Min, Myung Shik Lee, Moon Kyu Lee, Kwang Won Kim
Korean Diabetes J. 2000;24(2):180-190.   Published online January 1, 2001
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BACKGROUND
S: One of the main problems conditioning the outcome of islet transplantation is the ability to separate a sufficient number of viable islets with preserved function. Islet purification is critically affected by all of the isolation stages, Thus, it is necessary to set up the standard isolation method that islets are separate well from acinar without compromising islet yield and viability. METHODS: Twenty three adult mongrel dogs were used for the experiment of total pancreatectomy with islet isolation. The islets were properly isolated by a modified Recordi method. The obtained islets were further purified by centrifugation on discontinuous gradients using cell separation system (Model 2991, Cobe, Lakewood Colo). We evaluatad islet number (islet equivalent number, 150 gm equivalents/kg of recipient body weight, lEq/kg), purity. cell volume, viabilty, recovery rate, and comparison of outcome according to the isolation conditions. RESULTS: 1) The mean of islet numbers before purification were 13543+/-943 lEq/kg, digestion times were 13.8+/-2.6 min. digestion tamperature was b was 59,7+/-7.0%, viability was 90.0+/-2.1%, cell volume was 4.7+/-1.1 mL, islet number after purification were 4064+/-361 lEq/kg, and recovery rate was 29+2.9. 2) Isolated islet numbers were different according to the degree of pancreas distension with collagenase, digestion temperature, and digestion time. 3) The best conditions for islet isolation were above 37.5 degree C in temperature at recirculation of collagenase, within 12min in digestion time and well distended pancreas with collagenase. 4) According to multiple regression adjusted by variable factors, the degree of pancreas distension with collagenase and digestion time were independently associated factors for successful islet isolation. CONCLUSIONS: In this study, we concluded that the degree of pancreas distension with collagenase and digestion time were independent factors for successful islet isolation and the best conditions for islet isolation were above 37.5 degree C in temperature at recirculation of collagenase, within 12 min in digestion time and well distended pancreas with collagenase.
The Changes of Expression of Intermediate Flament in Pancreatic Duct Cells During Proliferation and Differentiation after 90% Pancreatectomy in Rats.
Seung Hyeon Ko, Kun Ho Yoon, Sun Hee Seo, Jung Min Lee, Ki Won Oh, Sang Ah Chang, Hye Soo Kim, Yoo Bae Ahn, Hyun Shik Son, Moo Il Kang, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang
Korean Diabetes J. 2000;24(2):191-201.   Published online January 1, 2001
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BACKGROUND
Neogenesis of the beta calls from ductal cells is the main mechanism of the increased beta cell mass after partial pancreatectomy. For the transdifferentiation from the duct cells to the beta cells, de-differentiation of the duct cells is needed because duct cells are also terminally differentiated cells already. But there was no clear evidence of de-differentiation of the duct cells during duct call proliferation so far. Herein we report the changes of intermediate filament protein expression in rapidly proliferating duct cells after partial pancreatectomy for the evidence of de-differentiation of the duct cells. METHODS: 45 week-old Sprague-Dawley rats weighing 80~120 g were used. 90% partial pancreatectomy was done. Experimental animals were divided into 5 subgroups by date of killing after surgery: 1, 3, 7, 14, 30 days, Pancreas remnant was excised and immunohistochemical stain was done for pancytokeratin (Pan-CK) as a epithelial cell marker and vimentin (VT) as a mesenchymal cell marker. We observed the double stained slide with pan-CK and VT antibody using confocal microscope for costaining analysis over time. The sections were also immunostained with anti-insulin antibody for the quantification of the beta cell mass by point-counting methods. RESULTS: We observed impaired glucose tolerance and diabetes were developed affer 90% pancreatectomy. Significant increase of the weight of pancreatic remnant, beta cell and duct cell mass were observed about 14 days after pancreatectomy. We observed the co-expression of VT and pan-CK intermediate filament protein in rapidly proliferating duct cells in the area of common pancreatic duct and main duct at one day after partial pancreatectomy. 3 days affer partial pancreatectomy, VT and pan-CK costained duct cells were mainly observed in the rageneration focus of the duct cell proliferation. 30 days after partial pancreatectomy, we could not find any costaining duct calls in the remnant pancreas. CONCLUSION: The vimentin intermediate filament, a marker of mesenchymal cell was expressed in proliferating ductal cells after pancreatectomy. We could suspect that pancytokeratin and vimentin co-expression is a good marker for de-differentiation of proliferating duct cells.
Devrease of Mitochondrial DNA Content in Non-Insulin Dependent Diabetic Rats.
Ji Hyun Song, Sun Hee Yim, Bok Ghee Han, Hong Kyu Lee, Young Mi Kim, Kyong Soo Park, S Suzuki
Korean Diabetes J. 2000;24(2):202-215.   Published online January 1, 2001
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BACKGROUND
Although genetic disorder in diabetes mellitus (DM) is not well understood, it has been suggested that the maternally inherited mitochondrial DNA which does not follow the Mendel's laws is a genetic factor for DM. It was reported that the mitochondrial DNA contents in DM patients were decreased compared to the normal control. Similar decrease in mitochondrial DNA content before DM development was tested in animal models. METHOD: The mitochondrial DNA (mtDNA) content in various tissues obtained from two types of non-insulin dependent diabetic rats, Goto-Kakizaki (GK) and Otsuka Long-Evans Tokushima Fatty (OLETF) rats at different ages were quantified. We also determined the quantity of hepatic COX subunit lll(COX III) mRNA, and the enzyme activities of succinate dehydrogenase (SDH) and cytochrome c oxidase (COX) in mitochondria isolated from liver and skeletal muscle were measured. RESULTS: At 6 weeks, mtDNA content of GK rat liver was 20% decreased compared to the Wistar control, The mtDNA content of Wistar rat liver was decreased to aging from 6 weeks to 24 weeks while mtDNA in GK rat liver remains relatively constant. In case of skeletal muscle, however, mtDNA contents in GK rats were 50% decreased compared to the control at 12 and 24 week old, Similarly, OLETF and LETO control rats showed the age-dependent decrease of mtDNA content in liver and pancreas. Especially the mtDNA contents in OLETF rat tissues were reduced at the younger age than the LETO control content. That is, at 6 weeks old mtDNA contents in OLETF rat pancreas and liver were only 50% of the control. The level of mitochondrial coded hepatic CDX subunit III mRNA tends to decrease with age. Despite the decrease of mtDNA content, hepatic COX lll mRNA level and COX activities and SDH activities were not altered significantly, implying that the change of mtDNA contents did not damage the mitochondrial gene transcription and mitochondrial function dramatically. CONCLUSIONS: This results suggest that mtDNA contents in pancreas and liver decrease age-dependently but it occurs at younger age in NIDDM. The decrease of mtDNA content at young age may be a cause of NIODM.
Serum Plasema Leptin Levels, Abdominal Obesity, and Insulin Resistance in Type 2 Diabetic Patients.
Dae Won Jun, Sung Hun Kim, Jae Hyung Lee, Woong Hwan Choi, Yong Soo Park, Tae Hwa Kim
Korean Diabetes J. 2000;24(2):216-224.   Published online January 1, 2001
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BACKGROUND
There is growing evidence for a adipoinsular axis, between adipose tissue and pancreatic beta cells via the hormones leptin and insulin, in mice models, Insulin is adipogenic and increases the production of leptin by adipose tissue, Leptin feeds back to reduce both insulin secretion and insulin gene expression. But human obesity is a complex disorder, with many factors playing a parts; the pathophysiology of leptin is not as simple as it seems to be in mice models of obesity. We therefore explored the dysregulation between leptin and insulin concentration in human model. METHOD: Using radioimmunoassay, we measured serum leptin concentrations in Type 2 diabetic patients (male 26, male 52). Using body composition, we measured total and regional adiposity. The data were analyzed using t-tast to test difference in serum leptin concentration, and other factors were evaluated by partial correlation analysis. RESULT: Serum leptin concentrations in both sex was strongly and positively correlated with total adiposity (r=0.588, p<0.001), Serum leptin concentration was correlated with serum insulin concentration (r=0.41, p=0.002) even after adjusting for adiposity in both sex (r=0.32, p=0.021). Serum leptin concentration was more highly correlated with abdominal adiposity than peripheral adiposity(r=0.693 vs r=0,628). Leptin concentration were higher in women than men, even at the same adiposity, However, no independent association was seen between leptin and hypertension as well as total cholesterol. CONCLUSION: Serum leptin concentration was correlated with serum insulin concentration even after adjusting for adiposity in both sex, In human, such a putative loss of leptin reception by beta cell could result in dysregulation of the adipoinsular axls and a corresponding failure to suppress insulin secretion, resulting in chronic hyperinsutinemia.
Risk Factors of Posttransplant Diabetes Mellitus after Allogeneic Bone Marrow Transplantation.
Ki Won Oh, Won Young Lee, Moo Il Kang, Hyun Shik Son, Kun Ho Yoon, Bong Yun Cha, Wan Sik Shin, Kwang Woo Lee, Ho Young Son, Sung Koo Kang, Woo Sung Min, Choon Choo Kim
Korean Diabetes J. 2000;24(2):225-234.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Although increasing number of patients are survived after organ transplantation, morbidity and mortality due to cardiovascular disease is thought to be the key risk factor for the long-term tranplant survivors. Many studies have shown that posttransplant diabetes mellitus, dyslipidemia, and hypsrtension are major causes of accerelated atherosclerosis after organ transplantation. Immunosuppressants, rejection, family history of DM, certain HLA phenotypes, pretransplant age and fasting glucose concentration are suggested as etiopathogenic factors of posttransplant diabetes mellitus (PTDM) after solid organ transplantation, while the risk factors of PTDM after bone marrow transplantation (BMT) is unknown. The aim of our study to investigate the clinical characteristics and possible risk factors for PTDM after BMT. METHODS: Age, male to female ratio, body mass index, mean daily steroid dosage, mean daily cyclosporin dosage, incidence of graft versus host disease(GVHD), incidence of cytomegalovirus (CMV) disease, fasting plasma glucose concentra-tion, serum lipid profiles, and HLA phenotypes were retrospectively examined in 15 PTDM patients and 68 non-diabetic patients after allogeneic BMT. RESULTS: 1. Among 490 allogeneic BMT, PTDM developed in 15 patiants (3.1%). The mean duration from BMT to onset of PTDM was 26,6+/-33,9 days. 2. When compared between the PTDM and non-diabetic patients, mean daily steroid dosage, incidence of GVHD, and incidence of CMV disease were significantly different. 3, HLA phenotypes, HLA-DR52 and DR53, were more frequently observed only in PTDM patients. 4. At the onset of PTDM, we observed that fasting plasma glucose, total cholesterol, and LDL-cholesterol concentration were significantly elevated in pre-BMT state. CONCLUSION: We conclude that posttransplant diabetes mellitus after BMT, frequently develops in patients with a predisposition of high-dose steroid, GVHD, HLA-DR52 and DR53 phenotypes. This study suggested that high-dose steroid therapy, mainly due to GVHD, might be the critical factor in the onset of PTDM after allogeneic BMT and that the risk may be affected by HLA-DR52 and DR53 phenotypes.
The Relation Between DHEA, DHEAS and Syndrome X, Cardiovascular Complication in Type 2 Diabetes Mellitus.
Yong Hyun Kim, Jeong Heon Oh, Nan Hee Kim, Kyung Mook Choi, Sang Jin Kim, Sei Hyun Baik, Dong Seop Choi
Korean Diabetes J. 2000;24(2):234-244.   Published online January 1, 2001
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BACKGROUND
Insulin is known as a major factor that regulates secretion of DHEA and DHEAS. Numerous studies are exist to investigate the relationship between DHEA(S) and insulin resistance. Furthermore, numerous previous studies revealed that insulin resistance plays a major role in the pathogenic relationship between DHEA(S) and type 2 diabetes mellitus. However, number of studies to investigate the difference of levels of DHEA(S) according to the presence of syndrome X in type 2 diabetes mellitus are limited. METHODS: In type 2 diabetes, aged from 40 to 70 years old, the levels of serum DHEA and DHEAS was compared between the subejcts with or without syndrome X as well as the normal age and sex matched control. Furthermore, correlation between serum DHEA/DHEAS and insulin resistance, and the levels of DHEA/DHEAS according to the cardiovascular complication status was also evaluated. RESULTS: 1. No statistical difference in serum DHEA and DHEAS was observed among the 3 groups. However, the serum DHEA and DHEAS levels were lower in type 2 diabetes with syndrome X and higher in normal control. 2. No correlation was observed between DHEA, DHEAS and insulin resistance factors. 3. No stastistical difference in serum DHEA and DHEAS was observed in type 2 diabetic patients with cardiovascular complications. However, the level of DHEA was lower in the patients with cardiovascular complications. 4. No stastistical difference in serum DHEA and DHEAS was observed according to the presence of cardiovascular complications when analysis was performed in 55 years and younger subjects. 5. The level of DHEA was lower in the presence of cardiovascular complication when only male diabetic subjects were included in the analysis, but the level of DHEAS showed no difference according to the cardiovascular complication status. CONCLUSION: No statistical difference of the levels of serum OHEA and DHEAS was observed according to the presence of syndrome X in type 2 diabetes patients, However, the level of serum DHEA tended to be lower in the presence of cardiovascular complications. The levels of DHEA in male diabetic subjects were lower in the presence of cardiovascular complication, thus, we suspected that DHEA may play a potential role as one of risk factors of cardiovascular complications in this subgroup.
Relationship Among Urinary Glycosaminoglycan (GAG) Excretion Rates, Urinary Albumin Excretion and Macrovascular Disease in Patients with Type 2 Diabetes Mellitus.
Yoon Sang Choi, Sang Hoon Kim, Hyang Kim, Yun Kyung Cho, Hyun Ju Um, Si Yong Kim, Byong Ik Kim, Yoo Lee Kim, Hwa Young Lee, Sang Jong Lee
Korean Diabetes J. 2000;24(2):245-255.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Increased loss of proteoglycan (PG) from glomerular basement membrane (GBM) has been postulated to alter glomerular charge selectivity which contributes to urinary loss of albumin. The glycosaminoglycan (GAG) is the degradation products of PG. Recently, one of the hypothesis suggested that urinary albumin execretion(UAE) reflects not only merely a glomerular manifes-tation but also a macrovascular disease (by Deckert et al), Wasty et al. reported a significant decrease in total GAG concentration and marked changes in their distribution in atherosclarotic plaques in human. Thus, the alterations in the metabolism of GAG might play a role in the pathogenesis of diabetic macroangiopathy. Therefore, we investigated the relationship among urinary GAG execretion rates, UAE and macrovascular disease in patients with type 2 diabetes mellitus. METHODS: We measured urinary excretion rates of GAS in type 2 diabetic patients with and without macrovascular disease ( cerebrovascular disease, ischemic heart disease and other peripheral vascular disease ) and investigated the relationships among urinary execretion of GAG, UAE and macrovascular disease in 103 patients with type 2 diabetes mellitus. RESULTS: 1) Among total 103 patients, 66 patients (64.0%) showed normoal-buminuria, 18 patients (17.5%) showed microabluminuria and 19 paitents (18.4%) showed macro albuminuria respectively. The duration of diabetes mellitus and the prevalence of hypertension, diabetic retinopathy and macrovascular disease were increased according to the degree of UAE. 2) The urinary excretion rates of GAG in type 2 diabetes mellitus with normo-, microand macro-albuminuria were 6.72+/-4.05, 9.17+/-3.26 and 14.20+/-6.13 microgram glucuronic acid/min respectively (p<0.05). The urinary GAG levels were significantly correlated with UAE (r=0.43, p<0.05). 3) The urinary excretion rates of GAG in type 2 diabetes mellitus with (n=26) and without (n=77) macrovascular disease were 6.21+/-2.75 and 9,31+/-5.59 ug glucuronic acid/min, respectively (p<0.05). CONCLUSION: 1) The urinary excretion rates of GAG were decreased in patients with macro vascular complications of type 2 diabetes mellitus. 2) The urinary excretion rates of GAG may be a possible marker of macrovascular disease in type 2 diabetes mellitus. Yet, further large prospective studies are necessary to confirm our findings.
Peripheral Polyneruopathy and Hypoinsulinemia in Patients with Type 2 Diabetes.
Y S Jung, K Y Lee, S K Lee, H K Kim, H Y Park, M H Kang
Korean Diabetes J. 2000;24(2):256-266.   Published online January 1, 2001
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BACKGROUND
There is little information on the risk factors for diabetic polyneuro-pathy other than glycemic control and duration of diabetes. The relation between diabetic polyneuropathy and hypoinsulinemia is controversial. This study is to determine whether hypoinsulinemia is an additional factor influencing the development of polyneuropathy in patients with type 2 diabetes. METHODS: We performed an oral glucose tolerance test with C-peptide measure-ment in 1'P2 patients with type 2 diabetes. Peripheral polyneuropathy was diagnosed when the patients had both typical symptoms of polyneuropathy and abnormal physical findings or NCV. We analysed the relation between metabolic variables including fasting and postprandial C-peptide levels and diabetic polyneuropathy. RESULTS: In addition to retinopathy and nephropathy, duration of diabetes, low C-peptide level (fasting and postprandial), insulin use, and high HDL-cholesterol level were associated with diabetic polyneuropathy. Multivariate logistic regression model revealed that an independent assoclation of diabetes duration and postprandial 2-hour C-peptide concentration with polyneuropathy. When we stratified the patients into the two groups according to the median duration of diabetes (8 years), the association of low postprandial C-peptide concentration with polyneuro-pathy was significant only in the shorter duration group(< 8 years). However, significant association of HbA(1c) level was shown in the longar duration group. CONCLUSION: Decreased insulin secretory function of the pancreas as well as increased duration of diabetes was indepandently associated with diabetic polyneuropathy in patients with type 2 diabetes. Hypoinsulinemia might be an additional risk factor for the development of diabetic polyneuropathy in type 2 diabetic patients, particularly with short duration, To confirm these relationship further longitudinal study in a large cohort is necessary.
Can the Oral Glucose Tolerance Test (OGTT) done at Postpartum (PPT) 1 Wddk Substitute OGTT at PPT 6 Week OGTT at PPT 6 Week in Diagnosing Rersistent PPT Glucose Intolerance in the Patients with Gastrational Diagetes Melltus (GDM)?.
Yoo Lee Kim, Yong Wook Cho, Seok Won Park, Yun Kyung Cho, Hwa Young Lee, In Hyun Kim, Jong Gun Won, Hye Sun Jun, Ho Taek Lee, Seog Ki Lee, Sang Jong Lee
Korean Diabetes J. 2000;24(2):267-280.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Although 75 g-OGTT at PPT 6 week is necessary to diagnose persistent PPT glucose intolerance (PPGI) in GDM patients, it 1s difficult to perform this test because many patients drop-out during the follow-up period. Thus we tested whether OGTT done at PPT 1 week can substitute OGTT at PPT 6 week in diagnosing PPGI in GDM patients. METHOD: In 370 GDM patients, 75 g-OGTT was performed at PPT 1 week and repeat OGTT was done in 196 patients at PPT 6 week. Results of OGTT were classified as normal glucose tolerance(NGT), impaired glucose tolerance(IGT), and diabetes mellitus (DM) according to National Diabetes Data Group(NDDG) criteria. Changes in glucose tolerance state between PPT 1 and 6 week were assessed, and the predictability of clinical characteristics for these changes were investigated by logistic regression analysis. RESULTS: Among 370 GDM patients who performed OGTT at PPT 1 week, 79.4% had NGT, 12.2% had IGT, and 8.4% had DM. 53% (196/370) of subjects repeated OGTT at PPT 6 week. In OGTT at PPT 6 week, 77.6% (152/196, 140/149 in NGT, 4/26 in IGT and 8/21 in DM) were in the same glucose tolerance state as at PPT 1 week. The glucose tolerance improved in 14.8% (29/196, 16/26 in IGT and 13/21 in DM) and deteriorated in 7,6% (15/196, 9/149 in NGT and 6/26 in IGT). 94%(140/149) of patients who had NGT at PPT 1 week had NGT at PPT b week and 48.9/o (23/47) of patients who had abnormal glucose tolerance at PPT 1 week had abnormal glucose tolerance at PPT 6 week. Mean fasting plasma glucose level on OGTT became lower at PPT 1 week than during pregnancy (4.6+/-0,8 vs 5.1+/-1.2mmol/L, p<0.05) and became higher at PPT 6 week than at PPT 1 week (5.4+/-1.1 vs 4.6+/-0.8 mmol/L, p<0.05). Mean plasma glucose level at 2 hour after glucose load was significantly lower at PPT 6 week than at PPT 1 week (7.2+/-2.7 vs 8.3+/-2.5 mmol/L). When the subjects were grouped into NGT, IGT, and DM according to glucose tolerance state at PPT 6 week, the NGT group already showed normal glucose tolerance at PPT 1 week. The IGT and DM group showed slightly lower glucose levels at PPT 1 week than during pregnancy but became high to the level during pregnancy at PPT 6 week. In the patients group showing deterioration in glucose tolerance state between PPT 1 and 6 week, prevalence of insulin treatment was higher (63.4% vs 9.4, 20.7%), the gestational age at diagnosis of GDM were lower (25.0+/-6.2 week vs 29.8+/-3.3, 29.9+/-4,8 waek), and prepregnant weight was higher (113.4+/-21.2% vs 102.5+/-12.4, 102.4+/-14.6%) than those in the patients groups showing no change and improvement in glucose tolerance state, Weight gain until diagnosis of GDM during pregnancy(5.7+/-4.4kg vs 9.4+/-3.4kg) and weight change between prepregnancy and PPT 5 week(-1,3+/-3.5kg vs 1.5+/-29kg) was smaller in the deterioration group than those in the no change group. Logistic regression analysis performed using improvement and deterioration of glucose tolerance state between PPT 1 and 6 week as an outcome of interest revealed that an earlier diagnosis of GDM and a smaller weight at PPT 6 week than prepregnant weight were independent predictors for deterioration of glucose tolerance between PPT 1 and 6 week. In conclusion, OGTT done at PPT 1 week can substitute OGTT at PPT 6 week in a large subgroup of GDM patients who has NGT at PPT 1 week without any risk factors for deterioration in glucose tolerance.
Case Report
A Case of Interstitial Deletion [del(6)(q21q23)] with type 2 diabetes Mellitus and Mental Retardation.
Ye Dal Jung, Sun Joo Cho, Hak Jun Kim, Wern Chan Yoon, Dong Geun Yeo, Jeong Ki Park, Ji Hyun Lee, Ho Sang Shon
Korean Diabetes J. 2000;24(2):281-284.   Published online January 1, 2001
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AbstractAbstract PDF
Chromosomal abnormalities such as Klinefelter syndrome, Down syndrome, Turner syndrome, Prader-Willi, Bardet-Biedl syndrome were associated with diabetes mellitus. Over 30 cases of interstitial deletions of the long arm of chromosome 6 with vastly variable breakpoints and clinical features have been reported in the literature, The clinical findings varies and most often includes mental retardation, microcephaly, and craniofacial anomalies. We report a case of interstitial deletion (del(6)(q21q23)) with type 2 diabetes mellitus and mental retardation.

Diabetes Metab J : Diabetes & Metabolism Journal