Increased life expectancy and increased obesity have contributed to an increasing incidence of osteoporosis and diabetes mellitus. Recent meta-analyses and cohort studies confirm that diabetes is associated with a higher risk of fracture. Patients with type 2 diabetes exhibit increased fracture risks despite a higher bone mass, which are mainly attributable to non-skeletal risk factors. Patients with type 1 diabetes may have impaired bone formation because of absence of the anabolic effects of insulin and insulin-like growth factor I (IGF-I) system. Several clinical studies have reported adverse skeletal actions of peroxisome proliferator-activated receptor gamma (PPARgamma) agonist in humans. Obesity regulates bone metabolism not only by increasing weight loading but also by modulating adipokines that are known to affect bone remodeling.
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Although diabetes mellitus (DM) is treatable, it is still not curable. Its chronicity is associated with a high prevalence of psychiatric disorders, especially depression in type 2 DM and learned helplessness in type 1 DM. In turn, this depression and helplessness may affect a patient's adherence to medical appointments, compliance to treatment, and effective doctor-patient relationships, which are vital to promising outcomes. This study reviews the existing literature regarding the interactional relationships between depression, DM and the doctor/patient relationship, and also suggests certain aspects of the doctor/patient relationship which can contribute to more successful treatment outcomes.
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BACKGROUND Vascular endothelial growth factor (VEGF) is associated with the development of diabetic complications. However, it is unknown whether systemic VEGF treatment has any effects on the pancreatic islets in an animal model of type 2 diabetes mellitus. METHODS: Anti-VEGF peptide (synthetic ATWLPPR, VEGF receptor type 2 antagonist) was injected into db/db mice for 12 weeks. We analyzed pancreatic islet morphology and quantified beta-cell mass. Endothelial cell proliferation and the severity of islet fibrosis were also measured. VEGF expression in isolated islets was determined using Western blot analysis. RESULTS: When anti-VEGF was administered, db/db mice exhibited more severe hyperglycemia and associated delayed weight gain than non-treated db/db mice. Pancreas weight and pancreatic beta-cell mass were also significantly decreased in the anti-VEGF-treated group. VEGF and VEGF receptor proteins (types 1 and 2) were expressed in the pancreatic islets, and their expression was significantly increased in the db/db group compared with the db/dm group. However, the elevated VEGF expression was significantly reduced by anti-VEGF treatment compared with the db/db group. The anti-VEGF-treated group had more prominent islet fibrosis and islet destruction than db/db mice. Intra-islet endothelial cell proliferation was also remarkably reduced by the anti-VEGF peptide. CONCLUSION: Inhibition of VEGF action by the VEGF receptor 2 antagonist not only suppressed the proliferation of intra-islet endothelial cells but also accelerated pancreatic islet destruction and aggravated hyperglycemia in a type 2 diabetes mouse model. Therefore, the potential effects of anti-VEGF treatment on pancreatic beta cell damage should be considered.
Woo Je Lee, Hyoun Sik Kim, Hye Sun Park, Mi Ok Kim, Mina Kim, Ji Young Yun, Eun Hee Kim, Sang Ah Lee, Seung Hun Lee, Eun Hee Koh, Joong Yeol Park, Ki Up Lee
Korean Diabetes J. 2009;33(3):198-205. Published online June 1, 2009
BACKGROUND Accumulating evidence has suggested that nitric oxide (NO) is involved in the regulation of insulin sensitivity in skeletal muscle. Recent studies also suggested NO as an important molecule regulating mitochondrial biogenesis. This study examined the effect of the NO donor, 3-morpholinosydnonimine (SIN-1), on glucose metabolism in skeletal muscle and tested the hypothesis that NO's effect on glucose metabolism is mediated by its effect on mitochondrial function. METHODS: In Sprague-Dawley (SD) rats treated with SIN-1 for 4 weeks, insulin sensitivity was measured by a glucose clamp study. Triglyceride content and fatty acid oxidation were measured in the skeletal muscle. In addition, mitochondrial DNA content and mRNA expression of mitochondrial biogenesis markers were assessed by real-time polymerase chain reaction and expression of insulin receptor substrate (IRS)-1 and Akt were examined by Western blot analysis in skeletal muscle. In C2C12 cells, insulin sensitivity was measured by 2-deoxyglucose uptake and Western blot analysis was used to examine the expression of IRS-1 and Akt. RESULTS: SIN-1 improved insulin sensitivity in C2C12 cells and skeletal muscles of SD rats. In addition, SIN-1 decreased triglyceride content and increased fatty acid oxidation in skeletal muscle. Mitochondrial DNA contents and biogenesis in the skeletal muscle were increased by SIN-1 treatment. Moreover, SIN-1 increased the expression of phosphor-IRS-1 and phosphor-Akt in the skeletal muscle and muscle cells. CONCLUSION: Our results suggest that NO mediates glucose uptake in skeletal muscle both in vitro and in vivo by improving mitochondrial function and stimulating insulin signaling pathways.
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Korean Diabetes J. 2009;33(3):206-214. Published online June 1, 2009
BACKGROUND Skeletal muscle is the most important tissue contributing to insulin resistance. Several studies have shown that accumulation of intramyocellular lipid is associated with the development of insulin resistance. Thus, proteins involved in lipid transport, storage and metabolism might also be involved in insulin action in skeletal muscle. Adipose differentiation-related protein (ADRP), which is localized at the surface of lipid droplets, is known to be regulated by peroxisome proliferator activated receptor gamma (PPARgamma). However, it is not known whether ADRP plays a role in regulating glucose uptake and insulin action in skeletal muscle. METHODS: ADRP expression in skeletal muscle was measured by RT-PCR and western blot in db/db mice with and without PPARgamma agonist. The effect of PPARgamma agonist or high lipid concentration (0.4% intralipos) on ADRP expression was also obtained in cultured human skeletal muscle cells. Glucose uptake was measured when ADRP was down-regulated with siRNA or when ADRP was overexpressed with adenovirus. RESULTS: ADRP expression increased in the skeletal muscle of db/db mice in comparison with normal controls and tended to increase with the treatment of PPARgamma agonist. In cultured human skeletal muscle cells, the treatment of PPARgamma agonist or high lipid concentration increased ADRP expression. siADRP treatment decreased both basal and insulin-stimulated glucose uptake whereas ADRP overexpression increased glucose uptake in cultured human skeletal muscle cells. CONCLUSION: ADRP expression in skeletal muscle is increased by PPARgamma agonist or exposure to high lipid concentration. In these conditions, increased ADRP contributed to increase glucose uptake. These results suggest that insulin-sensitizing effects of PPARgamma are at least partially achieved by the increase of ADRP expression, and ADRP has a protective effect against intramyocellular lipid-induced insulin resistance.
BACKGROUND We sought to determine the association between serum gamma-glutamyltransferase (GGT) levels within the normal range and the risk for development of impaired fasting glucose (IFG) or type 2 diabetes. METHODS: This retrospective cohort study spanned four years (2002~2006) with 1,717 Korean men who underwent periodic health examinations at a university hospital in Incheon, Korea and were not diagnosed with IFG or type 2 diabetes. Fasting plasma glucose levels were measured at the annual health examination. IFG and diabetes were defined as a serum fasting glucose concentration of 100~125 mg/dL and more than 126 mg/dL, respectively. Cox's proportional hazards model was used to evaluate the association between serum GGT levels and development of IFG or type 2 diabetes. RESULTS: There was a strong dose-response relationship between serum GGT levels and the incidence of IFG and diabetes. A total of 570 cases (33.2%) of incident IFG and 50 cases (2.9%) of diabetes were found. After controlling potential predictors, the relative risks for the incidence of IFG for GGT levels < or = 19, 20~25, 26~34, 35~50 and > or = 51 were 1.00, 0.99, 1.17, 1.23 and 1.38 respectively (P for trend 0.015), and for the incidence of diabetes were 1.00, 1.44, 1.80, 2.55 and 2.58 respectively (P for trend 0.050). CONCLUSION: The risk for development of IFG and type 2 diabetes increased in a dose-dependent manner as serum GGT increased within its normal range in Korean men.
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BACKGROUND Silent myocardial ischemia (SMI) is more common in diabetic patients than among the general population. It is not yet established whether a routine screening test for SMI is necessary, and which screening test would be most useful. The purpose of this study was to estimate the prevalence of SMI detected by Thallium-201 perfusion single photon emission computed tomography (SPECT) in type 2 diabetic patients. METHODS: A total of 173 asymptomatic type 2 diabetic patients were included in the study. Thallium-201 perfusion SPECT was performed to screen for SMI. RESULTS: Among the 173 patients, abnormal perfusion patterns were found in 11 patients. Coronary angiography was carried out for these patients, and significant coronary artery stenosis was found in ten of them (positive predictive value; 90.9%). There was a significant association between SMI and overt albuminuria (OR = 7.33, 95% CI, 1.825-29.437). CONCLUSION: Thallium-201 perfusion SPECT is not sensitive enough to identify SMI, but is accurate in detecting decreased myocardial perfusion. This may be a useful screening tool for detecting SMI in type 2 diabetic patients with impaired renal function.
Yun Jeong Lee, Mi Hyun Jeong, Joo Hyung Kim, Juri Park, Hee Young Kim, Ji A Seo, Sin Gon Kim, Nan Hee Kim, Kyung Mook Choi, Sei Hyun Baik, Dong Seop Choi
Korean Diabetes J. 2009;33(3):232-240. Published online June 1, 2009
BACKGROUND Cellular phones are extremely prevalent in modern society and they enable appropriate feedback mechanisms through real time monitoring and short message services regarding blood glucose levels. We investigated whether cellular phone-based telemedicine support system could improve blood glucose control in type 2 diabetes patients who were in inadequate glycemic control regardless of insulin therapy. METHODS: A randomized, controlled clinical trial was conducted involving 74 type 2 diabetic patients with suboptimal glycemic control (HbA1c levels > 7%) regardless of insulin therapy. The intervention (cellular phone-based telemedicine) group managed their blood glucose using a cellular phone for 3 months, while the control (self monitoring of blood glucose) group managed their blood glucose with a standard glucometer for the same period. RESULTS: Three months later, HbA1c levels were decreased in both groups. However, the decrease in the control group from 8.37% to 8.20% was only 0.20% (P = 0.152) which was not significant. In contrast, the intervention group had a significant reduction of 0.61% from 8.77% to 8.16% (P < 0.001). Moreover, among patients with a baseline > or = 8%, the patients in the intervention group showed a significant reduction of 0.81% from 9.16% to 8.34% (P < 0.001). CONCLUSION: HbA1c levels were significantly decreased in the cellular phone-based telemedicine group compared with the control group after 3 months. This study suggests that cellular phone-based telemedicine is helpful for better glucose control in type 2 diabetes patients who previously were unable to control glucose levels adequately with insulin therapy.
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BACKGROUND The prevalence of type 2 diabetes has increased worldwide, as have the incidence and mortality of associated cardiovascular complication. However current status of diabetes management is poor. This study was performed to evaluate the management of care for type 2 diabetes patients at a university hospital. METHODS: This study comprised 926 type 2 diabetes patients, over the age of 30, who were treated at the Dongguk University Gyeongju Hospital between January and December 2008. Medical records were reviewed to collect demographic information, biochemical test results and the pharmacologic agents prescribed. RESULTS: The mean age, duration of diabetes and body mass index were 62.5 +/- 11.8 years, 9.1 +/- 7.2 year and 24.7 +/- 6.3 kg/m2, respectively. There were 251/926 (27.1%) patients with cardiovascular disease. In addition, 49.2% and 27.5% of patients had HbA1c levels < 7% and < 6.5%, respectively. There were 66.3% of the patients with blood pressure < 130/80 mm Hg. Fifty one percent and 47.4% of the patients had an LDL-C < 100 mg/dL and a non-HDL-C < 130 mg/dL, respectively. In addition, 19.7% of the patients with cardiovascular disease had an LDL-C < 70 mg/dL. Antiplatelet agents were used in 81.2% of the patients. The mean number of HbA1c measurements was 1.07 +/- 0.7 /year. HbA1c and lipid profiles were not checked in 21.4% and 23.1% of the patients, respectively. Over the previous six months, 6.9% of the patients had not had their blood pressure monitored. CONCLUSION: Among the patients with type 2 diabetes evaluated, 30~70% received in inadequate level of care. These findings point to the need for more aggressive efforts for optimal metabolic control.
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We report a 45-year-old man with type 2 diabetes who presented with recurrent hypoglycemia. Biochemical and imagingstudies did not show any mass-like lesion in the pancreas, so prednisolone and diazoxide were administered for the treatment of hypoglycemia. However, the hypoglycemia persisted during and after the medical treatment. A selective arterial calcium stimulation test was performed and revealed a suspicious lesion at the head of the pancreas. The patient underwent enucleation of the pancreas head lesion. The lesion was confirmed histologically to be focal nesidioblastosis and surgical resection was successfully performed. The patient showed no hypoglycemic symptoms postoperatively.