Sang Ah Chang

Body mass index is the most important determining factor for the degree of insulin resistance in non-obese type 2 diabetic patients in Korea ☆

With obesity, increased insulin secretion is needed to compensate for the additional demands and to maintain euglycemia. In contrast to Caucasians, the majority of type 2 diabetic patients belong to the non-obese category in Korea. There appears to be an ethnic difference underlying the pathogenesis in type 2 diabetes mellitus. However, there is only limited data on these subjects. The degree of insulin resistance in 267 Korean non-obese (body mass index [BMI] < 25 kg/m(2)) >/= patients with type 2 diabetes mellitus was analyzed, and the factors responsible for the insulin resistance were examined. The mean age and BMI of the patients were 50.8 +/- 10.6 years and 22.6 +/- 1.8 kg/m(2). Homeostasis model assessment-insulin resistance (HOMA-IR) >/= 2.5 was defined as being insulin resistant according to our data (mean +/- 1.5 SD of 1,917 normal subjects). There was no significant difference according to age, the duration of disease, and the glycosylated hemoglobin (HbA(lc)) levels between the subjects with or without insulin resistance. The HOMA-IR values in the patients with insulin resistance and normal insulin sensitivity were 4.2 +/- 1.4 and 1.5 +/- 0.6, respectively. In the insulin-resistant group, the log-transformed triglyceride (TG) levels were higher and the high-density lipoprotein-cholesterol (HDL-C) levels were lower than those of the insulin-sensitive group (log-transformed TG: 5.2 +/-.6 v 4.9 +/-.7 and HDL-C: 1.13 +/- 0.3 v 1.25 +/- 0.3mmol/L). These differences were still observed after adjusting for BMI. The HOMA-IR value was independently predicted by BMI and HDL-C levels, which explained 7% and 3% in the variability of insulin resistance, respectively. However, the TG levels were not independently associated with the HOMA-IR. Logistic regression analysis showed that the significant factor associated with HOMA-IR was only BMI. These results suggest that the BMI is the most important determinant of insulin resistance, while TG and HDL-C levels might be good markers of insulin resistance in non-obese patients with type 2 diabetes mellitus in Korea.

Smoking and Type 2 Diabetes Mellitus

Cigarette smoking is a well-known risk factor in many diseases, including various kinds of cancer and cardiovascular disease. Many studies have also reported the unfavorable effects of smoking for diabetes mellitus. Smoking increases the risk of developing diabetes, and aggravates the micro- and macro-vascular complications of diabetes mellitus. Smoking is associated with insulin resistance, inflammation and dyslipidemia, but the exact mechanisms through which smoking influences diabetes mellitus are not clear. However, smoking cessation is one of the important targets for diabetes control and the prevention diabetic complications.

Severe Hypoglycemia Is a Serious Complication and Becoming an Economic Burden in Diabetes

Background The prevalence of hypoglycemia is increasing due to the growing incidence of diabetes and the latest strict guidelines for glycated hemoglobin (HbA1c) levels under 7%. This study examined the clinical characteristics, causal factors, and medical costs of severely hypoglycemic patients in an emergency room (ER) of Uijeongbu St. Marys Hospital. Methods The study consisted of a retrospective analysis of the characteristics, risk factors, and medical costs of 320 severely hypoglycemic patients with diabetes who presented to an ER of Uijeongbu St. Marys Hospital from January 1, 2006 to December 31, 2009. Results Most hypoglycemic patients (87.5%, 280/320) were over 60 years old with a mean age of 69.5±10.9 years and a mean HbA1c level of 6.95±1.46%. Mean serum glucose as noted in the ER was 37.9±34.5 mg/dL. Renal function was decreased, serum creatinine was 2.0±2.1 mg/dL and estimated glomerular filtration rate (eGFR) was 48.0±33.6 mL/min/1.73 m2. In addition, hypoglycemic patients typically were taking sulfonylureas or insulin and a variety of other medications, and had a long history of diabetes. Conclusion Severe hypoglycemia is frequent in older diabetic patients, subjects with low HbA1c levels, and nephropathic patients. Therefore, personalized attention is warranted, especially in long-term diabetics with multiple comorbidities who may not have been properly educated or may need re-education for hypoglycemia.

Thyrotoxic Periodic Paralysis Presenting as Polymorphic Ventricular Tachycardia Induced by Painless Thyroiditis

Thyrotoxic periodic paralysis (TPP) can occur with any form of thyrotoxicosis. The most common cause of TPP in thyrotoxicosis is the Graves’ disease (1). Only one patient with TPP due to a painless thyroiditis (PT) has been reported (2). Here we describe an additional patient with TTP due to PT who had polymorphic ventricular tachycardia. This is an extremely unusual presentation of TTP. A 38-year-old Korean man was admitted to the emergency room for flaccid paralysis of the lower limbs for 6 hours duration. His past medical history was unremarkable. He had not taken any prescribed medications, and he did not have a history of drug abuse. There was no family history of Graves’ disease. On arrival at the emergency room, his blood pressure was 150=100 mmHg, and the heart rate was 96 beats=minutes. He was alert with a respiratory rate of 20 breaths=minutes and a body temperature of 368C. There was no proptosis. Palpation of the thyroid showed slight enlargement of the right lobe without tenderness or palpable nodule. Auscultation of the thyroid revealed no bruit. The lower limbs had flaccid paralysis with intact sensory function. Baseline laboratory data indicated normal serum sodium, magnesium, and calcium levels. The potassium level was 2.5 mEq=L (normal range 3.5–5.1 mEq=L), free thyroxine was 2.4 ng=dL (0.9–1.8 ng=dL), thyroid-stimulating hormone was 0.02 mIU=mL (0.17–4.65 mIU=mL), triiodothyronine was 179.41 ng=dL (78–200 ng=dL), thyroid-binding inhibitory immunoglobulins was 4% (normal rage <15%), and the antimicrosomal antibody was 1:6400. The initial electrocardiogram showed normal sinus rhythm (Fig. 1A). Twenty minutes after admission, he had polymorphic ventricular tachycardia with loss of consciousness (Fig. 1B). He was successfully resuscitated with 250 J cardioversion. He regained consciousness and his cardiac rhythm converted to atrial fibrillation (Fig. 1C). Cardiac enzyme measurements were as follows: creatine phosphokinase 626 U=L; creatine phosphokinase-MB 2.55 ng=mL; and troponin T< 0.010 mg=dL. A repeat electrocardiogram showed normal sinus rhythm (heart rate: 100 beats=minutes) and normal corrected QT interval. An echocardiogram performed 2 days later showed normal cardiac function without structural heart disease. Twenty-four hour holter monitoring did not show arrhythmias. A thyroid scan with Tc-99m revealed little or no uptake in the thyroid area compatible with thyroiditis (Fig. 2A). Therefore, no antithyroid drugs were administered. He was discharged from the hospital without further untoward events. The serum potassium and thyroid function was normal for 3 months (free thyroxine 1.07 ng=dL, thyroid-stimulating hormone 1.07 mIU=mL, potassium 4.1 mEq=L), and there were no symptoms of hypokalemia and muscle paralysis. A repeat thyroid scan with Tc-99m performed 3 months after the initial test revealed normal uptake in the thyroid area (Fig. 2B). Although PT is a self-limited disease associated with transient mild thyrotoxicosis and hypothyroidism, our patient not only had TPP but also a near-fatal ventricular arrhythmia.

The Effect of an Angiotensin Receptor Blocker on Arterial Stiffness in Type 2 Diabetes Mellitus Patients with Hypertension

Background Hypertension and type 2 diabetes mellitus are major risk factors for cardiovascular disease. This study analyzed the changes in central aortic waveforms and pulse wave velocity as well as related parameters after treatment with valsartan, an angiotensin II type 1 receptor blocker, in patients with type 2 diabetes and hypertension. Methods We used pulse wave analysis to measure central aortic waveform in a total of 98 subjects. In 47 of these patients, pulse wave velocity measurements were obtained before and after 12 weeks of treatment with valsartan. Results In the central aortic waveform analysis, the aortic pulse pressure and augmentation index were significantly decreased after valsartan treatment, as was the aortic pulse wave velocity. Factors contributing to the improvement in pulse wave velocity were the fasting blood glucose and haemoglobin A1c levels. Conclusion Short-term treatment with valsartan improves arterial stiffness in patients with type 2 diabetes and hypertension, and the glucose status at baseline was associated with this effect.

Angiotensin II Inhibits Insulin Binding to Endothelial Cells

Background Insulin-mediated glucose uptake in insulin target tissues is correlated with interstitial insulin concentration, rather than plasma insulin concentration. Therefore, insulin delivery to the interstitium of target tissues is very important, and the endothelium may also play an important role in the development of insulin resistance. Methods After treating bovine aortic endothelial cells with angiotensin II (ATII), we observed the changes in insulin binding capacity and the amounts of insulin receptor (IR) on the cell membranes and in the cytosol. Results After treatment of 10-7M ATII, insulin binding was decreased progressively, up to 60% at 60 minutes (P<0.05). ATII receptor blocker (eprosartan) dose dependently improved the insulin binding capacity which was reduced by ATII (P<0.05). At 200 µM, eprosartan fully restored insulin binding capacity, althogh it resulted in only a 20% to 30% restoration at the therapeutic concentration. ATII did not affect the total amount of IR, but it did reduce the amount of IR on the plasma membrane and increased that in the cytosol. Conclusion ATII decreased the insulin binding capacity of the tested cells. ATII did not affect the total amount of IR but did decrease the amount of IR on the plasma membrane. Our data indicate that ATII decreases insulin binding by translocating IR from the plasma membrane to the cytosol. The binding of insulin to IR is important for insulin-induced vasodilation and transendothelial insulin transport. Therefore, ATII may cause insulin resistance through this endothelium-based mechanism.