Tae-Wha Kim

Chromium picolinate supplementation improves insulin sensitivity in Goto-Kakizaki diabetic rats

Chromium picolinate (CrP) supplementation has been studied as a potential therapy of insulin resistance and lipid abnormalities. There have been some reports involving chromium supplementation in patients with diabetes, but the results are varied. The present study was conducted to assess the effects of CrP on insulin sensitivity and body weight in Goto-Kakizaki (GK) diabetic rats. We supplemented normal Sprague-Dawley (SD) rats and GK diabetic rats with supplemental CrP, 100 mg/kg/day once a day for 4 weeks. In the normal SD rats, the mean body weight of the control group increased by 50.5%, whereas that of the CrP-treated group increased by 65.9% (P < 0.05 vs control). Similarly, in the diabetic GK rats, CrP supplementation showed increased weight gain compared to the control group (133.4% vs 119.6% of the baseline weight, P < 0.01). Glucose tolerance tests (GTT) [ip injection of glucose; 2 g/kg] and insulin sensitivity tests [SQ injection of insulin (5 U/kg) plus ip injection of glucose (30 min after insulin injection)] were conducted. During insulin sensitivity tests at the end of treatment, the glucose levels were significantly lower in CrP-treated rats compared with the control rats (AUC0-->120; 113.1 +/- 32.0 vs 170.5 +/- 49.0 mg-min/mL, P < 0.05). During GTTs, the glucose levels and insulin concentrations in the CrP-treated rats were not different from those in the control rats. The results of these studies suggest that CrP supplementation in GK diabetic rats leads to increase of weight gain and improvement of insulin sensitivity. This raises the possibility that CrP supplementation can be considered to improve carbohydrate metabolism in patients with type 2 diabetes mellitus.

Differential Expression of Nonislet Autoimmunity: Comparison of Korean and U.S. Patients with Type 1 Diabetes

Abstract: Type 1 diabetes (T1D) is frequently associated with other autoimmune diseases. The occurrence of common features of autoimmune diseases and the coassociation of multiple autoimmune diseases in the same individual or family support the notion that there may be common genetic factors. We previously reported that immunogenetic markers of T1D were similar in Korean and U.S. families. We hypothesized that nonislet autoimmunity might be expressed in a similar manner in Korean as well as in Caucasian patients and correlated with the DRB1‐DQB1 haplotypes. Twenty‐five percent of Korean patients with T1D (32/128) had antithyroid autoantibodies (ATA+), whereas eight percent of age‐matched controls were ATA+ [OR = 3.7 (95% CI:1.0‐12.0), P < 0.05]. Twenty‐three percent (84/369) of age‐matched T1D patients from the U.S. had ATA (not statistically different from that in Koreans). None of the Korean patients nor the family members were positive for 21‐hydroxylase (21OH) or transglutaminase autoantibodies (TG). In contrast, in U.S. patients, nine T1D patients (2.4%) were 21OH+ (not statistically different from that in Koreans) and 39 T1D patients (10.6%) were TG+ [OR = 30.7 (95% CI: 4.6‐111), P < 10−4 vs. Korean patients]. Nonislet autoimmunity is prevalent in Korean and U.S. patients with T1D and their family members, but specific forms of autoimmunity differ even after matching for their HLA haplotypes. Individuals with T1D and their relatives frequently develop a panel of autoantibodies, perhaps due to other common susceptibility genes that are shared among first‐degree relatives.

Development and evaluation of a measurement method and system for solar heat gain coefficient and thermal transmittance

Abstract Evaluation of the thermal performance of a fenestration system during the cooling season is based on heat gains by temperature difference and solar radiation, characterised by thermal transmittance (U-value) and solar heat gain coefficient, respectively. While U-value testing and calculation methods have been long established, solar heat gain coefficient has been evaluated only by calculation under the lack of any established testing method. However, calculation alone cannot yield exact solar heat gain coefficient values for various types of fenestration. To address this problem, this study aims to develop a solar heat gain coefficient apparatus for measuring the energy performance of fenestration in terms of U-value and solar heat gain coefficient, and to evaluate that system. The proposed measurement system can be used in measuring U-values and solar heat gain coefficient values for fenestration with complicated shapes, such as an awning device.

Thyrotropin-releasing hormone increases phospholipase D activity through stimulation of protein kinase C in GH3 cells

Activation of phospholipase D was investigated after treatment of GH3 cells with thyrotropin-releasing hormone. Thyrotropin-releasing hormone treatment resulted in both time- and dose-dependent increases of phospholipase D activity, translocation of protein kinase C-α and -βl isozymes from cytosol to membrane within 30 min, and approx 43-fold increase of phosphatidylinositol-specific phospholipase C activity. Intracellular calcium concentration was rapidly increased and diacyglycerol level remained high up to 3 h after the treatment. Pretreatment of the cells with U73122, a potent inhibitor of phosphatidylinositol-specific phospholipase C, inhibited thyrotropin-releasing hormone-induced phospholipase D activation. Protein kinase C activity was down-regulated by pretreatment of the GH3 cells with either protein kinase C inhibitors (RO320432, GF109203X) or preincubation of the cells with phorbol myristrate acetate (500 nM) for 24 h. This treatment largely abolished the thyrotropin-releasing hormone-induced activation of phospholipase D, thus further confirming the involvement of protein kinase C in the activation. These results suggest that thyrotropin-releasing hormone-induced phospholipase D activation may be due to phosphatidylinositol-specific phospholipase C, and activation of protein kinase C isozymes is responsible for this stimulation.