• YAKHAK HOEJI
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• v.42 no.4
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• pp.408-413
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• 1998

To establish prediabetes in vitro/ model concerning the etiology of Insulin Dependent Diabetes Mellitus (IDDM) in cellular level we have designed experimental prediabefic model in pancreatic beta cells. RINm5F, HIT-T15 and isolated rat islets were chosen as pancreatic beta cells. Since interleukin-$1{\beta}$-induced beta cell cytotoxicity has been implicated in the autoimmune cytotoxicity of IDDM, we used inteleukin-$1{\beta}$ as diabetogenic agent. For establishment of prediabetic in vitro model, the degree of beta cell deterioration was determined by cell proliferation, insulin release and morphological appearance. Cell proliferation, insulin release and morphology were changed dose-dependently in condition that inteleuldn-$1{\beta}$ was exposured to pancreatic beta cells. The concentration and exposure time of interleukin-$1{\beta}$ to set up prediabetic model in beta cell lines and isolated rat islets were 100${\sim}$1000U/ml, 48hr. And 25${\sim}$100U/ml, 48hr, respectively.

• Biomolecules & Therapeutics
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• v.6 no.4
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• pp.371-377
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• 1998

The aim of the present study was to investigate the effect of Palmiwon on the type 1-prediabetic models induced by streptozotocin (STZ) in RINm5F cells and HIT-T15 cells. Palmiwon increased the cell proliferation and insulin release when pre- and post-treated for the STZ-exposed pancreatic beta cells. The cell proliferation and insulin release of these beta cells were measured by $^3$H-thymidine uptake and RIA, respectively. We also analyzed nutrients such as sugars, fatty acid and amino acids and minerals containing in Palmiwon using by gas chromatography, amino acid analyzer and AA spectrometer, respectively. Palmiwon seems to have protective and recovery properties on the prediabetic model in cellular level, which were ascribe to various nutrients and minerals containing in Palmiwon. From these results, it could be suggested that Palmiwon may be available as preventive and therapeutic prescription of type 1 diabetes mellitus.

• YAKHAK HOEJI
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• v.41 no.2
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• pp.260-267
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• 1997

To establish prediabetes in vitro model concerning the etiology of IDDM(Insulin Dependent Diabetes Mellitus) in cellular level we have designed prediabetes in vitro models in pa ncreatic beta cells. HIT-T15, RINm5F and isolated rat islets were chosen as pancreatic beta cells, and streptozotocin (STZ) used as diabetogenic agent. Degree of beta cell destruction to establish prediabetic in vitro model was determined by cell proliferation and insulin release using thymidine uptake and radio immuno assay. When HIT-T15 and RINm5F cells were treated with STZ, the degree of cell deterioration was dependent upon the origin and passage number of beta cells, and in the case of isolated islets STZ showed the more sensitivity than above two beta cell lines. The concentration and exposure time of STZ treatment to establish prediabetes in vitro model in beta cell lines and isolated rat islets were 2 ~ 10mM, 30 min. and 1 ~ 5mM, 30 min., respectively.

• Journal of Korean Academy of Nursing
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• v.50 no.2
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• pp.298-312
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• 2020

Purpose: This study had two objectives: 1) to develop a scale for the process of exercise engagement (SPEE) for prediabetic individuals (PDIs); 2) to validate a structural model for the process of exercise engagement for PDIs. Methods: A cross-sectional survey with simple random sampling was conducted from September 2013 to December 2015 (in Taiwan). A total of 310 PDIs were enrolled for scale development and model validation via item analysis, factor analyses, and structural equation modeling. The Kuo model was used as the basis for developing the Chinese version of the SPEE for PDIs. Results: The SPEE contains five subscales with a total of twenty-one items that account for 54.9% to 65.9% of the total variance explained for assessing participants' process of engagement during exercise. For Kuo model validation, the model measures indicated goodness of fit between the Kuo model and sample data. Analysis further revealed a direct effect between the creating health blueprints (CHB) stage and the spontaneous regular exercise (SRE) stage (β=.60). Conclusion: The SPEE includes five subscales for assessing the psychological transition and behavioral expression at each stage of the process of exercise engagement for PDIs. The SPEE for people with prediabetes provides deeper insights into the factors of behavioral change stages that are required to initiate long-term health care outcomes and avoid developing diabetes. These insights are significant as they allow for patient-specific mapping and behavior modification to effect exercise.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.4
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• pp.309-318
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• 2015

Alcohol consumption increases the risk of type 2 diabetes. However, its effects on prediabetes or early diabetes have not been studied. We investigated endoplasmic reticulum (ER) stress in the pancreas and liver resulting from chronic alcohol consumption in the prediabetes and early stages of diabetes. We separated Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a type-2 diabetic animal model, into two groups based on diabetic stage: prediabetes and early diabetes were defined as occurrence between the ages of 11 to 16 weeks and 17 to 22 weeks, respectively. The experimental group received an ethanol-containing liquid diet for 6 weeks. An intraperitoneal glucose tolerance test was conducted after 16 and 22 weeks for the prediabetic and early diabetes groups, respectively. There were no significant differences in body weight between the control and ethanol groups. Fasting and 120-min glucose levels were lower and higher, respectively, in the ethanol group than in the control group. In prediabetes rats, alcohol induced significant expression of ER stress markers in the pancreas; however, alcohol did not affect the liver. In early diabetes rats, alcohol significantly increased most ER stress-marker levels in both the pancreas and liver. These results indicate that chronic alcohol consumption increased the risk of diabetes in prediabetic and early diabetic OLETF rats; the pancreas was more susceptible to damage than was the liver in the early diabetic stages, and the adaptive and proapoptotic pathway of ER stress may play key roles in the development and progression of diabetes affected by chronic alcohol ingestion.

• Nutrition Research and Practice
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• v.12 no.3
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• pp.233-242
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• 2018

BACKGROUND/OBJECTIVES: The effects of fish consumption by subjects with prediabetes on the metabolic risk factors were examined based on the data from the $6^{th}$ Korea National Health and Nutrition Examination Surveys in 2015. SUBJECTS/METHODS: A total of 1,520 subjects who agreed to participate in a blood test and dietary intake survey were divided into a prediabetes group and normal blood glucose group, and the level of the subjects' fish consumption was divided into ${\leq}17.0g/day$, 18.0-93.0 g/day, and ${\geq}94g/day$. The correlation between the level of fish intake and the metabolic risk factors was evaluated by multinomial logistic regression analysis. RESULTS: A significant difference in the gender distribution was observed in the prediabetes group, which is a group with a high risk of non-communicable diseases, according to the fish intake, and there were significant differences in the total energy intake, protein intake, n-3 fatty acids intake, and the intakes of sodium and micro-nutrients according to the intake group (P < 0.05). In addition, the blood total cholesterol (TC) decreased 0.422 fold in model 1 (unadjusted) [95% confidence interval (CI): 0.211-0.845] and 0.422 fold in model 2 (adjusted for sex) (95% CI: 0.210-0.846) in those with a fish intake of 18.0-93.0 g/day (P < 0.05) compared to those with a fish intake of ${\leq}17.0g/day$. The blood TC decreased 0.555 fold (95% CI: 0.311-0.989) in model 1 and 0.549 fold (95% CI: 0.302-0.997) in model 2 in those with a fish intake of ${\geq}94g/day$ compared to those with a fish intake of ${\leq}17.0g/day$ (P < 0.05). CONCLUSION: Subjects with prediabetes or the metabolic risk factors can maintain their blood low density lipoprotein cholesterol (LDL-C) and blood TC concentrations at the optimal level by consuming fish (18.0-93.0 g/day).

• Nutrition Research and Practice
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• v.17 no.2
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• pp.228-240
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• 2023

BACKGROUND/OBJECTIVES: Cocoa consumption is associated with health benefits due to its high content of polyphenols. However, the effects of short-term cocoa consumption remain unclear. We aimed to determine the effects generated by cocoa consumption (for 7 days) in young adults in normoweight and class II obesity. SUBJECTS/METHODS: Before-and-after study was carried out in normoweight (NW) (n = 15) and class II obesity (CIIO) (n = 15) young adults. The NW and CIIO participants consumed 25 and 39 g of cocoa, respectively, per day for 7 days. The effect of cocoa consumption was evaluated on the lipid profile, insulin resistance (IR), and inflammation. Oxidative damage was also examined by assessing the biomarkers of oxidative damage in plasma. In addition, recombinant human insulin was incubated with blood obtained from the participants, and the molecular damage to the hormone was analyzed. RESULTS: Cocoa consumption resulted in decreased low-density lipoprotein-cholesterol in both groups (P = 0.04), while the total cholesterol, high-density lipoprotein cholesterol, and triglycerides were maintained at the recommended levels. Initially, IR was detected in the CIIO group (homeostasis model assessment [HOMA] = 4.78 ± 0.4), which is associated with molecular damage to insulin. Interestingly, intervention with cocoa resulted in improved IR (HOMA = 3.14 ± 0.31) (P = 0.0018) as well as molecular damage to insulin. Finally, cocoa consumption significant decreased the arginase activity (P = 0.0249) in the CIIO group; this is a critical enzymatic activity in the inflammatory process associated with obesity. CONCLUSIONS: The short-term consumption of cocoa improves the lipid profile, exerts anti-inflammatory effects, and protects against oxidative damage. Results of this study indicate that cocoa consumption can potentially improve IR and restore a healthy redox status.