• Journal of Nutrition and Health
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• v.40 no.3
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• pp.221-228
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• 2007

We determined the effects of dietary manipulations on messenger RNA of peroxisome proliferators activated receptor isoforms (i.e., PPAR ${\alpha},\;{\beta}/{\delta},\;{\gamma}$) in red vastus lateralis muscle of rats. Total 16 male Sprague-Dawley rats were used, and animals were divided into one of two dietary conditions: either chow diet group (CHOW; n=8) in which animals were 134 with standard rodent chow (61.8% carbohydrate, 15.7% fat, 22.5% protein) or high fat diet group (FAT n=8) in which animals were fed 24.3% carbohydrate, 52.8% fat, 22.9% protein. At the end of the 8 weeks of experimental period, red vastus lateralis muscle was dissected out from all animals, and PPAR ${\alpha},\;{\beta}/{\delta},\;{\gamma}$ mRNA expression was determined. There was no significant difference in body mass (BM) between CHOW and FAT. As expected, blood glucose and free fatty acid (FFA) concentration was higher in FAT than CHOW (p<0.05), and lactate concentration was significantly lower in FAT compared to CHOW (p<0.05). Insulin concentration tended to higher in FAT than CHOW ($67.2{\pm}21.9\;vs.\;27.0{\pm}5.2$ pmol/L), but it did not reach to the statistical significance. Gene expression of PPAR ${\alpha}$ was not significantly different between CHOW and FAT. It was not also significantly different in PPAR ${\beta}/{\delta}$. Interestingly, expression of mRNA in PPAR ${\gamma}$ however, was markedly depressed in FAT compared to CHOW (approximately 3 fold higher in CHOW; p<0.05). Results obtained from present study implies that PPAR ${\gamma}$ (as compensatory function of PPAR ${\alpha}$ is expressed) possibly exerts another major tuning roles in fatty acid transport, utilization, as well as biosynthesis in skeletal muscle cells. The situations and conditions that can be postulated for this implication need to be further examined.

• Asian-Australasian Journal of Animal Sciences
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• v.28 no.6
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• pp.870-875
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• 2015

The purpose of this study was to investigate the alternative splicing in equine cordon-bleu WH2 repeat protein-like 1 (COBLL1) gene that was identified in horse muscle and blood leukocytes, and to predict functional consequences of alternative splicing by bioinformatics analysis. In a previous study, RNA-seq analysis predicted the presence of alternative spliced isoforms of equine COBLL1, namely COBLL1a as a long form and COBLL1b as a short form. In this study, we validated two isoforms of COBLL1 transcripts in horse tissues by the real-time polymerase chain reaction, and cloned them for Sanger sequencing. The sequencing results showed that the alternative splicing occurs at exon 9. Prediction of protein structure of these isoforms revealed three putative phosphorylation sites at the amino acid sequences encoded in exon 9, which is deleted in COBLL1b. In expression analysis, it was found that COBLL1b was expressed ubiquitously and equivalently in all the analyzed tissues, whereas COBLL1a showed strong expression in kidney, spinal cord and lung, moderate expression in heart and skeletal muscle, and low expression in thyroid and colon. In muscle, both COBLL1a and COBLL1b expression decreased after exercise. It is assumed that the regulation of COBLL1 expression may be important for regulating glucose level or switching of energy source, possibly through an insulin signaling pathway, in muscle after exercise. Further study is warranted to reveal the functional importance of COBLL1 on athletic performance in race horses.

• Korean Journal of Community Nutrition
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• v.10 no.4
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• pp.525-535
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• 2005

This study was conducted to investigate the effect of a 3 week low calorie diet (LCD) and a 9 week of behavior modification (BM) program on the weight loss, mineral and vitamin status in 22 obese women. The subject were healthy, obese (PIBW> $120\%$) women aged 20 - 50 Yr and not taking any medications known to influence body composition, mineral or vitamin metabolism During the LCD program, subjects were provided commercial liquid formulas with 125 kcal per pack and were instructed to have a formula for replacement of one meal and at least one regular meal per day within the range of daily 800 - 1200 kcal intake. During the BM program the subjects weekly attended the group nutrition counseling session to encourage themselves to modify their eating behavior and spontaneously restrict their energy intakes. The BM program focused on stimulus control, control of portion sizes and modification of binge eating and other adverse habits. The initial mean energy intake of subjects was 2016.9 $\pm$ 129.8 kcal ($100.8\%$ of RDA) and dropped to 1276.5 $\pm$ 435.7 kcal at the end of a 3 week of LCD program and elevated to 1762 $\pm$ 329.3 kcal at the end of a 9 week of BM program. Carbohydrate, protein and fat intakes were significantly decreased at the end of the LCD but carbohydrate was the only macro nutrient that showed significant decrease (p < 0.05) at the end of the BM program compared to baseline. Calcium and iron intakes decreased significantly (p < 0.01, respectively) with no significant changes in other micronutrients at the end of the LCD. The mean weight of the subjects decreased from 73.8 $\pm$ 8.0 kg to 69.2 $\pm$ 7.7 kg with LCD and ended up with 67.7 $\pm$ 7.1 kg after 9 weeks of BM. The 3 weeks of LCD reduced most of the anthropometric indices such as BMI, PIBW, fat weight, wast-to-hip ratio and subscapular and suprailiac skinfold thickness. The 9 weeks of behavior modification showed slight change or maintenance of each anthropometric measurements. Weight loss and decreased WHR with the diet program induced significantly decreased systolic blood pressure. SGOT, SGPT and serum insulin levels with improved serum lipid profiles. Biochemical parameters related to iron status such as hemoglobin, hematocrit were significantly decreased (p < 0.01) at the end of the LCD. But their mean values were within normal range. The mean serum 25 (OH) vitamin $D_3$ level significantly increased after whole diet program. Serum folate level significantly decreased after 12 weeks of diet program. In conclusion 3 weeks of LCD brought 4.6 kg reduction in body weight without risk of iron, zinc or vitamin D deficiency and 9 weeks of the BM was effective to maintain nutritional status with slightly more weight reduction (1.5 kg). However calcium intake and serum folate should be monitored during the LCD and BM because of increased risk of deficiencies.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.16 no.3
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• pp.148-154
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• 2016

A urea cycle disorder is a condition caused by a defect of the enzymes in the urea cycle, and deficiency of ornithine transcarbamylase (OTC), which converts carbamoyl phosphate and ornithine into citrulline, is the most common type of the disorder. OTC deficiency induces the accumulation of precursors of urea, ammonia, and glutamine, leading to neurological symptoms including hypotonia, respiratory failure, seizure, lethargy, and coma and sometimes to death. Because OTC deficiency is inherited in an X-linked manner, typical symptoms such as vomiting, poor feeding, and lethargy appear mainly in male neonates. We recently had a case that presented with neonatal onset lethargy, vomiting, and apnea in a 4-day-old boy. He was diagnosed with OTC deficiency by biochemical phenotype, including hyperammonemia and an increased orotic acid level in the urine. Genetic analysis of the OTC gene showed a novel mutation c.780_781insCAGGCAGTGT (p.Ile261Glnfs*35). He was treated for hyperammonemia using continuous venovenous hemofiltration (CVVH) at 118 hours after birth. After 4 days of CVVH, his consciousness and blood ammonia concentration were normalized, and he was discharged at the age of 53 days. At around 12 months of age, bilateral femur fractures and osteomyelitis occurred in this patient. Two months after the fracture, he died of septic shock, insulin-resistant hyperglycemia, and multi-organ failure.

• Childhood Kidney Diseases
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• v.14 no.2
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• pp.132-142
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• 2010

Hypokalemia usually reflects total body potassium deficiency, but less commonly results from transcellular potassium redistribution with normal body potassium stores. The differential diagnosis of hypokalemia includes pseudohypokalemia, cellular potassium redistribution, inadequate potassium intake, excessive cutaneous or gastrointestinal potassium loss, and renal potassium wasting. To discriminate excessive renal from extrarenal potassium losses as a cause for hypokalemia, urine potassium concentration or TTKG should be measured. Decreased values are indicative of extrarenal losses or inadequate intake. In contrast, excessive renal potassium losses are expected with increased values. Renal potassium wasting with normal or low blood pressure suggests hypokalemia associated with acidosis, vomiting, tubular disorders or increased renal potassium secretion. In hypokalemia associated with hypertension, plasam renin and aldosterone should be measured to differentiated among hyperreninemic hyperaldosteronism, primary hyperaldosteronism, and mineralocorticoid excess other than aldosterone or target organ activation. Hypokalemia may manifest as weakness, seizure, myalgia, rhabdomyolysis, constipation, ileus, arrhythmia, paresthesias, etc. Therapy for hypokalemia consists of treatment of underlying disease and potassium supplementation. The evaluation of hyperkalemia is also a multistep process. The differential diagnosis of hyperkalemia includes pseudohypokalemia, redistribution, and true hyperkalemia. True hyperkalemia associated with decreased glomerular filtration rate is associated with renal failure or increased body potassium contents. When glomerular filtration rate is above 15 mL/min/$1.73m^2$, plasma renin and aldosterone must be measured to differentiate hyporeninemic hypoaldosteronism, primary aldosteronism, disturbance of aldosterone action or target organ dysfunction. Hyperkalemia can cause arrhythmia, paresthesias, fatigue, etc. Therapy for hyperkalemia consists of administration of calcium gluconate, insulin, beta2 agonist, bicarbonate, furosemide, resin and dialysis. Potassium intake must be restricted and associated drugs should be withdrawn.

• Korean Journal of Food Science and Technology
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• v.45 no.4
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• pp.488-494
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• 2013

The anti-diabetic effect of green tea fermented by cheonggukjang was evaluated using KK-$A^y$ mice, an animal model of type 2 diabetes mellitus. Over a 90 day testing period, food and water intake decreased significantly in the group fed fermented green tea (FGT) and a group fed commercially available health functional food (PC), when compared with a diabetic control group (DC). The blood glucose levels of FGT mice were lower than in DC mice throughout the test period and were similar to the levels in PC after 60 days. Levels of Hemoglobin A1c (HbA1c) levels and insulin resistance were lower in mice of the FGT group than in mice of the DC group. DNA microarray analysis showed that administration of FGT increased the abundance of 12 mRNA transcripts related to diabetes. Whereas FGT increased hexokinase transcripts related to glycolysis more than 37 fold, levels of Pdx1 (pancreatic and duodenal homeobox1) and Cacna1e (calcium channel) transcripts increased more than 1.8 fold.

• Korean Journal of Clinical Laboratory Science
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• v.50 no.2
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• pp.190-196
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• 2018

Obesity has been reported to be a cluster of risk factors in the pathological ecology, In particular, there is increasing evidence that inflammation-related factors are associated with diabetes. This study examined the relationship between the hs-CRP level and FBG, fructosamine, and $HbA_1c$ in 4,734 non-diabetic adults aged 20 years or older, who were approved by the National Health and Nutrition Survey in 2015. The results showed that the FBG, fructosamine, and $HbA_1c$ levels increased with increasing BMI; the hs-CRP levels were the highest in the obese group, and HOMA-IR, an index of insulin resistance, was also significantly higher in the obese group. The hs-CRP level was the highest in obese adults. The levels of FBG, fructosamine. and $HbA_1c$, which are involved in blood glucose control, increased with increasing hs-CRP level. The FBG, fructosamine, and $HbA_1c$ levels increased significantly with increasing hs-CRP level after adjusting for various related variables. These results suggest that the obesity-induced increase in hs-CRP is a risk factor for diabetes mellitus in non-diabetic adults. Therefore, proper dietary habits and regular exercise should prevent diabetes by preventing obesity in non-diabetic adults.

• The Korean Journal of Food And Nutrition
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• v.31 no.3
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• pp.425-434
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• 2018

Metabolic syndrome is a risk factor for cardiovascular and type 2 diabetes. This study was conducted to examine the relevance between nutrition intake, meal quality, and high-sensitivity C-reactive protein in Koreans with metabolic syndrome. The 2,536 subjects, aged 19~64, who participated in 2015 National Nutrition Survey were included in this study. The 24-hour recall method was employed to analyze nutrition intake and dietary quality. Subjects were grouped into either the non-metabolic syndrome group (n=1,938) or the metabolic syndrome group (n=598). Total males and females were divided into 3 groups according to the high-sensitivity C-reactive protein (hs-CRP) level to study its relationship to metabolic syndrome and its components, including odds ratio (OR) and confidence interval (CI). Results showed the homeostasis model assessment of insulin resistance (HOMA-IR) value was higher in the metabolic syndrome group (3.37) than non-metabolic syndrome group (1.57) (p<0.001). In the Index of Nutrition Quality, males in the non-metabolic syndrome group showed higher niacin (p<0.05) than males in metabolic syndrome group. Females in the non-metabolic syndrome group had higher vitamin $B_1$ (p<0.01), vitamin $B_2$ (p<0.001), niacin (p<0.05), calcium (p<0.001), and phosphate (p<0.01). Female in the high hs-CRP group showed high OR in blood glucose component (OR 2.488, 95% CI: 1.269~4.879) and metabolic syndrome risk (OR 2.856, 95% CI: 1.292~6.314). Females in the middle hs-CRP group had high triglycerides component (OR 2.956, 95% CI: 1.920~4.551), compared to the low hs-CRP group. The study showed females with higher hs-CRP had a higher risk of metabolic syndrome.

• Journal of Digital Convergence
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• v.14 no.9
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• pp.471-478
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• 2016

The purpose of this study to examine the effect of 12 hours fasting resistance exercise on metabolic efficiency and fatigue of middle-aged female for 8 weeks. 50 middle-aged female target group pre-test exercise group(EX) and the control over the homogeneity in the control group(CON) were selected for this purpose divided into two groups. Exercise group(EX) is maintained after 8 weeks four times weeks 12 hours fasting resistance was performed for 60 minutes, the control group(CON) were compared to a normal life with the group of the exercise group(EX). Resistance applied to the exercise group(EX) were using free weights and a fixed mechanism applied around the upper and lower body exercise program for heart muscle, exercise intensity based on the 70% 1RM until 4 weeks, 5-8, which was performed by the aid program set to 80%. Through this procedure were as follows. First, 12 hours fasting resistance exercise showed the significance of the interaction effect in metabolic efficiency, blood pressure(SBP, DBP), fat, fasting glucose, fasting insulin(p<.01). Second, 12 hours fasting resistance exercise showed the significance of the interaction effect in the treatment program in which lactic acid, uric acid(p<.01).

• Journal of Ginseng Research
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• v.44 no.2
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• pp.362-372
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• 2020

Background: The non-saponin fraction of Korean Red Ginseng has been reported to have many biological activities. However, the effect of this fraction on anti-diabetic activity has not been elucidated in detail. In this study, we investigated the effects of KGC05P0, a non-saponin fraction of Korean Red Ginseng, on anti-diabetic activity in vitro and in vivo. Methods: We measured the inhibition of commercially obtained α-glucosidase and α-amylase activities in vitro and measured the glucose uptake and transport rate in Caco-2 cells. C57BL/6J mice and C57BLKS/J^db/db (diabetic) mice were fed diets with or without KGC05P0 for eight weeks. To perform the experiments, the groups were divided as follows: normal control (C57BL/6J mice), db/db control (C57BLKS/J^db/db mice), positive control (inulin 400 mg/kg b.w.), low (KGC05P0 100 mg/kg b.w.), medium (KGC05P0 200 mg/kg b.w.), and high (KGC05P0 400 mg/kg b.w.). Results: KGC05P0 inhibited α-glucosidase and α-amylase activities in vitro, and decreased glucose uptake and transport rate in Caco-2 cells. In addition, KGC05P0 regulated fasting glucose level, glucose tolerance, insulin, HbA1c, carbonyl contents, and proinflammatory cytokines in blood from diabetic mice and significantly reduced urinary glucose excretion levels. Moreover, we found that KGC05P0 regulated glucose production by down-regulation of the PI3K/AKT pathway, which inhibited gluconeogenesis. Conclusion: Our study thereby demonstrated that KGC05P0 exerted anti-diabetic effects through inhibition of glucose absorption and the PI3K/AKT pathway in in vitro and in vivo models of diabetes. Our results suggest that KGC05P0 could be developed as a complementary food to help prevent T2DM and its complications.