• Journal of Nutrition and Health
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• v.53 no.4
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• pp.356-368
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• 2020

Purpose: Histidine-containing dipeptides, which are rich in chicken, have been reported to reduce the risk of metabolic abnormalities via anticarbonylation mechanism in animal models. To determine the effect of dietary histidine-containing dipeptides on metabolic risk factors in humans, the relation between chicken consumption and insulin resistance were determined in a population consuming high carbohydrate and low protein. Methods: A total of 7,183 subjects (2,929 men and 4,254 women) aged ≥ 50 years from the Korea National Health and Nutrition Examination Survey (KNHANES) were divided into three groups according to chicken consumption (rarely, monthly, and weekly), and evaluated for the metabolic risk factors using homeostasis model assessment for insulin resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI) in this cross-sectional study. The fourth and fifth (IV-1-3 & V-1) KNHANES, which had blood insulin data, were chosen for the current study. Results: The chicken consumption was significantly associated with insulin (p for trend = 0.018) and HOMA-IR (p for trend = 0.023) in men. In particular, the 'weekly' chicken consuming men in the lowest tertile (< 65.0%) of carbohydrate intake group had significantly lower HOMA-IR (p for trend = 0.033) and higher QUICKI (p for trend = 0.043) than the 'rarely' intake group. In addition, the odds ratio for abnormal HOMA-IR was 0.55 (95% confidence interval [CI], 0.31-0.99) and QUICKI was 0.47 (95% CI, 0.26-0.86) for the 'weekly' chicken consuming group. Conclusion: The 'weekly' chicken consumption had a beneficial effect on insulin resistance and it may partially be due to the major bioactive components in chicken, histidine-containing dipeptides.

• Asian-Australasian Journal of Animal Sciences
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• v.19 no.7
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• pp.1033-1039
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• 2006

The metabolic response of Labeo rohita to thermal acclimation was assessed. Advanced fingerlings of L. rohita (average weight $31{\pm}1.4g$) were acclimated to 31, 33 and $36^{\circ}C$ compared with ambient temperatures ($26^{\circ}C$) for 30 days and different enzymes associated with stress response were estimated. Glycolytic enzyme-Lactate dehydrogenase, (LDH, E.C.1.1.1.27), TCA cycle enzyme-Malate dehydrogenase (MDH, E.C.1.1.1.37), Protein metabolizing enzymes-Aspartate amino transferase (AST, E.C.2.6.1.1) and Alanine amino transferase (ALT, E.C.2.6.1.2) of liver, gill and muscle, Gluconeogenic enzymes-Fructose 1,6 Bi phosphatase (FBPase, E.C. 3.1.3.11) and Glucose 6 phosphatase (G6Pase, E.C. 3.1.3.9) of liver and kidney were significantly (p<0.05) different with increasing acclimation temperatures. Heat Shock Protein-70 (HSP-70) was expressed in increasing intensity at 31, 33 and $36^{\circ}C$ but was not expressed at $26^{\circ}C$. Results suggest that higher acclimation temperatures enhance metabolism and L. rohita maintains homeostasis between $26-36^{\circ}C$ via an acclimation episode. Such adaptation appears to be facilitated by resorting to gluconeogenic and glycogenolytic pathways for energy mobilization and induction of HSPs.

• Journal of Animal Science and Technology
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• v.59 no.1
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• pp.1.1-1.11
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• 2017

Background: Intrauterine environment plays a pivotal role in the origin of fatal diseases such as the metabolic syndrome. Diabetes is associated with low-grade inflammatory state and dysregulated adipokines production. The aim of this study is to investigate the effect of maternal diabetes on adipocytokines (adiponectin, leptin and TNF-${\alpha}$) production in F1 offspring in rats. Methods: The offspring groups were as follows: F1 offspring of control mothers under control diet (CD) (CF1-CD), F1 offspring of control mothers under high caloric diet (HCD) (CF1-HCD), F1 offspring of diabetic mothers under CD (DF1-CD), and F1 offspring of diabetic mothers under HCD (DF1-HCD). Every 5 weeks post-natal, 10 pups of each subgroup were culled to obtain blood samples for biochemical analysis. Results: The results indicate that DF1-CD and DF1-HCD groups exhibited hyperinsulinemia, dyslipidemia, insulin resistance and impaired glucose homeostasis compared to CF1-CD (p > 0.05). DF1-CD and DF1-HCD groups had high hepatic and muscular depositions of TGs. The significant elevated NEFA level only appeared in offspring of diabetic mothers that was fed HCD. DF1-CD and DF1-HCD groups demonstrated low serum levels of adiponectin, high levels of leptin, and elevated levels of TNF-${\alpha}$ compared to CF1-CD (p > 0.05). These results reveal the disturbed metabolic lipid profile of offspring of diabetic mothers and could guide further characterization of the mechanisms involved. Conclusion: Dysregulated adipocytokines production could be a possible mechanism for the transgenerational transmittance of diabetes, especially following a postnatal diabetogenic environment. Moreover, the exacerbating effects of postnatal HCD on NEFA in rats might be prone to adipcytokine dysregulation. Furthermore, dysregulation of serum adipokines is a prevalent consequence of maternal diabetes and could guide further investigations to predict the development of metabolic disturbances.

• Molecules and Cells
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• v.38 no.12
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• pp.1044-1053
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• 2015

This study first investigated the effects of corn gluten hydrolysate (CGH) (1.5 g/day) administration for 7 days on appetite-responsive genes in lean Sprague-Dawley (SD) rats. In a second set of experiments, the metabolic changes occurring at multiple time points over 8 weeks in response to CGH (35.33% wt/wt) were observed in high-fat (HF, 60% of energy as fat) diet-fed SD rats. In lean rats, the hypothalamus neuropeptide-Y and proopiomelanocortin mRNA levels of the CGH group were significantly changed in response to CGH administration. In the second part of the study, CGH treatment was found to reduce body weight and perirenal and epididymal fat weight. CGH also prevented an increase in food intake at 2 weeks and lowered plasma leptin and insulin levels in comparison with the HF group. This reduction in the plasma and hepatic lipid levels was followed by improved insulin resistance, and the beneficial metabolic effects of CGH were also partly related to increases in plasma adiponectin levels. The Homeostasis Model of Assessment - Insulin Resistance (HOMA-IR), an index of insulin resistance, was markedly improved in the HF-CGH group compared with the HF group at 6 weeks. According to the microarray results, adipose tissue mRNA expression related to G-protein coupled receptor protein signaling pathway and sensory perception was significantly improved after 8 weeks of CGH administration. In conclusion, the present findings suggest that dietary CGH may be effective for improving hyperglycemia, dyslipidemia and insulin resistance in diet-induced obese rats as well as appetite control in lean rats.

• Animal Bioscience
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• v.34 no.1
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• pp.143-153
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• 2021

Objective: To explore the molecular mechanisms of fatty liver hemorrhagic syndrome (FLHS) in laying hens, an experiment was conducted to reveal the differences in histopathological observation and gene expression between FLHS group and normal group. Methods: We compared the histopathological difference using hematoxylin and eosin staining and proceeded with RNA sequencing of adipose tissue to search differentially expressed genes and enriched biological processes and pathways. Then we validated the mRNA expression levels by real-time polymerase chain reaction and quantified protein levels in the circulation by enzyme-linked immunosorbent assay. Results: We identified 100 differentially expressed transcripts corresponding to 66 genes (DEGs) were identified between FLHS-affected group and normal group. Seven DEGs were significantly enriched in the immune response process and lipid metabolic process, including phospholipase A2 group V, WAP kunitz and netrin domain containing 2, delta 4-desaturase sphingolipid 2, perilipin 3, interleukin-6 (IL-6), ciliary neurotrophic factor (CNTF), and suppressor of cytokine signaling 3 (SOCS3). And these genes could be the targets of immune response and be involved in metabolic homeostasis during the process of FLHS in laying hens. Based on functional categories of the DEGs, we further proposed a model to explain the etiology and pathogenesis of FLHS. IL-6 and SOCS3 mediate inflammatory responses and the satiety hormone of leptin, induce dysfunction of Jak-STAT signaling pathway, leading to insulin resistance and lipid metabolic disorders. Conversely, CNTF may reduce tissue destruction during inflammatory attacks and confer protection from inflammation-induced insulin resistance in FLHS chickens. Conclusion: These findings highlight the therapeutic implications of targeting the JAK-STAT pathway. Inhibition of IL6 and SOCS3 and facilitation of CNTF could serve as a favorable strategy to enhance insulin action and improve glucose homoeostasis, which are of importance for treating obesity-related disorders for chickens.

• BMB Reports
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• v.54 no.6
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• pp.323-328
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• 2021

Periodontal diseases have been reported to have a multidirectional association with metabolic disorders. We sought to investigate the correlation between periodontitis and diabetes or fatty liver disease using HFD-fed obese mice inoculated with P. gingivalis. Body weight, alveolar bone loss, serological biochemistry, and glucose level were determined to evaluate the pathophysiology of periodontitis and diabetes. For the evaluation of fatty liver disease, hepatic nonalcoholic steatohepatitis (NASH) was assessed by scoring steatosis, inflammation, hepatocyte ballooning and the crucial signaling pathways involved in liver metabolism were analyzed. The C-reactive protein (CRP) level and NASH score in P. gingivalis-infected obese mice were significantly elevated. Particularly, the extensive lobular inflammation was observed in the liver of obese mice infected with P. gingivalis. Moreover, the expression of metabolic regulatory factors, including peroxisome proliferator-activated receptor γ (Pparγ) and the fatty acid transporter Cd36, was up-regulated in the liver of P. gingivalis-infected obese mice. However, inoculation of P. gingivalis had no significant influence on glucose homeostasis, insulin resistance, and hepatic mTOR/AMPK signaling. In conclusion, our results indicate that P. gingivalis can induce the progression of fatty liver disease in HFD-fed mice through the upregulation of CD36-PPARγ axis.

• Clinical and Experimental Reproductive Medicine
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• v.50 no.3
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• pp.200-205
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• 2023

Objective: Polycystic ovary (PCO), a diagnostic component of polycystic ovary syndrome (PCOS), requires either an ovarian volume (OV) criterion or a follicle number per ovary (FNPO) criterion. This study investigated the association of OV and FNPO criteria with various manifestations of PCOS. Methods: This cross-sectional study was conducted at a university hospital among 100 patients newly diagnosed with PCOS (according to the revised Rotterdam criteria). Fasting blood samples were collected to measure glucose, total testosterone (TT), luteinizing hormone (LH), follicle-stimulating hormone (FSH), lipid, insulin, and hemoglobin A1c levels. An oral glucose tolerance test was performed. Transabdominal or transvaginal ultrasound of the ovaries was done, depending on patients' marital status. All investigations were conducted in the follicular phase of the menstrual cycle. OV >10 mL and/or FNPO ≥12 indicated PCO. A homeostasis model assessment of insulin resistance (IR) value ≥2.6 indicated IR, and metabolic syndrome (MS) was defined according to the international harmonization criteria. Results: Seventy-six participants fulfilled the OV criterion, 70 fulfilled the FNPO criterion, and 89 overall had PCO. Both maximum OV and mean OV had a significant correlation with TT levels (r=0.239, p=0.017 and r=0.280, p=0.005, respectively) and the LH/FSH ratio (r=0.212, p=0.034 and r=0.200, p=0.047, respectively). Mean OV also had a significant correlation with fasting insulin levels (r=0.210, p=0.036). Multivariate binary logistic regression analysis showed that IR (odds ratio [OR], 9.429; 95% confidence interval [CI], 1.701 to 52.271; p=0.010) and MS (OR, 7.952; 95% CI, 1.821 to 34.731; p=0.006) had significant predictive associations with OV alone, even after adjustment for age and body mass index. Conclusion: OV may be more closely related to the androgenic and metabolic characteristics of PCOS than FNPO.

• Journal of the Korean Applied Science and Technology
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• v.38 no.4
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• pp.1117-1128
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• 2021

The purpose of the current study was to investigate the effects of 4-week health promotion intervention program consisting of high-intensity aerobic exercise to improve energy consumption and cardiorespiratory capacity, circuit training to strengthen muscular strength and endurance and education for lifestyle changes on the obesity level, physical fitness, insulin resistance and metabolic syndrome among overweight or obese elementary school students. Twenty three overweight or obese children as obese group and 15 normal body weight children as normal group were recruited. The health promotion program consisted of two exercise sessions and one education session, 3days/week in 4-week. Obesity level(body mass index, waist circumference, %body fat), physical fitness(muscular strength, muscular endurance, flexibility, cardiopulmonary fitness), insulin resistance(homeostasis model assessment of insulin resistance) and metabolic syndrome risk factors(blood pressure, fasting glucose, triglycerides, high density lipoprotein cholesterol) were measured. There was not significant decrease in obesity level; however, there were significant improvement in physical fitness, insulin resistance and metabolic syndrome risk factors after program participation among obese children. As a result, through participation in the summer camp consisting mainly of exercise, the improvement of the physical fitness level and the decrease of insulin resistance had an effect on the reduction of the metabolic syndrome frequency.

• Molecules and Cells
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• v.38 no.9
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• pp.750-758
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• 2015

Genomic instability and altered metabolism are key features of most cancers. Recent studies suggest that metabolic reprogramming is part of a systematic response to cellular DNA damage. Thus, defining the molecules that fine-tune metabolism in response to DNA damage will enhance our understanding of molecular mechanisms of tumorigenesis and have profound implications for the development of strategies for cancer therapy. Sirtuins have been established as critical regulators in cellular homeostasis and physiology. Here, we review the emerging data revealing a pivotal function of sirtuins in genome maintenance and cell metabolism, and highlight current advances about the phenotypic consequences of defects in these critical regulators in tumorigenesis. While many questions should be addressed about the regulation and context-dependent functions of sirtuins, it appears clear that sirtuins may provide a promising, exciting new avenue for cancer therapy.

• BMB Reports
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• v.53 no.5
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• pp.241-247
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• 2020

As an intracellular degradation system, autophagy is an essential and defensive cellular program required for cell survival and cellular metabolic homeostasis in response to various stresses, such as nutrient deprivation and the accumulation of damaged organelles. In general, autophagy flux consists of four steps: (1) initiation (formation of phagophore), (2) maturation and completion of autophagosome, (3) fusion of autophagosomes with lysosomes (formation of autolysosome), and (4) degradation of intravesicular components within autolysosomes. The number of genes and reagents that modulate autophagy is increasing. Investigation of their effect on autophagy flux is critical to understanding the roles of autophagy in many physiological and pathological processes. In this review, we summarize and discuss ways to analyze autophagy flux quantitatively and qualitatively with the use of imaging tools. The suggested imaging method can help estimate whether each modulator is an inhibitor or a promoter of autophagy and elucidate the mode of action of specific genes and reagents on autophagy processes.