• Integrative Medicine Research
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• v.3 no.1
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• pp.4-10
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• 2014

Green tea and coffee consumption have been widely popular worldwide. These beverages contain caffeine to activate the central nervous system by adenosine receptor blockade, and due to the caffeine, addiction or tolerance may occur. In addition to this caffeine effect, green tea and coffee consumption have always been at the center of discussions about human health, disease, and longevity. In particular, green tea catechins are involved in many biological activities such as antioxidation and modulation of various cellular lipid and proteins. Thus, they are beneficial against degenerative diseases, including obesity, cancer, cardiovascular diseases, and various inflammatory diseases. Some reports also suggest that daily consumption of tea catechins may help in controlling type 2 diabetes. However, other studies have reported that chronic consumption of green tea may result in hepatic failure, neuronal damage, and exacerbation of diabetes, suggesting that interindividual variations in the green tea effect are large. This review will focus on the effect of green tea catechins extracted from the Camellia sinensis plant on type 2 diabetes and obesity, and the possible mechanistic explanation for the experimental results mainly from our laboratory. It is hoped that green tea can be consumed in a suitable manner as a supplement to prevent the development of type 2 diabetes and obesity.

• Journal of Korean Medicine Rehabilitation
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• v.31 no.4
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• pp.117-127
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• 2021

Objectives Previously, we demonstrated that a 5% ethanol extract of unripe Rubus coreanus (5-uRCK) and ellagic acid has hypocholesterolemic and antiobesity activity in high-fat diet-fed animals. Therefore, we conducted a clinical study on the anti-obesity effect of 5-uRCK in 140 Korean adults (aged 19-70 years, body mass index (BMI) ≥25 kg/m²). Methods The participants were randomly assigned to two groups and were administered the placebo (n=70) or 5-uRCK extract (800 mg, n=70) daily for 12 weeks. The subjects were instructed to maintain their usual dietary intake and normal physical activity. Anthropometrics, body composition (dual-energy X-ray absorptiometry), and blood parameters were compared between the two groups. Results Average body weight and BMI did not show any significant changes; however, changes in upper body fat mass between the two groups was significantly different, as determined using analysis of covariance adjusted for baseline of percent body fat and drinking units. Moreover, Although not significant, the trunk fat mass and percent trunk fat tended to decrease after 5-uRCK supplementation. There was no significant difference in other laboratory biomarkers between the two groups. All safety parameters were within normal ranges in the both group. Conclusions In the present study, 5-uRCK significantly reduced upper body fat in obese subjects after 12 weeks, which indicates that it may help improve android-type obesity. Furthermore, the supplement is safe and well tolerated.

• Molecules and Cells
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• v.47 no.3
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• pp.100007.1-100007.11
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• 2024

Recent evidence establishes a pivotal role for obesity-induced inflammation in precipitating insulin resistance and type-2 diabetes. Central to this process is the proinflammatory M1 adipose-tissue macrophages (ATMs) in epididymal white adipose tissue (eWAT). Notably, natural killer (NK) cells are a crucial regulator of ATMs since their cytokines induce ATM recruitment and M1 polarization. The importance of NK cells is shown by the strong increase in NK-cell numbers in eWAT, and by studies showing that removing and expanding NK cells respectively improve and worsen obesity-induced insulin resistance. It has been suggested that NK cells are activated by unknown ligands on obesity-stressed adipocytes that bind to NKp46 (encoded by Ncr1), which is an activating NK-cell receptor. This was supported by a study showing that NKp46-knockout mice have improved obesity-induced inflammation/insulin resistance. We therefore planned to use the NKp46-knockout mice to further elucidate the molecular mechanism by which NKp46 mediates eWAT NK-cell activation in obesity. We confirmed that obesity increased eWAT NKp46⁺ NK-cell numbers and NKp46 expression in wild-type mice and that NKp46-knockout ablated these responses. Unexpectedly, however, NKp46-knockout mice demonstrated insulin resistance similar to wild-type mice, as shown by fasting blood glucose/insulin levels and glucose/insulin tolerance tests. Obesityinduced increases in eWAT ATM numbers and proinflammatory gene expression were also similar. Thus, contrary to previously published results, NKp46 does not regulate obesity-induced insulin resistance. It is therefore unclear whether NKp46 participates in the development of obesity-induced inflammation and insulin resistance. This should be considered when elucidating the obesity-mediated molecular mechanisms that activate NK cells.

• Journal of Korean Academy of Nursing
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• v.31 no.6
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• pp.1034-1043
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• 2001

To determine the frequency of past and present obesity among patients with NIDDM and to identify the differences of body fat, blood pressure and C-peptide/glucose ratio according to obese diabetic patients (BMI$\geq$25 kg/$m^2$) and nonobese (BMI<25 kg/$m^2$). Also the final factor is to observe the anthrometric change patterns in the study. Method: The weight at 20 years-old, previous maximal body weight, and acute weight loss were queried. Current height, body weight, BMI, waist & hip circumferences, waist-hip ratio, skinfold thicknesses, blood pressure, fasting blood glucose, and fasting C-peptide were measured in one hundred sixty-seven NIDDM patients. The differences of the parameters ccording to obese and nonobese, and three anthropometric change patterns were analyzed. Result: Results were as follows: 1. 66.5 % of the NIDDM patients had a history of past obesity as assessed by their maximum weight, while only 33.2% of them were currently obese (p's < 0.001). 2. The waist & hip circumferences, skinfold thicknesses, systolic, diastolic & mean arterial blood pressure in obese patients were greater than those of nonobese patients (all p's < 0.001). 3. The waist and the hip circumferences, and skinfold thicknesses (subscapula & triceps) were highest among the obese-obese group. WHR and abdominal skinfold thickness in the obese-obese and obese-nonobese groups were higher than those in the nonobese- nonobese group. Systolic & diastolic and mean arterial blood pressures in the obese-obese group were higher than those of obese-nonobese and nonobese-nonobese groups(all p's < 0.005). 4. The abdominal and subscapular skinfold thicknesses in female diabetic patients were greater than those of male patients (all p's <0.0001). Conclusion: Although most Korean NIDDM patients were previously obese, many of them were not obese during the course of the study. Greater central and upper body adiposicity and higher blood pressure was shown in obese diabetic patients. Also, greater central and upper body adiposicity was demonstrated in female diabetic patients.

• Clinical and Experimental Pediatrics
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• v.53 no.10
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• pp.892-897
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• 2010

Purpose: This study evaluated the prevalence of the metabolic syndrome (MetS) and risk factors for metabolic derangement in young adults with childhood-onset hypopituitary growth hormone deficiency (ACOHGHD). Methods: Thirty patients with ACOHGHD who were treated with hormone-replacement therapy, aged 18 to 29 years, who visited the Seoul National University Children's Hospital between September 2009 and February 2010 were enrolled. Height, weight, waist circumference, hip circumference, and blood pressure were measured, and the clinical and hormonal features were reviewed retrospectively. We evaluated measures of metabolic derangement in the enrolled patients and in the data of healthy adults aged 20 to 29 years taken from the 2005 Korean National Health and Nutrition Examination Survey (KNHANES) as part of the National Cholesterol Education Program-the Adult Treatment Panel III. Results: Compared with the KNHANES participants, patients with ACOHGHD had significantly large waist circumference (men and women), high systolic blood pressure (BP) (women) and diastolic BP (men), and high serum triglyceride levels (women). The duration of illness correlated significantly with central obesity ($r^2$=0.546, $P$=0.003). The prevalence of MetS was 10% in patients with ACOHGHD and 2.3% in KNHANES participants. The prevalence of central obesity and MetS was higher in patients with ACOHGHD than in KNHANES participants ($P$<0.001 and $P$=0.042, respectively). Conclusion: Abdominal obesity correlated with the duration of illness in patients with ACOHGHD. Waist circumference should be measured in the clinic to prevent MetS, particularly in patients with a long history of ACOHGHD, regardless of age or sex.

• Journal of Society of Preventive Korean Medicine
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• v.22 no.2
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• pp.77-107
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• 2018

Objectives : In present study, therefore, possible beneficial pharmacological activities of standard potato protein extracts (SPE) were observed on the mild diabetic obese mice. Methods : After end of 12 weeks of continuous oral administrations of three different dosages of SPE 400, 200 and 100 mg/kg, or metformin 250 mg/kg, analyzed the hepatoprotective, hypolipidemic, hypoglycemic, nephroprotective and anti-obesity effects, separately. In addition, liver antioxidant defense systems were additionally measured with lipid metabolism-related genes expressions and hepatic glucose-regulating enzyme activities for action mechanism. Results : All of diabetes and related complications including obesity were significantly inhibited by treatment of SPE 400, 200 and 100 mg/kg, dose-dependently, and they also dramatically normalized the hepatic lipid peroxidation and depletion of liver endogenous antioxidant defense system, the changes of the hepatic glucose-regulating enzyme activities, also changes of the lipid metabolism-related genes expressions including hepatic $AMPK{\alpha}1$ and $AMPK{\alpha}2$ mRNA expressions, dose-dependently. Especially, SPE 200 mg/kg constantly showed favorable inhibitory activities against type II diabetes and related complications as comparable to those of metformin 250 mg/kg in HFD mice, respectively. Conclusions : The present work demonstrated that SPE 400, 200 and 100 mg/kg showed favorable anti-diabetic and related complications including obesity refinement activities in HFD mice, through AMPK upregulation mediated hepatic glucose enzyme activity and lipid metabolism-related genes expression, antioxidant defense system and pancreatic lipid digestion enzyme modulatory activities.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.4067-4073
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• 2012

Obesity is an established risk factor for colorectal cancer. Pioglitazone is a peroxisome proliferator activated receptor$receptor{\gamma}$ ($PPAR{\gamma}$) agonist that induces differentiation in adipocytes and induces growth arrest and/or apoptosis in vitro in several cancer cell lines. In the present study, we investigated the effect of pioglitazone on the development of azoxymethane-induced colon aberrant crypt foci (ACF) in KK-$A^{\mathcal{Y}}$ obesity and diabetes model mice, and tried to clarify mechanisms by which the $PPAR{\gamma}$ ligand inhibits ACF development. Administration of 800 ppm pioglitazone reduced the number of colon ACF/mouse to 30% of those in untreated mice and improved hypertrophic changes of adipocytes in KK-$A^{\mathcal{Y}}$ mice with significant reduction of serum triglyceride and insulin levels. Moreover, mRNA levels of adipocytokines, such as leptin, monocyte chemoattractant protein-1 and plasminogen activator inhibitor-1, in the visceral fat were decreased. PCNA immunohistochemistry revealed that pioglitazone treatment suppressed cell proliferation in the colorectal epithelium with elevation of p27 and p53 gene expression. These results suggest that pioglitazone prevented obesity-associated colon carcinogenesis through improvement of dysregulated adipocytokine levels and high serum levels of triglyceride and insulin, and increase of p27 and p53 mRNA levels in the colorectal mucosa. These data indicate that pioglitazone warrants attention as a potential chemopreventive agent against obesity-associated colorectal cancer.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.23 no.3
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• pp.189-230
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• 2020

The metabolic syndrome, by definition, is not a disease but is a clustering of individual metabolic risk factors including abdominal obesity, hyperglycemia, hypertriglyceridemia, hypertension, and low high-density lipoprotein cholesterol levels. These risk factors could dramatically increase the prevalence of type 2 diabetes and cardiovascular disease. The reported prevalence of the metabolic syndrome varies, greatly depending on the definition used, gender, age, socioeconomic status, and the ethnic background of study cohorts. Clinical and epidemiological studies have clearly demonstrated that the metabolic syndrome starts with central obesity. Because the prevalence of obesity has doubly increased worldwide over the past 30 years, the prevalence of the metabolic syndrome has markedly boosted in parallel. Therefore, obesity has been recognized as the leading cause for the metabolic syndrome since it is strongly associated with all metabolic risk factors. High prevalence of the metabolic syndrome is not unique to the USA and Europe and it is also increasing in most Asian countries. Insulin resistance has elucidated most, if not all, of the pathophysiology of the metabolic syndrome because it contributes to hyperglycemia. Furthermore, a major contributor to the development of insulin resistance is an overabundance of circulating fatty acids. Plasma fatty acids are derived mainly from the triglycerides stored in adipose tissues, which are released through the action of the cyclic AMP-dependent enzyme, hormone sensitive lipase. This review summarizes the latest concepts in the definition, pathogenesis, pathophysiology, and diagnosis of the metabolic syndrome, as well as its preventive measures and therapeutic strategies in children and adolescents.

• Journal of Acupuncture Research
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• v.17 no.3
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• pp.168-175
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• 2000

Stimulation of the auricle is known to be effective in reducing obesity. The aim of the present study is to investigate whether stimulating a specific auricular acupuncture point is effective on suppression of appetite. Cholesystokinin (CCK) is known to induce a powerful feeding response after central administration and particularly abundant in the cerebral cortex. In food-deprived rats exhibiting a strong drive for feeding, decreased CCK release was markedly detected in the cerebral cortex of the brain. Needling the fasted rats on the specific auricular region increased the CCK level of the cerebral cortex. In conclusion, stimulating the specific auricular points increases CCK-expression in the cerebral cortex of the fasted rats and may be useful for controlling obesity.

• Biomedical Science Letters
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• v.17 no.1
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• pp.13-20
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• 2011

The peroxisome proliferator-activated receptor ${\alpha}$ ($PPAR{\alpha}$) is a nuclear transcription factor that plays a central role in lipid and lipoprotein metabolism. To investigate whether swim training improves obesity and lipid metabolism through $PPAR{\alpha}$ activation in female sham-operated (Sham) and ovariectomized (OVX) mice, we measured body weight, visceral adipose tissue mass, serum free fatty acid at 6 weeks as well as the expression of hepatic $PPAR{\alpha}$ target genes involved in fatty acid oxidation. Swim-trained mice had decreased body weight, visceral adipose tissue mass and serum free fatty acid levels compared to high fat diet fed control mice in both female Sham and OVX mice. These reductions were more prominent in OVX than in Sham mice. Swim training significantly increased hepatic mRNA levels of $PPAR{\alpha}$ target genes responsible for mitochondrial fatty acid ${\beta}$-oxidation, such as carnitine palmitoyltransgerase-1 (CPT-1), very long chain acyl-CoA dehydrogenase (VLCAD), and medium chain acyl-CoA dehydrogenase (MCAD) in OVX mice. However, swim trained female Sham mice did not increase hepatic mRNA levels of $PPAR{\alpha}$ target genes responsible for mitochondrial fatty acid ${\beta}$-oxidation compared to Sham control mice. These results indicate that swim training differentially regulates body weight and adipose tissue mass between OVX and Sham mice, at least in part due to differences in liver $PPAR{\alpha}$ activation.