• Biomedical Science Letters
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• v.16 no.3
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• pp.151-159
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• 2010

The peroxisome proliferator-activated receptor $\alpha$ (PPAR$\alpha$) is a nuclear transcription factor that plays a central role in lipid metabolism and obesity. Exercise also is a powerful modifier of the manifestations of the lipid metabolism and obesity in animal models and humans with obesity and metabolic syndrome. However, effects of exercise on lipid metabolism and obesity in normal-weight younger female subjects, having functional ovaries and not metabolic disease, remain unexplained. To explore the effects of exercise on the development of obesity and its molecular mechanism in high fat diet-fed female C57BL/6J mice, we experimented the effects of swim training on body weight, adipose tissue mass, serum lipid levels, morphological changes of adipocytes and the expression of PPAR$\alpha$ target genes involved in fat oxidation in skeletal muscle tissue of female C57BL/6J mice. Swim-trained mice had significantly decreased body weight, adipose tissue mass, serum triglycerides compared with female control mice. Histological studies showed that swim training significantly decreased the average size of adipoctyes in parametrial adipose tissue. Swim training did not affect the expression of PPAR$\alpha$ mRNA in skeletal muscle. Concomitantly, swim training did not increase mRNA levels of PPAR$\alpha$ target genes responsible for fatty acid $\beta$-oxidation, such as carnitine palmitoyltransferase 1, medium chain acyl-CoA dehydrogenase, enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase, and thiolase in skeletal muscle. In conclusion, these results indicate that swim training regulates lipid metabolism and obesity in high fat diet fed-female mice although swim training did not increase mRNA levels of PPAR$\alpha$ target genes involved in fatty acid $\beta$-oxidation in skeletal muscle, suggesting that swim training may prevent obesity and improve fitness through other mechanisms in female with ovaries, not through the activation of skeletal muscle PPAR$\alpha$.

• Nutrition Research and Practice
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• v.18 no.1
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• pp.78-87
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• 2024

BACKGROUND/OBJECTIVES: The prevalence of obesity, a worldwide pandemic, has been increasing steadily in Korea. Reports have shown that increased intermuscular adipose tissue (IMAT) is associated with an increased risk of cardiovascular disease, independent of body mass index. However, the relationship between dietary intake and IMAT accumulation in the Korean population remains undetermined. The objective of this study was to evaluate regional fat compartments using advanced magnetic resonance imaging (MRI) techniques. We also aimed to investigate the association between IMAT amounts and dietary intake, including carbohydrate intake, among Korean individuals with obesity. SUBJECTS/METHODS: This cross-sectional study, performed at a medical center in South Korea, recruited 35 individuals with obesity (15 men and 20 women) and classified them into 2 groups according to sex. Anthropometry was performed, and body fat distribution was measured using MRI. Blood parameters, including glucose and lipid profiles, were analyzed using commercial kits. Linear regression analysis was used to test whether the IMAT was associated with daily carbohydrate intake. RESULTS: Carbohydrate intake was positively associated with IMAT in all individuals, with adjustments for age, sex, height, and weight. No significant differences in blood indicators were found between the sexes. CONCLUSIONS: Regardless of sex and age, higher carbohydrate intake was strongly correlated with greater IMAT accumulation. This suggests the need to better understand sex differences and high carbohydrate diet patterns in relation to the association between obesity and metabolic risk, which may help reduce obesity prevalence.

• Journal of Life Science
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• v.30 no.7
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• pp.640-650
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• 2020

Fibroblast growth factor 21 (FGF21) is an atypical member of the FGF protein family which is highly synthesized in the liver, pancreas, and adipose tissue. Depending on the expression tissue, FGF21 uses endo- or paracrine features to regulate several metabolic pathways including glucose metabolism and energy homeostasis. Different physiologically stressful conditions such as starvation, a ketogenic diet, extreme cold, and mitochondrial dysfunction are known to induce FGF21 synthesis in various tissues to exert either adaptive or defensive mechanisms. More specifically, peroxisome proliferator-activated receptor gamma and peroxisome proliferator-activated receptor alpha control FGF21 expression in adipose tissue and liver, respectively. In addition, the pharmacologic administration of FGF21 has been reported to decrease the body weight and improve the insulin sensitivity and lipoprotein profiles of obese mice and type 2 diabetes patients meaning that FGF21 has attracted huge interest as a therapeutic agent for type 2 diabetes, obesity, and non-alcoholic fatty liver disease. However, understanding FGF21 remains complicated due to the paradoxical condition of its tissue-dependent expression. For example, nutrient deprivation largely increases hepatic FGF21 levels whereas adipose tissue-derived FGF21 is increased under feeding condition. This review discusses the issues of interest that have arisen from existing publications, including the tissue-specific function of FGF21 and its action mechanism. We also summarize the current stage of a clinical trial using several FGF21 analogs.

• Biomolecules & Therapeutics
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• v.29 no.5
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• pp.455-464
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• 2021

Uncontrolled inflammation is considered the pathophysiological basis of many prevalent metabolic disorders, such as nonalcoholic fatty liver disease, diabetes, obesity, and neurodegenerative diseases. The inflammatory response is a self-limiting process that produces a superfamily of chemical mediators, called specialized proresolving mediators (SPMs). SPMs include the ω-3-derived family of molecules, such as resolvins, protectins, and maresins, as well as arachidonic acid-derived (ω-6) lipoxins that stimulate and promote resolution of inflammation, clearance of microbes, and alleviation of pain and promote tissue regeneration via novel mechanisms. SPMs function by binding and activating G protein-coupled receptors, such as FPR2/ALX, GPR32, and ERV1, and nuclear orphan receptors, such as RORα. Recently, several studies reported that SPMs have the potential to attenuate lipid metabolism disorders. However, the understanding of pharmacological aspects of SPMs, including tissue-specific biosynthesis, and specific SPM receptors and signaling pathways, is currently limited. Here, we summarize recent advances in the role of SPMs in resolution of inflammatory diseases with metabolic disorders, such as nonalcoholic fatty liver disease and obesity, obtained from preclinical animal studies. In addition, the known SPM receptors and their intracellular signaling are reviewed as targets of resolution of inflammation, and the currently available information on the therapeutic effects of major SPMs for metabolic disorders is summarized.

• Endocrinology and Metabolism
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• v.31 no.1
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• pp.1-6
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• 2016

Immoderate energy intake, a sedentary lifestyle, and aging have contributed to the increased prevalence of obesity, sarcopenia, metabolic syndrome, type 2 diabetes, and cardiovascular disease. There is an urgent need for the development of novel pharmacological interventions that can target excessive fat accumulation and decreased muscle mass and/or strength. Adipokines, bioactive molecules derived from adipose tissue, are involved in the regulation of appetite and satiety, inflammation, energy expenditure, insulin resistance and secretion, glucose and lipid metabolism, and atherosclerosis. Recently, there is emerging evidence that skeletal muscle and the liver also function as endocrine organs that secrete myokines and hepatokines, respectively. Novel discoveries and research into these organokines (adipokines, myokines, and hepatokines) may lead to the development of promising biomarkers and therapeutics for cardiometabolic disease. In this review, I summarize recent data on these organokines and focus on the role of adipokines, myokines, and hepatokines in the regulation of insulin resistance, inflammation, and atherosclerosis.

• Journal of radiological science and technology
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• v.39 no.1
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• pp.81-88
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• 2016

The body of the fat tissue increased in obese represented by risk factors such as cardiovascular diseases, diabetes, metabolic disease and dyslipidemia. Such metabolic diseases and the like of the cardiovascular and cerebrovascular disease, hypertension, dyslipidemia, increase in the adipose tissue of the pancreas is known to be a risk factor of these diseases. Study on the diagnosis and treatment of pancreatic cancer was conducted actively, case studies on pancreatic steatosis is not much. In this study, divided into a control group diagnosed with pancreatic steatosis as a result of ultrasonography to evaluation the physical characteristics and serologic tests and blood pressure and arterial stiffness. The control group and the test pancreas steatosis age and waist circumference, body mass index, total cholesterol, HDL cholesterol, LDL cholesterol, and systolic and diastolic blood pressure, fasting blood glucose, arterial elasticity is higher in pancreatic steatosis. And the lower ankle brachial stenosis and HDL-cholesterol were lower than the normal control group, so the pancreatic steatosis harmful to blood vessels.(P <0.05). The difference between the control group and it was confirmed that the pancreatic jibanggun statistically significant. In conclusion, pancreatic steatosis at abdominal ultrasound can predict the risk of metabolic diseases, and there was a correlation with cardiovascular disease.

• Culinary science and hospitality research
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• v.23 no.6
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• pp.173-183
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• 2017

Conditions related to body composition and aging, such as osteopenic obesity, sarcopenia/ sarcopenic obesity, and the newly termed osteosarcopenic obesity(triad of bone, muscle and adipose tissue impairment), are beginning to gain recognition. Currently, it has begun to attract the attention of scholars from all over the world, however, for this disease, it still needs a more clear understanding and perception. Therefore, this article considered the osteoporosis, muscle depression, and obesity, these diseases as a gate to study the relationship among muscle, bone, and fat. In addition, in the aging process, the formation of IGF-cortisol, testosterone, and estrogen is sensitive. These hormones can not only absorb muscle protein metabolism, but also affect alienation. The decrease in IGF-cortisol in the elderly resulted in increased visceral fat, decreased muscle mass and bone mineral density, and then affected decreased skeletal muscle atrophy and decreased quality. The reduction of skeletal muscle quality and strength and increase body fat affected the adipose tissue to produce inflammatory cytokines, thereby reduced skeletal muscle, promoted cardiovascular disease, metabolic syndrome and insulin resistance in chronic diseases. Almost all chronic inflammatory diseases were associated with bone, muscle and fat. These mechanisms were complex and interrelated. Inflammation reduces bone formation, increases fat and reduces muscle mass. And thus not only had a significant impact on the motor system, but also made the incidence increase of fracture, osteoporosis, fragile syndrome, fall, osteomalacia and other bone disease. This article aimed to start from the interaction between the muscles and bones of the elderly, extended to obesity, muscle deficiency, osteoporosis and other diseases, finally, from a nutritional point of view, to discuss how to treat osteoporosis obesity.

• Journal of Dairy Science and Biotechnology
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• v.28 no.1
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• pp.17-28
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• 2010

A substantial body of evidence has emerged over the last decade in support of the novel concept that dietary calcium and dairy foods play an important role in regulating energy metabolism and thereby promote healthy weight management and reduce obesity risk. This concept has been demonstrated in experimental animals studies, cross-sectional and prospective population studies and a number of randomized clinical trials. Notably, the effects of dairy foods in weight management are more consistent than the effects of supplemental calcium across clinical trials, and calcium per se is responsible for approximately 40-50% of the effects of dairy. The calcium component is only effective in individuals with chronically low calcium intake, as it serves to prevent the endocrine response to low calcium diets which otherwise favors adipocyte energy storage; calcium also serves to promote energy loss via formation of calcium soaps in the gastrointestinal tract and thereby reduce fat absorption. The calcium-independent anti-obesity bioactivity of dairy resides primarily in whey. The key components identified to date are leucine and bioactive peptides resulting from whey protein digestion. The high concentration of leucine in whey stimulates a repartitioning of dietary energy from adipose tissue to skeletal muscle where it provides the energy required for leucine-stimulated protein synthesis, resulting in increased loss of adipose tissue and preservation of skeletal muscle mass during weight loss. Finally, dairy rich diets suppress the oxidative and inflammatory responses to obesity and thereby attenuate the diabetes and cardiovascular disease risk associated with obesity.

• Biomedical Science Letters
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• v.24 no.4
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• pp.311-318
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• 2018

Vitamin C (ascorbic acid) supplementation has been suggested to negatively correlate with obesity in humans and other animals. Previous studies, including ours, have demonstrated that a high-fat diet (HFD) induces obesity and related diseases such as hyperlipidemia, hyperglycemia, insulin resistance, and nonalcoholic fatty liver disease. Here, we investigated the effects of vitamin C on visceral adipocyte hypertrophy and glucose intolerance in C57BL/6J mice. Mice received a low-fat diet (LFD, 10% kcal fat), HFD (45% kcal fat), or the same HFD supplemented with vitamin C (HFD-VC, 1% w/w) for 15 weeks. Visceral adiposity and glucose intolerance were examined using metabolic measurements, histology, and gene expression analyses. Mice in the HFD-VC supplementation group had reduced body weight, mesenteric fat mass, and mesenteric adipocyte size compared with HFD-fed mice. Vitamin C intake in obese mice also decreased the mRNA levels of lipogenesis-related genes (i.e., stearoyl-CoA desaturase 1 and sterol regulatory element-binding protein 1c) in mesenteric adipose tissues, inhibited hyperglycemia, and improved glucose tolerance. In addition, vitamin C attenuated the HFD-induced increase in the size of pancreatic islets. These results suggest that vitamin C suppresses HFD-induced visceral adipocyte hypertrophy and glucose intolerance in part by decreasing the visceral adipose expression of genes involved in lipogenesis.

• Journal of the Korean Applied Science and Technology
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• v.36 no.1
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• pp.34-46
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• 2019

Obesity is frequently associated with metabolic disease. This study showed whether fenofibrate, a hypolipidemic agent, swimming and swimming combined with fenofibrate (: combination) regulate obesity, and whether combination is more effective than fenofibrate on regulation of obesity in high-fat diet-fed mice for 8 weeks. Both fenofibrate and swimming decreased obesity-associated factors such as body weight, adipose tissue mass, serum lipid levels and adipoctye size, compared with control mice. When mice were concomitantly treated with fenofibrate and swimming, combination reduced further the inhibitory effects on obesity-associated factors, compared with fenofibrate. Both fenofibrate, swimming and combination decreased serum glucose levels, compared with control mice. The evidence is presented herein that combination were effective to control obesity and serum glucose levels, suggesting that swimming combined with fenofibrate might contribute to inhibition of high-fat diet fed-induced metabolic syndrome.