• Biomedical Science Letters
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• v.11 no.2
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• pp.89-101
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• 2005

Obesity is increasing worldwide and has become a major health burden in Western societies affecting every third American and every fifth European. Obesity makes a major contribution to morbidity and mortality, predisposing individuals to cardiovascular disease and diabetes. Many new substances are currently being investigated for their usefulness in the pharmacotherapy of obesity. Most anti-obesity drugs can be divided into four groups: those that reduce food intake; those that alter metabolism; those that increase thermogenesis; and those that regulate hormone involved in feeding behavior. In this article we review these and other agents available in various countries for the treatment of obesity. Perhaps more importantly, we have focussed on areas of potential productivity in the future. Over the last 5 or so years, this impetus in obesity research has provided us with exciting new drugs targets involved in the regulation of feeding behavior and cellular mechanism involved in energy expenditure. Recent development in the quest for control of human obesity include the discovery of hormones, neuropeptides, receptors and transcription factors involved in feeding behavior, metabolic rate and adipocyte development. For developing new, perhaps even more specific pharmacological agents, further research is needed to understand the individual different genetic and physiological basis of obesity. It remains the hope of research scientists that in the not too distant future we shall see a new class of anti-obesity drugs arising logically from the molecular biology revolutions.

• Journal of Korean Medicine for Obesity Research
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• v.3 no.1
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• pp.95-105
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• 2003

The obesity is the matter of the energy balance in essential. The energy balance in human body is energy expenditure subtracted from energy intake. The energy intake is mainly supplied by carbohydrates, proteins and lipids in food, and the energy expenditure is composed of basal metabolic rate or resting energy expenditure, physical activity and thermogenesis including diet-induced thermogenesis. The resting energy expenditure is measured by direct calorimetry and indirect calorimetry. Generally we can simply use predictive equation with the variables of weight, height, age and fat-free mass to yield metabolic rate. But there is discrepancy between the estimate and real metabolic rate because the equations can not reflect individuality and environments. The resting energy expenditure is influenced by many factors but the fundamental factor is fat-free mass. We briefly reviewed the concept and evaluation of the energy balance, intake and expenditure, which are important parts in the study of obesity. Finally, we surveyed the correlation between metabolic rate and obesity and suggested applicable herb medication to increase metabolic rate.

• Archives of Obesity and Metabolism
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• v.3 no.1
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• pp.35-42
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• 2024

Serotonin, a biogenic amine widely found in many organisms, functions as both a neurotransmitter and hormone. Although serotonin is involved in various physiological processes, this study aimed to review its role in energy metabolism. Given that serotonin cannot cross the blood-brain barrier and is synthesized by two different isoforms of tryptophan hydroxylase in the central nervous system (CNS) and peripheral tissues, it is reasonable to assume that serotonin in the CNS and peripheral tissues functions independently. Recent studies have demonstrated how serotonin influences energy metabolism in metabolic target organs such as the intestines, liver, pancreas, and adipose tissue. In summary, serotonin in the CNS induces satiety and appetite suppression, stimulates thermogenesis, and reduces body weight. Conversely, serotonin in the periphery increases intestinal motility, stimulates gluconeogenesis in the liver, suppresses glucose uptake by hepatocytes, promotes fat uptake by liver cells, stimulates insulin secretion while suppressing glucagon secretion in the pancreatic islets, promotes lipogenesis in white adipose tissue, inhibits lipolysis and browning of white adipose tissue, and suppresses thermogenesis in brown adipose tissue, thereby storing energy and increasing body weight. However, considering that most experimental results were obtained using mice and conducted under specific nutritional conditions, such as high-fat diets, whether serotonin acts in the same way in humans, whether it will act similarly in individuals with normal versus obese weights, and whether its effects vary depending on the type of food consumed, remain unknown.

• Journal of Applied Biological Chemistry
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• v.66
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• pp.186-196
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• 2023

Dyglomera^® is an aqueous ethanol extract derived from the fruit and pods of Dichrostachys glomerata. A previous study has revealed that Dyglomera regulates adipogenesis and lipolysis by modulating AMP-activated protein kinase (AMPK) phosphorylation and increased expression levels of lipolysis-related proteins in white adipose tissue of high fat diet-induced mice and 3T3-L1 adipocyte cells. To further investigate mechanisms of Dyglomera, additional studies were performed using 3T3-L1 cells. Results revealed that Dyglomera downregulated adipogenesis by inhibiting the protein kinase B/mammalian target of rapamycin signaling pathway and reconfirmed that it downregulated gene expression levels of proliferator-activated receptor (PPAR)-γ, CCAAT enhancer binding protein α, sterol-regulation element-binding protein-1c. Dyglomera also reduced adipokines such as tumor necrosis factor alpha, interleukin-1β, and interleukin 6 by regulating leptin expression. Moreover, Dyglomera promoted beige-and-brown adipocyte-related phenotypes and regulated metabolism by increasing mitochondrial number and expression levels of genes such as T-box protein 1, transmembrane protein 26, PR domain 16, and cluster of differentiation 40 as well as thermogenic factors such as uncoupling protein 1, proliferator-activated receptor-gamma co-activator-1α, Sirtuin 1, and PPARα through AMPK activation. Thus, Dyglomera not only can inhibit adipogenesis, but also can promote lipolysis and thermogenesis and regulate metabolism by affecting adipokine secretion from 3T3-L1 adipocytes.

• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.4
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• pp.474-483
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• 2016

Enzymatically modified isoquercitrin (EMIQ) is a mixture of quercetin glycodsides consisting of isoquercitrin and its ${\alpha}-glucosylated$ derivatives containing one to seven additional linear glucose moieties. The aim of this study was to assess whether or not EMIQ attenuates high-fat diet (HFD)-induced body weight gain and changes in plasma indices of obesity in mice. Male C57BL/6N mice were fed chow diet, HFD, and HFD containing 1.2% EMIQ for 10 weeks. EMIQ significantly (P<0.05) reduced body weight gain (-21%), total visceral fat-pad weights (-31%), and plasma levels of triglycerides (-17%), total cholesterol (-19%), and free fatty acids (-26%) in HFD-fed mice. EMIQ significantly increased protein kinase A (PKA) expression in the epididymal adipose tissue of HFD-fed mice. Expression of adipogenesis-related genes significantly decreased, whereas expression of fatty acid oxidation-related and thermogenesis-related genes increased in epididymal adipose tissue of EMIQ-fed mice compared with HFD-fed mice. These results suggest that the protective effects of EMIQ against HFD-induced adiposity in mice appear to be associated with PKA-mediated signaling cascades involved in adipogenesis, fatty acid oxidation, and thermogenesis in adipose tissue.

• Journal of Nutrition and Health
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• v.57 no.2
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• pp.171-184
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• 2024

Purpose: Although activating thermogenic adipocytes is a promising strategy to reduce the risk of obesity and related metabolic disorders, emerging evidence suggests that it is difficult to induce adipocyte thermogenesis in obesity. Therefore, this study aimed to investigate the regulation of adipocyte thermogenesis in diet-induced obesity. Methods: Adipose progenitor cells were isolated from the white and brown adipose tissues of control diet (CD) or high-fat diet (HFD) fed mice, and fully differentiated white and brown adipocytes were treated with β-agonists or 18-carbon fatty acids for β-adrenergic activation or peroxisome proliferator-activated receptor (PPAR) activation. Results: Compared to the CD-fed mice, the expression of uncoupling protein 1 (Ucp1) was lower in the white adipose tissue of the HFD-fed mice; however, this was not observed in the brown adipose tissue. The expression of peroxisome proliferator-activated receptor gamma (Pparg) was lower in the brown adipose progenitor cells isolated from HFD-fed mice than in those isolated from the CD-fed mice. Norepinephrine (NE) treatment exerted lesser effect on peroxisome proliferator-activated receptor-γ coactivator (Pgc1a) upregulation in white adipocytes derived from HFD-fed mice than those derived from CD-fed mice. Regardless which 18-carbon fatty acids were treated, the expression levels of thermogenic genes including Ucp1, Pgc1a, and positive regulatory domain zinc finger region protein 16 (Prdm16) were higher in the white adipocytes derived from HFD-fed mice. Oleic acid (OLA) and γ-linolenic acid (GLA) upregulated Pgc1a expression in white adipocytes derived from HFD-fed mice. Brown adipocytes derived from HFD-fed mice had higher expression levels of Pgc1a and Prdm16 compared to their counterparts. Conclusion: These results indicate that diet-induced obesity may downregulate brown adipogenesis and NE-induced thermogenesis in white adipocytes. Also, HFD feeding may induce thermogenic gene expression in white and brown primary adipocytes, and OLA and GLA could augment the expression levels.

• Journal of applied mathematics & informatics
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• v.9 no.2
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• pp.731-744
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• 2002

The temperature distribution in human skin and subdermal tissue layer is presented using bioheat transfer equation. The body temperature is determined by the balance between heat produced and heat lost by our body. The time-dependent solutions have been found to be affected by the metabolic heat generation rate, blood mass flow, the rate of evaporation of perspiration and also by the atmospheric temperature. The analytic solutions for different layers have been calculated numerically and are also shown graphically.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.262.1-262.1
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• 2002

Uncoupling proteins (UCPs) are transmembrane proton transporters present in the mitochondria. In UCPs. UCP1 and UCP3 play an important role in adaptive thermogenesis by uncoupling mitochondrial oxidation of substrates from ATP synthesis. PPARg coactivator 1(PGC-1) regulates transcriptional activity of PPARg and other nuclear receptors and controls the expression of UCPs. (omitted)

• Journal of Microbiology and Biotechnology
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• v.33 no.1
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• pp.96-105
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• 2023

Probiotic supplements have promising therapeutic effects on chronic diseases. In this study, we demonstrated the anti-obesity effects of two potential probiotics, Bifidobacterium bifidum DS0908 (DS0908) and Bifidobacterium longum DS0950 (DS0950). Treatment with DS0908 and DS0950 postbiotics significantly induced the expression of the brown adipocyte-specific markers UCP1, PPARγ, PGC1α, PRDM16 and beige adipocyte-specific markers CD137, FGF21, P2RX5, and COX2 in C3H10T1/2 mesenchymal stem cells (MSCs). In mice with high-fat diet (HFD)-induced obesity, both potential probiotics and postbiotics noticeably reduced body weight and epididymal fat accumulation without affecting food intake. DS0908 and DS0950 also improved insulin sensitivity and glucose use in mice with HFD-induced obesity. In addition, DS0908 and DS0950 improved the plasma lipid profile, proved by reduced triglyceride, low-density lipoprotein, and cholesterol levels. Furthermore, DS0908 and DS0950 improved mitochondrial respiratory function, confirmed by the high expression of oxidative phosphorylation proteins, during thermogenesis induction in the visceral and epididymal fat in mice with HFD-induced obesity. Notably, the physiological and metabolic changes were more significant after treatment with potential probiotic culture-supernatants than those with the bacterial pellet. Finally, gene knockdown and co-treatment with inhibitor-mediated mechanistic analyses showed that both DS0908 and DS0950 exerted anti-obesity-related effects via the PKA/p38 MAPK signaling activation in C3H10T1/2 MSCs. Our observations suggest that DS0908 and DS0950 could potentially alleviate obesity as dietary supplements.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2023.04a
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• pp.46-46
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• 2023

It has been reported that Rosa acicularis has anti-obesity activity by inhibiting the digestive lipase activity. However, there is a lack of clear in vitro studies regarding the anti-obesity activity of Rosa acicularis. Therefore, in this study, we aimed to verify the anti-obesity activity of Rosa acicularis leaves (RAL) and elucidate its mechanism of action in 3T3-L1 preadipocytes. RAL dose-dependently inhibited the accumulation of lipid droplets and triacylglycerol. RAL had no effect on cell proliferation and survival in undifferentiated 3T3-L1 cells, but it inhibited cell proliferation in differentiating 3T3-L1 cells. RAL increased ATGL, p-HSL, and HSL, and decreased perilipin-1 in differentiating 3T3-L1 cells. In addition, RAL reduced lipid droplet accumulation and increased free glycerol content in differentiated 3T3-L1 cells. RAL increased ATGL and HSL in differentiated 3T3-L1 cells. Also, RAL increased p-AMPK, PPARγ, UCP-1, and PGC-1α in differentiating 3T3-L1 cells. AMPK inhibition by Compound C attenuated RAL-mediated increase of ATGL, HSL, PPARγ, and UCP-1 in 3T3-L1 cells. Taken together, it is thought that RAL may inhibit lipid accumulation through lipolysis and thermogenesis via the activation of AMPK in adipocytes.