• Biomedical Science Letters
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• v.9 no.4
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• pp.215-222
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• 2003

As the obesity has been known to be related with the hyperlipidemia, cardiovascular disease, cerebral apoplexy, fatty liver, and other chronic diseases, recent researches have focused on the functional food materials and their anti-obesity activities. This study was performed to study the effects of vanilloid family capsaicin, major pungent ingredient of hot chillies and peppers, on anti-obesity activities. ICR male mice were fed one of the pellet diet, basal diet, and high fat diet with capsaicin (45 $\mu\textrm{g}$/day) solution for 5 days. Mice in the corresponding control groups were given water for 5 days. In results, capsaicin reduced body weights in any diet groups. Percent weight and cell size of the abdominal white adipose tissue in mice on the high fat diet with capcaicin were significantly lower compared with those in mice on the high fat diet with water. However, percent brown adipose tissue weight per body weight in mice on the high fat diet was not affected by capsaicin. Capsaicin reduced the levels of s-triglyceride and s-total cholesterol in the pellet diet or high fat diet groups. There was no difference in the s-protein levels between the capsaicin group and the control water group. These data indicate that 1) orally administered capsaicin has a reducing effect on the blood triglyceride and total cholesterol levels, and 2) capsaicin has lowering effects on the body weight, percent weight and cell size of the abdominal white adipose tissue.

• Preventive Nutrition and Food Science
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• v.8 no.1
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• pp.105-112
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• 2003

Animals possess a highly sophisticated mechanism of storing energy in adipose tissue inside their bodies. However, in humans it has been clarified that adipocyte (fat cell), which composes the body fat (adipose) tissues, development and the extent of subsequent fat accumulation are closely associated with the occurrence and advancement of various common diseases (e.g., type-2 diabetes, coronary artery disease, and hypertension) resulting from obesity. Recent exciting progress in clinical and biochemical studies of adipocytes has rapidly clarified the functions of adipocytes and adipose tissue. Interesting findings are the function of white adipocytes as "secreting cells" and the molecular mechanism undelying adipocyte differentiation at the transcriptional level in relation to nuclear receptors. Consequently, the adipose tissue is being targeted for the prevention or treatment of many common diseases. In this review, I will focus on recent information on characteristics of adipocytes and the relationship between obesity and common obesity-related diseases. diseases.

• BMB Reports
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• v.53 no.3
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• pp.142-147
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• 2020

Lipid accumulation in white adipose tissue is the key contributor to the obesity and orchestrates numerous metabolic health problems such as type 2 diabetes, hypertension, atherosclerosis, and cancer. Nonetheless, the prevention and treatment of obesity are still inadequate. Recently, scientists found that brown adipose tissue (BAT) in adult humans has functions that are diametrically opposite to those of white adipose tissue and that BAT holds promise for a new strategy to counteract obesity. In this study, we evaluated the potential of sinapic acid (SA) to promote the thermogenic program and lipolysis in BAT. SA treatment of brown adipocytes induced the expression of brown-adipocyte activation-related genes such as Ucp1, Pgc-1α, and Prdm16. Furthermore, structural analysis and western blot revealed that SA upregulates protein kinase A (PKA) phosphorylation with competitive inhibition by a pan-PKA inhibitor, H89. SA binds to the adenosine triphosphate (ATP) site on the PKA catalytic subunit where H89 binds specifically. PKA-cat-α1 gene-silencing experiments confirmed that SA activates the thermogenic program via a mechanism involving PKA and cyclic AMP response element-binding protein (CREB) signaling. Moreover, SA treatment promoted lipolysis via a PKA/p38-mediated pathway. Our findings may allow us to open a new avenue of strategies against obesity and need further investigation.

• Journal of the Korea Institute of Information and Communication Engineering
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• v.17 no.12
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• pp.2995-3000
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• 2013

We investigated the effects of testosterone on the improvement of white adipose tissue explant and its molecular mechanism in adipose tissue of high fat diet-fed male castrated (CAST) mice. The CAST mice treated with testosterone had lower adipose tissue weights, the average size of adipocytes and mRNA levels of $C/EBP{\alpha}$ as well as adipocyte marker genes than the vehicle-treated CAST mice. These results suggest that testosterone prevent the expression of $C/EBP{\alpha}$ and $C/EBP{\alpha}$-mediated adipocyte marker genes, resulting in decreased adipose tissue mass and adipocyte metabolism in male CAST mice. Moreover, this study give a valuable molecular and biological knowledge on testosterone therapy in obese hypogonadal men.

• Biomedical Science Letters
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• v.14 no.3
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• pp.139-146
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• 2008

The peroxisome proliferator-activated receptor ${\gamma}$ $(PPAR{\gamma})$ plays a central role in adipogenesis and lipid storage. The $(PPAR{\gamma})$ ligands, thiazolidinediones (TZDs), enhance in vitro adipogenesis in several cell types, but the role of the TZDs on in vivo adipogenesis is still poorly understood. To investigate how $PPAR{\gamma}$ ligand troglitazone regulates adipogenesis in female mice, we examined the effects of the troglitazone on adipose tissue mass, morphological changes of adipocytes, and the expression of $PPAR{\gamma}$ target and adipocyte-specific genes in low fat diet-fed female C57BL/6 mice. Administration of troglitazone for 13 weeks did not change body and total white adipose tissue weights compared with control mice. Troglitazone treatment also did not cause a significant decrease in the average size of adipocytes in parametrial adipose tissue although it is reported to increase the number of small adipocytes in male animals. Troglitazone did not affect the mRNA expression of $PPAR{\gamma}$ and its target genes as well as adipocyte-specific genes in parametrial adipose tissue. These results suggest that $PPAR{\gamma}$ does not seem to be associated with adipogenesis in females with functioning ovaries and that its inability to induce adipogenesis may be due to sex-related factors.

• Journal of Pharmacopuncture
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• v.20 no.4
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• pp.235-242
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• 2017

Irisin is a novel hormone like polypeptide that is cleaved and secreted by an unknown protease from fibronectin type III domain-containing protein 5 (FNDC5), a membrane-spanning protein and which is highly expressed in skeletal muscle, heart, adipose tissue, and liver. Since its discovery in 2012, it has been the subject of many researches due to its potent physiological role. It is believed that understanding irisin's function may be the key to comprehend many diseases and their development. Irisin is a myokine that leads to increased energy expenditure by stimulating the 'browning' of white adipose tissue. In the first description of this hormone, increased levels of circulating irisin, which is cleaved from its precursor fibronectin type III domain-containing protein 5, were associated with improved glucose homeostasis by reducing insulin resistance. Irisin is a powerful messenger, sending the signal to determine the function of specific cells, like skeletal muscle, liver, pancreas, heart, fat and the brain. The action of irisin on different targeted tissues or organs in human being has revealed its physiological functions for promoting health or executing the regulation of variety of metabolic diseases. Numerous studies focus on the association of irisin with metabolic diseases which has gained great interest as a potential new target to combat type 2 diabetes mellitus and insulin resistance. Irisin is found to improve insulin resistance and type 2 diabetes by increasing sensitization of the insulin receptor in skeletal muscle and heart by improving hepatic glucose and lipid metabolism, promoting pancreatic ${\beta}$ cell functions, and transforming white adipose tissue to brown adipose tissue. This review is a thoughtful attempt to summarize the current knowledge of irisin and its effective role in mediating metabolic dysfunctions in insulin resistance and type 2 diabetes mellitus.

• Journal of Microbiology and Biotechnology
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• v.27 no.4
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• pp.660-667
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• 2017

PineXol, extracted from Korean red pine bark, has beneficial effects, such as antioxidant, antiinflammatory, and antilipogenic activities in vitro. We tested the hypothesis that PineXol supplementation could have anti-obesity effects on mice fed a high-fat diet (HFD). Four-week-old male C57BL/6 mice were fed normal chow (18% kcal from fat) or a HFD (60% kcal from fat). HFD-fed animals were also subjected to PineXol treatment at a dose of 10 or 50 mg/kg body weight (BW) (PX10 or PX50, respectively) body weight. The body weight and body fat mass in the PX50 group were statistically lower than those in the HFD group (p < 0.05 and p < 0.001, respectively). The concentration of hepatic triglycerides, total cholesterol, and low-density lipoprotein cholesterol were reduced in the PX50 group compared with the HFD group (p < 0.01). Acetyl CoA carboxylase (p < 0.01), elongase of very long chain fatty acids 6 (p < 0.01), stearoyl CoA desaturase 1 (p < 0.05), microsomal triglyceride transfer protein (p < 0.01), and sterol regulatory element-binding protein 1 (p < 0.05) were significantly decreased in the PX50 group compared with that in the HFD group. In white adipose tissue, CCAAT-enhancer-binding protein alpha (p < 0.05), peroxisome proliferator-activated receptor gamma (p < 0.001), and perilipin (p < 0.01) were decreased in the PX50 group compared with those in the HFD group. Therefore, the current study implies the potential of PineXol for the prevention and/or amelioration of obesity, in part by inhibition of both hepatic lipid synthesis and adipogenesis in white adipose tissue.

• Preventive Nutrition and Food Science
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• v.16 no.3
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• pp.210-216
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• 2011

Capsaicin is a pungent component of red pepper, which is widely consumed as food adjuncts. The present study was performed to investigate anti-obesity effects of capsaicin in diet-induced obese rats. Male Sprague-Dawley rats (n=14) were fed with a high-fat diet (Control) or high-fat diet containing 0.016% capsaicin (w/w) (Capsaicin) for 8 weeks. The final body weight and the mass of white adipose tissue were significantly lower in capsaicin supplemented group compared to control. Dietary capsaicin ameliorated lipid profiles with decrease in the plasma concentrations of triglycerides and total cholesterol, and decrease in the levels of total lipids and triglycerides in the liver. Activity of glycerol-3-phosphate dehydrogenase (GPDH), an indicator of triglyceride biosynthesis in white adipose tissue, decreased by 35% in the group supplemented with capsaicin. However, consumption of capsaicin increased the expression of uncoupling protein 2 (UCP2) in white adipose tissue, which is related to energy consumption. Our data suggests that capsaicin may reduce body weight and fat accumulation in high fat diet-induced obese rats. These effects may be mediated, at least partially, by the upregulation of UCP2 gene expression and its ability to inhibit GPDH activity.

• Journal of Life Science
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• v.29 no.8
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• pp.922-940
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• 2019

Obesity, represented by abnormal fat accumulation due to an imbalance between energy intake and expenditure, is a major public health issue worldwide, leading to multiple noncommunicable diseases, including atherosclerosis, hypertension, type 2 diabetes, and cancer. Diverse solutions have been proposed to combat obesity. Attention has focused on two types of adipose tissues as a promising therapeutic target in obesity: traditional brown and beige or brite. Unlike energy-storing white adipose (endocrine) tissue, traditional brown adipose tissue and beige adipose tissue have energy-dissipating thermogenic properties. Both types of tissue are present in adult humans and inducible through external stimuli, such as cold exposure, ${\beta}3$-adrenergic receptor agonists, and phytochemicals. Among these stimuli, microbiota present in the human intestinal tract participate in multiple metabolic activities. Modulation of gut microbiota may offer a potent and possibly curative strategy against various metabolic diseases. Numerous studies have focused on the effects of established antiobesity treatments on the gut microenvironment or brown-adipose-tissue activation. In this review, we focus mainly on stimuli known to alleviate obesity, weight gain, and metabolic diseases, in addition to known and possible inter-relations between gut microbiota modulation and similar interventions and adipose tissue browning. The findings may pave the way toward new strategies against obesity.

• Journal of Nutrition and Health
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• v.57 no.4
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• pp.376-388
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• 2024

Purpose: Adipocyte dysfunction has been reported in diabetes, and stimulating thermogenesis and suppressing senescence in adipocytes potentially alleviates metabolic dysregulation. This study aimed to investigate thermogenesis and cellular senescence in diabetic adipocytes under basal conditions and in response to stimuli. Methods: White and brown primary adipocytes derived from control (CON) and db/db (DB) mice were treated with β-agonists, such as norepinephrine (NE) and CL316,243, and 18-carbon fatty acids, including stearic acid, oleic acid (OLA), linoleic acid (LNA), and α-linolenic acid, and the expression of the genes related to thermogenesis and cellular senescence was measured. Results: Although no difference in the thermogenic and cellular senescence gene expression in white adipose tissue (WAT) was noted between the CON and DB mice, brown adipose tissue (BAT) from the DB mice exhibited lower uncoupling protein 1 (Ucp1) expression and higher cyclin-dependent kinase inhibitor (Cdkn)1a and Cdkn2a expression levels compared to that from the CON mice. Stromal vascular cells isolated from the BAT of the DB mice displayed higher peroxisome proliferator-activated receptor gamma (Pparg), CCAAT/enhancer-binding protein alpha (Cebpa), Cdkn1a, and Cdkn2a expression levels. White adipocytes from the DB mice exhibited lower Ucp1, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (Pgc1a), and PR domain containing 16 (Prdm16) expression levels regardless of β-agonist treatment. NE upregulated Pgc1a in both white and brown adipocytes from the CON mice, but not in those from the DB mice. Although none of the fatty acids were observed to downregulate the cellular senescence genes in fully differentiated adipocytes, the OLA-treated brown adipocytes derived from DB mice exhibited lower Cdkn1a and Cdkn2b expression levels than the LNA-treated cells. Conclusion: These results indicate that the lower thermogenic capacity of diabetic adipocytes may be related to their cellular senescence, and different fatty acids potentially exert divergent effects on the expression of cellular senescence genes.