• Molecules and Cells
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• v.47 no.2
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• pp.100030.1-100030.14
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• 2024

Both brown and white adipose tissues (BAT/WAT) are innervated by the peripheral nervous system, including efferent sympathetic nerves that communicate from the brain/central nervous system out to the tissue, and afferent sensory nerves that communicate from the tissue back to the brain and locally release neuropeptides to the tissue upon stimulation. This bidirectional neural communication is important for energy balance and metabolic control, as well as maintaining adipose tissue health through processes like browning (development of metabolically healthy brown adipocytes in WAT), thermogenesis, lipolysis, and adipogenesis. Decades of sensory nerve denervation studies have demonstrated the particular importance of adipose sensory nerves for brown adipose tissue and WAT functions, but far less is known about the tissue's sensory innervation compared to the better-studied sympathetic nerves and their neurotransmitter norepinephrine. In this review, we cover what is known and not yet known about sensory nerve activities in adipose, focusing on their effector neuropeptide actions in the tissue.

• Journal of the Korean Applied Science and Technology
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• v.37 no.3
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• pp.385-397
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• 2020

This study investigated whether swimming exercises improves obesity through regulation of angiogenesis in white adipose tissue. Female mice with high-fat diets were divided into sham-operated group (Sham), ovariectomized group (OVX), and swim-trained ovariectomized group (OVX + Swim). Compared to the Sham, OVX increased body weight, adipose tissue mass and size of adipocyte. However, these factors (: such as body weight, adipose tissue mass and size of adipocyte) of OVX + Swim decreased compared with OVX. Compared with the Sham, OVX increased the mRNA expression of angiogenic activator and MMPs and decreased the mRNA expression of angiogenic inhibitors in white adipose tissue. But OVX + Swim decreased the mRNA expression of angiogenic activator and MMPs and increased the mRNA expression of angiogenic inhibitors in white adipose tissue, compared with the OVX. Theses results suggested that swimming exercises the angiogenesis in white adipose tissue, resulting to improve obesity in high-fat diet-fed female OVX mice.

• Biomedical Science Letters
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• v.18 no.3
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• pp.227-236
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• 2012

Previous study showed that swimming improved obesity but was not through $PPAR{\alpha}$ activation in liver and skeletal muscle in high fat diet-fed female mice with functioning ovaries as an animal model of obese premenopausal women. Thus, this study was aimed at investigation of the effects of swimming on the promotion of health and its molecular mechanism in adipose tissue of high fat diet-fed female mice. Eight-week-old female C57BL/6J mice were randomly divided into two groups (a non-swim control group and a swim group, n=8/group). Mice in the swim group swam for 2 h daily for 6 weeks in water bath with temperature of $35{\pm}1^{\circ}C$. All the animals received high fat diet (45% kcal fat) for 6 weeks. Reverse transcription-polymerase chain reaction was used to elucidate the molecular mechanism. Female mice subjected to swimming had significantly decreased body weight gain and white adipose tissue mass compared with the female control mice. Histological studies illustrated that swimming decreases the hepatic lipid accumulation. As expected, swimming did not affect the expression of mRNA levels of peroxisome proliferator-activated receptor (PPAR) ${\alpha}$ and $PPAR{\alpha}$ target genes responsible for mitochondrial fatty acid ${\beta}$-oxidation, such as carnitine palmitoyltransgerase-1 and medium chain acyl-CoA dehydrogenase in the white adipose tissue. However, mice that underwent 6-weeks of swimming exercise had decreased the mRNA expression of lipogenic genes, such as sterol regulatory element-binding proteins-1C and fatty acid synthase in comparison to sedentary control mice, with decreased $PPAR{\gamma}$ target genes involved in adipocyte-specific marker genes, such as adipocyte fatty acid binding protein and leptin in the white adipose tissue. These results suggest that swimming can effectively prevent obesity induced by high fat diet-fed, in part through down-regulation of adipogenesis and lipogenesis in white adipose tissue of female obese mice. Moreover, these results suggest that swimming maybe contributing the promotion of health through regulation of adipogenesis and lipogenesis in overweight premenopausal women.

• Food Science and Industry
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• v.50 no.1
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• pp.26-35
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• 2017

Obesity is a worldwide problem that is associated with metabolic disorders. Obesity is caused by the accumulation of an abnormal amount of body fat in adipose tissue. Adipose tissue is a major metabolic organ, and it has been classified as either white adipose tissue (WAT) or brown adipose tissue (BAT). WAT and BAT are characterized by different anatomical locations, morphological structures, functions, and gene expression patterns. WAT is mainly involved in the storage and mobilization of energy in the form of triglycerides. On the other hand, BAT specializes in dissipating energy as heat through uncoupling protein-1 (UCP-1)-mediated non-shivering thermogenesis. Novel type of brown-like adipocyte within WAT called beige/brite cells was recently discovered, and this transdifferentiation process is referred to as the "browning" or "britening" of WAT. Recently, Brown fat and/or browning of WAT have been highlights as a new therapeutic target for treatment of obesity and its related metabolic disorders. Here, we describe recent advances in the study of BAT and browning of WAT, focusing on proteomic approaches.

• Journal of the Korean Applied Science and Technology
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• v.40 no.5
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• pp.925-935
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• 2023

It was investigated whether PPARα activator more effectively inhibits angiogenesis of white adipose tissue in exercise mice that ate high fat diet compared to non-exercise mice that ate high fat diet. Male mice were randomly divided into a control group not treated with a PPARα activator fenofibrate and exercise (Con), a group treated with fenofibrate alone (FF), a group treated with exercise alone (Ex), and a group treated with a combination of fenofibrate and exercise (Ex+FF). (Ex+FF). All mice was fed high-fat diet for 8 weeks. The weight of white adipose tissue and the size of white adipocytes decreased in FF, Ex, and Ex+FF compared to Con, and decreased more in Ex+FF Ex+FF compared to FF. In white adipose tissue, the gene expression of MMPs and angiogenic factors decreased in FF, Ex, and Ex+FF compared to Con, and more decreased in Ex+FF compared to FF. On the other hand, gene expression of angiogenic inhibitors increased in FF, Ex and Ex+FF compared to Con, and increased more in Ex+FF compared to FF. Therefore, this study revealed that the combined treatment of fenofibrate and exercise effectively inhibits the angiogenesis of white adipose tissue, reducing the increase in white adipose tissue and suppressing abdominal obesity, rather than the single treatment of fenofibrate.

• Biomedical Science Letters
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• v.13 no.2
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• pp.91-97
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• 2007

Obesity is defined as increased mass of adipose tissue, conferring a higher risk of cardiovascular and metabolic disorders such as diabetes, hyperlipidemia, and coronary heart disease. To get a better understanding of the role of a male sex hormone testosterone on obesity, we thus measured the effects of testosterone on white adipose tissue (WAT) mass, adipocyte histology and hepatic lipid accumulation in male castrated (CAST) C57BL/6J mice. Compared to male CAST control mice, testosterone-treated mice had the decreased WAT mass and the increased the number of adipocytes. Especially, histological data showed that the adipocyte size was reduced in a dose-dependent manner and was most effective at dose 150 $\mu$g per mouse for testosterone. In addition, the administration of testosterone resulted in the inhibition of hepatic lipid accumulation compared with control mice. Our results suggest that testosterone regulates adipocytes development and hepatic lipid metabolism, resulting in the prevention of obesity in male CAST mice.

• Biomedical Science Letters
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• v.15 no.3
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• pp.171-177
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• 2009

This study investigated whether increased adiposity is prevented by estrogen replacement in female ovariectomized (OVX) C57BL/6J mice, an animal model of human menopause and whether these metabolic changes reflect the inhibitory action of estrogen on peroxisome proliferator-activated receptor $\gamma$ ($PPAR{\gamma}$)-regulated gene expression. Treatment of $17{\beta}$-estradiol for the last one week of the experiment decreased high fat diet-induced body weight gain and white adipose tissue mass compared to OVX control mice. Histological analysis showed that administration of $17{\beta}$-estradiol to mice decreased the size of adipocytes in parametrial adipose tissue versus OVX control mice. In addition, $17{\beta}$-estradiol reduced the adipose expression of $PPAR{\gamma}$ as well as $PPAR{\gamma}$ target genes such as adipocyte fatty acid binding protein and tumor necrosis factor $\alpha$. These results suggest that $17{\beta}$-estradiol may inhibit adiposity through reducing the $PPAR{\gamma}$ activities in female OVX mice.

• Nutrition Research and Practice
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• v.7 no.4
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• pp.267-272
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• 2013

The anti-obesity effects of a hot water extract from wasabi (Wasabia japonica Matsum.) leaves (WLE), without its specific pungent constituents, such as allyl-isothiocyanate, were investigated in high fat-diet induced mice. C57J/BL mice were fed a high-fat diet (control group) or a high-fat diet supplemented with 5% WLE (WLE group). Physical parameters and blood profiles were determined. Gene expression associated with lipid metabolism in liver and white adipose tissue were analyzed. After 120 days of feeding, significantly lower body weight gain, liver weight and epididymal white adipose tissue weight was observed in the WLE group compared to the control group. In liver gene expression within the WLE group, PPAR${\alpha}$ was significantly enhanced and SREBP-1c was significantly suppressed. Subsequent downstream genes controlled by these regulators were significantly suppressed. In epididymal white adipose tissue of the WLE group, expression of leptin, PPAR${\gamma}$, and C/EBP${\alpha}$ were significantly suppressed and adiponectin was significantly enhanced. Acox, related to fatty acid oxidization in adipocytes, was also enhanced. Our results demonstrate that the WLE dietary supplement induces mild suppression of obesity in a high-fat diet induced mice, possibly due to suppression of lipid accumulation in liver and white adipose tissue.

• Journal of the Korean Applied Science and Technology
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• v.40 no.1
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• pp.1-12
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• 2023

It was investigated whether a combination of PPARα activator fenofibrate and swimming exercise (H/F/S) would have a beneficial synergistic effect on improving inflammation of white adipose tissue compared to the single prescription of fenofibrate (H/F) and swimming exercise (H/S) in male mice that fed high fat diet. The body weight, weight of white adipose tissue and total cholesterol levels in the serum increased in mice-fed high fat diets (H) compared to mice-fed low fat diets (L). Compared to H, both H/F and H/S decreased these. These levels reduced by fenofibrate were more effectively reduced by the combination of fenofibrate and swimming exercise (H/F/S). As a result of examining the expression of inflammatory cytokines genes and fatty acid oxidation genes in white adipose tissue, H increased compared to L, both H/F and H/S decreased compared to H, and H/F/S decreased further compared to H/F. Thus, this study revealed that the combination of fenofibrate and swimming exercise in male mice fed high-fat diet suppresses inflammation of white adipose tissue caused by obesity through promoted fatty acid oxidation more effectively than the fenofibrate alone, and suggested a practical way to improve inflammation of adipose tissue caused by obesity.

• Molecules and Cells
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• v.41 no.10
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• pp.900-908
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• 2018

Insulin resistance is closely associated with metabolic diseases such as type 2 diabetes, dyslipidemia, hypertension and atherosclerosis. Thiazolidinediones (TZDs) have been developed to ameliorate insulin resistance by activation of peroxisome proliferator-activated receptor (PPAR) ${\gamma}$. Although TZDs are synthetic ligands for $PPAR{\gamma}$, metabolic outcomes of each TZD are different. Moreover, there are lack of head-to-head comparative studies among TZDs in the aspect of metabolic outcomes. In this study, we analyzed the effects of three TZDs, including lobeglitazone (Lobe), rosiglitazone (Rosi), and pioglitazone (Pio) on metabolic and thermogenic regulation. In adipocytes, Lobe more potently stimulated adipogenesis and insulin-dependent glucose uptake than Rosi and Pio. In the presence of pro-inflammatory stimuli, Lobe efficiently suppressed expressions of pro-inflammatory genes in macrophages and adipocytes. In obese and diabetic db/db mice, Lobe effectively promoted insulin-stimulated glucose uptake and suppressed pro-inflammatory responses in epididymal white adipose tissue (EAT), leading to improve glucose intolerance. Compared to other two TZDs, Lobe enhanced beige adipocyte formation and thermogenic gene expression in inguinal white adipose tissue (IAT) of lean mice, which would be attributable to cold-induced thermogenesis. Collectively, these comparison data suggest that Lobe could relieve insulin resistance and enhance thermogenesis at low-concentration conditions where Rosi and Pio are less effective.