• 대한한방내과학회지
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• 제37권4호
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• pp.609-623
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• 2016

Objective: This study was undertaken to investigate the effects of Mori folium on insulin resistance and adipose tissue inflammation in an experimental mouse model of obesity.Methods: Obesity was induced in C57BL/6 mice by feeding them a high-fat diet. The mice were divided into four groups (n=6): a normal diet, high-fat diet, high-fat diet with 40 mg of Mori folium, and high-fat diet with 800 mg of Mori folium groups. After 13 wk, the body weights, fasting blood glucose and fasting serum insulin levels, insulin resistance (homeostatic model assessment) levels, oral glucose tolerance test levels, epididymal fat and liver weights, and gene expression of tumor necrosis factor-α, interleukin-6, and interferon-γ were measured. In addition, adipose tissue macrophages were analyzed by fluorescence-activated cell sorting.Results: Mori folium significantly reduced blood glucose levels, oral glucose tolerance levels, and liver weights. It also reduced adipose tissue macrophage numbers and tumor necrosis factor receptor-α gene expression.Conclusions: These results show that Mori folium has insulin resistance reduction and anti-inflammatory effects in an experimental mouse model of obesity.

• 대한한방내과학회지
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• 제36권4호
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• pp.447-457
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• 2015

Objectives: This study was undertaken to investigate how Cortex Phellodendri affects metabolic functional change in an experimental rat model of obesity.Methods: An obesity model was induced in a C57BL/6 mouse with a high-fat diet. Mice were divided into three groups (n=6) of normal diet, high-fat diet (=control), and high-fat diet with Cortex Phellodendri. After 12 weeks, we measured the three mice groups’ body weight, FBG, FBI, HOMA-IR, OGTT, the weight of epididymal fat and liver, the percentage of ATM, and the gene expression of TNF-α, IL-10, and CD68.Results: Cortex Phellodendri significantly reduced blood glucose and oral glucose tolerance levels. It also reduced ATM numbers and TNF-α and CD68 gene expression and increased IL-10 gene expression.Conclusions: This study suggests that Cortex Phellodendri normalized the blood glucose and reduced the expression of inflammatory markers. However, with respect to other indicators of metabolic function in obesity, there were no significant results.

• Journal of Nutrition and Health
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• 제56권4호
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• pp.349-360
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• 2023

Purpose: Ketogenic diets (KDs) have anti-obesity effects that may be related to glucose control and the gut microbiota. This paper hypothesizes that KD reduces body weight and changes the insulin sensitivity and gut microbiota composition in a mouse model of diet-induced obesity. Methods: In this study, C57BL/6 male mice were assigned randomly to 3 groups. The assigned diets were provided to the control and high-fat (HF) diet groups for 14 weeks. The KD group was given a HF diet for 8 weeks to induce obesity, followed by feeding the KD for the next 6 weeks. Results: After the treatment period, the KD group exhibited a 35.82% decrease in body weight gain compared to the HF group. In addition, the KD group demonstrated enhanced glucose control, as shown by the lower levels of serum fasting glucose, serum fasting insulin, and the homeostatic model assessment of insulin resistance, compared to the HF group. An analysis of the gut microbiota using 16S ribosomal RNA sequencing revealed a significant decrease in the proportion of Firmicutes when the KD was administered. In addition, feeding the KD reduced the overall alpha-diversity measures and caused a notable separation of microbial composition compared to the HF diet group. The KD also led to a decrease in the relative abundance of specific species, such as Acetatifactor_muris, Ligilactobacillus_apodemi, and Muribaculum_intestinale, compared with the HF group. These species were positively correlated with the body weight, whereas the abundant species in the KD group (Kineothrix_alysoides and Saccharofermentans_acetigenes) showed a negative correlation with body weight. Conclusion: The current study presents supporting evidence that KD reduced the body weight and altered the insulin sensitivity and gut microbiota composition in a mouse model of diet-induced obesity.

• BMB Reports
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• 제48권12호
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• pp.647-654
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• 2015

Energy homeostasis in our body system is maintained by balancing the intake and expenditure of energy. Excessive accumulation of fat by disrupting the balance system causes overweight and obesity, which are increasingly becoming global health concerns. Understanding the pathogenesis of obesity focused on studying the genes related to familial types of obesity. Recently, a rare human genetic disorder, ciliopathy, links the role for genes regulating structure and function of a cellular organelle, the primary cilium, to metabolic disorder, obesity and type II diabetes. Primary cilia are microtubule based hair-like membranous structures, lacking motility and functions such as sensing the environmental cues, and transducing extracellular signals within the cells. Interestingly, the subclass of ciliopathies, such as Bardet-Biedle and Alström syndrome, manifest obesity and type II diabetes in human and mouse model systems. Moreover, studies on genetic mouse model system indicate that more ciliary genes affect energy homeostasis through multiple regulatory steps such as central and peripheral actions of leptin and insulin. In this review, we discuss the latest findings in primary cilia and metabolic disorders, and propose the possible interaction between primary cilia and the leptin and insulin signal pathways which might enhance our understanding of the unambiguous link of a cell's antenna to obesity and type II diabetes.

• 사상체질의학회지
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• 제30권2호
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• pp.8-27
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• 2018

Objective This study investigated the effects of Jeoreongchajeonja-tang in a high-fat diet-induced obesity mouse model. Methods The study examined 9-week-old male mice (C57bl/6J) divided into four groups: the normal(C57bl/6J-Nr), control (high-fat diet only; HFD-CTL), positive-control (high-fat diet with Garcinia cambogia), and experimental (high-fat diet with Jeoreongchajeonja-tang; HFD-JCT) groups. After 7 weeks, the body weight, food efficiency ratio, organ weight, and visceral fat weight of the mice were measured. Blood serum tests, mRNA, liver histopathology, and epididymis adipocytes were also examined. Results Compared with the Control(HFD-CTL) group, the Experimental(HFD-JCT) group given Jeoreongchajeonja-tang showed significant reductions in absolute body weight and food efficiency ratio. The serum alanine aminotransferase, total-cholesterol, triglyceride, low-density lipoprotein (LDL)-cholesterol, high-density lipoprotein (HDL)-cholesterol, insulin-like growth factor-1, and leptin levels were significantly lower in the experimental group than in the control group. The serum adiponectin levels were significantly higher in the experimental group than in the control group. Compared with the control group, the experimental group showed significant reductions in absolute abdominal subcutaneous fat, epididymal adipose tissue, kidney adipose tissue, intestine adipose tissue, and liver, kidney and spleen adipose tissue weights. The C/EBP-${\beta}$, leptin, and SREBP1c/ADD1 mRNA expression were significantly lower in the experimental group than in the control group, while the UCP-2 and adiponectin mRNA expression were significantly higher. Compared with the control group, the experimental group showed a significant reduction in the absolute adipocyte area in the liver and epididymal adipose tissue. Conclusion Jeoreongchajeonja-tang has an anti-obesity effect. Additional clinical studies are expected.

• 대한한의학회지
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• 제34권1호
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• pp.1-14
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• 2013

Objectives: This study was designed to investigate the anti-obesity, anti-diabetic and anti-inflammatory effects of Platycodi radix on obese type 2 diabetes mouse model. Methods: Obese type 2 diabetes mouse model was induced by Surwit's high fat, high sucrose diet for 8 weeks. Models were divided into 4 groups of normal diet (ND, n=10), high fat and high sucrose diet (HFD, n=10), high fat and high sucrose diet with Platycodi radix (PR, n=10), and high fat and high sucrose diet with Metformin (Met, n=10). Body weights were measured every week. After 7 weeks fasting, blood sugar and oral glucose tolerance tests were conducted. After 8 weeks blood samples were taken from mouse hearts and analyzed biochemically. Lipid profile, fructosamine, leptin and weight of epididymal fat pad and liver were measured. Adipose tissue macrophage percentage was analyzed by fluorescence-activated cell sorting (FACS). Results: Compared with the HFD group, body weight, glucose level, fructosamine, weight of epididymal fat pad and adipose tissue macrophage percentage decreased in the PR group. Conclusions: These results suggest that Platycodi Radix has anti-obesity, anti-diabetic, and anti-inflammatory effects on obese type 2 diabetes mouse model.

• 한국가축번식학회지
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• 제26권4호
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• pp.321-328
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• 2002

The hormone resistin is associated with type II diabetes mellitus in rodent model. Resistin impairs glucose tolerance and insulin action. A new class of anti-diabetic drugs were called thiazolidinediones (TZDs) downreguates a resistin. Resistin gene expression is induced during adipocyte differentiation and resistin polypeptide is secreted by adipocytes. But, the correlation between increased adiposity and resistin remains unknown. The objectives of this study was to clone a mouse resistin CDNA and to generate transgenic mice overexpressing mouse resistin gene. The pCMV-mus/resistin gene was prepared from previous recombinant pTargeT$^{TM}$-mus/resistin by digestion of Bgl II, and has used for microin- jection into pronuclei of one cell embryos. Mouse resistin expression was detected in transgenic F$_1$mice by RT-PCR. The transgenic mouse with resistin gene expression has heavier body weight which was measured higher level of plasma glucose than that of normal mouse. And in diet-induced experiments, in fasting group, resistin expression was higher than that of re-feeding group. This result demonstrates that the resistin gene overexpressing mice may be became to obesity and be useful as an animal disease model to be diabetes caused by insulin resistance of resistin.n.

• BMB Reports
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• 제55권4호
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• pp.187-191
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• 2022

Obesity is caused by an imbalance between energy intake and energy expenditure. Exercise is attracting attention as one of the ways to treat obesity. Exercise induces 'beige adipogenesis' in white adipose tissue, increasing total energy expenditure via energy dissipation in the form of heat. Also, beige adipogenesis can be induced by treatment with a beta-adrenergic receptor agonist. We developed a Cidea-dual reporter mouse (Cidea-P2A-Luc2-T2A-tdTomato, Luciferase/tdTomato) model to trace and measure beige adipogenesis in vivo. As a result, both exercise and injection of beta-adrenergic receptor agonist induced beige adipogenesis and was detected through fluorescence and luminescence. We confirmed that exercise and beta-adrenergic receptor agonist induce beige adipogenesis in Cidea-dual reporter mouse, which will be widely used for detecting beige adipogenesis in vivo.

• 한방비만학회지
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• 제17권2호
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• pp.145-145
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• 2017

• 한방비만학회지
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• 제16권1호
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• pp.19-26
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• 2016

Objectives: The prevalence of obesity continues rise and obesity and metabolic syndrome is a major problem in global health care. Animal models are used in the drug discovery of novel treatment for obesity. One of common models of obesity is a high fat diet induced obesity in a C5BL/6 mouse, and the development of obesity and glucose tolerance in mouse model is different according to period of diet. Therefore, this study was performed to observe the development of obesity and glucose tolerance during a high fat diet (HFD). Methods: Male C57BL/6 mice, 5 weeks of age, were fed on a standard chow diet as a normal diet (18 kcal% fat) or a HFD (60 kcal% fat) for up to 16 weeks. The various factors related with obesity and insulin resistance were measured at 8, 12, and 16 weeks. Results: The weights of body and epididymal fat were gradually increased for 8~16 weeks, however the change of hyperglycaemia and glucose tolerance have shown different with that of body weight. Blood glucose, oral glucose tolerance and insulin tolerance were increased more clearly at week 12 and 16 than week 8. Lipid accumulation of liver and body temperature were also significantly increased at week 16, compared with normal group. Conclusions: The developments of obesity and related factors were different by a HFD period in a C57BL/6 obese mice. This result suggests that the development of obesity with glucose tolerance and liver lipid may induce clearly by a HFD for 16 weeks.