• Title/Summary/Keyword: Diet-induced obesity

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Effects of White Pan Bread Added with Kamut (Triticum turgidum spp.) on High Fat Diet-Induced Obese C57BL/6 Mice (Kamut (Triticum turgidum spp.) 식빵 급여가 고지방식이 유도 비만 C57BL/6 마우스에 미치는 효과)

  • Jung, Hyun Gi;Baek, Ji Yun;Choi, Ye Jung;Kang, Ki Sung;Kim, Hyun Young;Kim, Ji Hyun;Choi, Jine Shang
    • Journal of Korean Medicine for Obesity Research
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    • v.21 no.2
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    • pp.49-58
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    • 2021
  • Objectives: The purpose of this study was to investigate the effect of white pan bread added with Kamut (Triticum turgidum spp.) on high fat diet (HFD)-induced obese C57BL/6 mice. Methods: The white pan bread or white pan bread with Kamut (BK) were administered for 8 weeks in HFD-induced obese C57BL/6 mice. To evaluate the effect and its mechanisms of BK on obese mice, we measured body weight change, serum lipid profiles, histopathological analysis, and protein expression of CCAAT/enhancer binding protein-α (C/EBPα) in the liver. Results: Administration of BK significantly decreased body weight in HFD-induced obese mice. In addition, BK-administered group significantly reduced serum total cholesterol, glucose, and high-density lipoprotein cholesterol levels compared with the HFD-induced control group. The HFD-induced mice had damaged liver tissue and increased the size of adipose tissue, but BK-administered group attenuated liver damage and decreased the size of adipocyte. Furthermore, administration of BK significantly down-regulated C/EBPα in the liver compared with HFD-fed mice. In particular, BK-administered group has higher inhibited body weight, serum lipid profiles, and C/EBPα expressions than white pan bread-administered group. Conclusions: This study demonstrated that administration of BK attenuated HFD-induced obesity by regulation of C/EBPα than consumption of white pan bread. Therefore, BK could be developed as a bread for prevention of obesity.

Effect of Mixture of Atractylodes macrocephala and Amomum villosum Extracts on Body Weight and Lipid Metabolism in High Fat Diet-Induced Obesity Model (고지방식이 유도 비만 모델에서 백출과 사인 추출 혼합물이 체중 및 지질대사에 미치는 영향)

  • Kim, Ha Rim;Kwon, Yong Kwan;Choi, Bong Keun;Jung, Hyun Jong;Baek, Dong Gi
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.34 no.2
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    • pp.75-80
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    • 2020
  • In this study, we investigated the dose-dependent effects of mixtures of Atractylodes macrocephala (AM) and Amomum villosum (AV) water extracts in a ratio of 3:1 on high fat diet (HFD)-induced obesity model. Oral administration of various concentrations with mixtures of AM and AV extracts in a ratio of 3:1 for 6 weeks inhibited HFD-induced increases of body, liver and epididymal fat weights in a dose-dependent fashions. Those effects may be mediated by decreased expressions of lipogenesis-related genes such as acetyl coA carboxylase (ACC) and fatty acid synthase (FAS) in liver. Also, increase of insulin and decrease of adiponectin in serum by HFD supply were inhibited by three different dosages of mixtures of AM and AV extracts in a ratio of 3:1. HFD supply induced increases of serum total cholesterol, triglyceride and LDL cholesterol. However, hyperlipidemia was significantly decreased in dose-dependent manners by treatment with mixtures of AM and AV extracts. Based on the results of the present study, hypolipidemic and anti-obesity effects by mixtures of AM and AV extracts were found in HFD-induced obesity model. Further clinical investigation is needed to develop anti-obesity therapeutic or preventive agents by using mixtures of AM and AV extracts.

Ameliorative effect of myricetin on insulin resistance in mice fed a high-fat, high-sucrose diet

  • Choi, Ha-Neul;Kang, Min-Jung;Lee, Soo-Jin;Kim, Jung-In
    • Nutrition Research and Practice
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    • v.8 no.5
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    • pp.544-549
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    • 2014
  • BACKGROUND/OBJECTIVES: Obesity-associated insulin resistance is a strong risk factor for type 2 diabetes mellitus. The aim of this study was to investigate the effect of myricetin on adiposity, insulin resistance, and inflammatory markers in mice with diet-induced insulin resistance. MATERIALS/METHODS: Five-week-old male C57BL/6J mice were fed a basal diet, a high-fat, high-sucrose (HFHS) diet, or the HFHS diet containing 0.06% myricetin or 0.12% myricetin for 12 weeks after a 1-week adaptation, and body weight and food intake were monitored. After sacrifice, serum lipid profiles, glucose, insulin, adipocyte-derived hormones, and proinflammatory cytokines were measured. The homeostasis model assessment for insulin resistance (HOMA-IR) was determined. RESULTS: Myricetin given at 0.12% of the total diet significantly reduced body weight, weight gain, and epidydimal white adipose tissue weight, and improved hypertriglyceridemia and hypercholesterolemia without a significant influence on food intake in mice fed the HFHS diet. Serum glucose and insulin levels, as well as HOMA-IR values, decreased significantly by 0.12% myricetin supplementation in mice fed the HFHS diet. Myricetin given at 0.12% of the total diet significantly reduced serum levels of leptin, tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interleukin-6 (IL-6) in mice fed the HFHS diet. CONCLUSIONS: These findings suggest that myricetin may have a protective effect against diet-induced obesity and insulin resistance in mice fed HFHS diet, and that alleviation of insulin resistance could partly occur by improving obesity and reducing serum proinflammatory cytokine levels.

Treatment Effect of FD Extract on Obesity-Induced High-lipid Diet in Zucker Rats

  • Kim Dong Kyu;Lee Nam-Jin;Hong Seong-Hee;Cho Jung-Hee;Park Jung-Hui;Kim Yun-Bae;Kang Jong-Koo;Hwang Seock-Yeon
    • Biomedical Science Letters
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    • v.11 no.3
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    • pp.417-420
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    • 2005
  • To investigate the anti-obesitic effect of FD extract which consisted of Mori radicis Cortex, Hoelen, Pueraria radix, Schizonepetae spica, Carthami Flos, Bupleuri radix and Saposhnikoviae radix in high-fat diet-fed female lean Zucker rats. Obesity was induced by feeding high-lipid diet contained $3\%$ corn oil and $1\%$ cholesterol for 8 weeks, in which FD extract was added to the diet for treatment group. The rats fed on the high fat diet showed increased gain of body weights, leading to enhanced feed efficiency ratio. Moreover high-fat diet induced hepatic lipid peroxidation and hyperlipemia. The body weight, food efficiency ratio and lipid peroxidation in the liver was decreased as compared with the rats fed on the high fat diet by FD extract. With all such changes, the blood biochemistry about lipid was, if anything, risen. These results suggest that FD extract was supposed to have effective ingredients for improving obesity for controlling adipose tissue.

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Supplementation of a Fermented Soybean Extract Reduces Body Mass and Prevents Obesity in High Fat Diet-Induced C57BL/6J Obese Mice

  • Lee, Jae Yeon;Aravinthan, Adithan;Park, Young Shik;Hwang, Kyo Yeol;Seong, Su-Il;Hwang, Kwontack
    • Preventive Nutrition and Food Science
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    • v.21 no.3
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    • pp.187-196
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    • 2016
  • Obesity is a growing health problem that many countries face, mostly due to the consumption of a Westernized diet. In this present study we observed the effects of a soybean extract fermented by Bacillus subtilis MORI (BTD-1) containing 1-deoxynojirimycin against high fat diet-induced obesity. The results obtained from this study indicated that BTD-1 reduced body weight, regulated hepatic lipid content and adipose tissue, and also affected liver antioxidant enzymes and glucose metabolism. These results suggest that administration of BTD-1 affects obesity by inhibiting hyperglycemia and free radical-mediated stress; it also reduces lipid accumulation. Therefore, BTD-1 may be potentially useful for the prevention of obesity and its related secondary complications.

Role of Hypothalamic Reactive Astrocytes in Diet-Induced Obesity

  • Sa, Moonsun;Park, Mingu Gordon;Lee, C. Justin
    • Molecules and Cells
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    • v.45 no.2
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    • pp.65-75
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    • 2022
  • Hypothalamus is a brain region that controls food intake and energy expenditure while sensing signals that convey information about energy status. Within the hypothalamus, molecularly and functionally distinct neurons work in concert under physiological conditions. However, under pathological conditions such as in diet-induced obesity (DIO) model, these neurons show dysfunctional firing patterns and distorted regulation by neurotransmitters and neurohormones. Concurrently, resident glial cells including astrocytes dramatically transform into reactive states. In particular, it has been reported that reactive astrogliosis is observed in the hypothalamus, along with various neuroinflammatory signals. However, how the reactive astrocytes control and modulate DIO by influencing neighboring neurons is not well understood. Recently, new lines of evidence have emerged indicating that these reactive astrocytes directly contribute to the pathology of obesity by synthesizing and tonically releasing the major inhibitory transmitter GABA. The released GABA strongly inhibits the neighboring neurons that control energy expenditure. These surprising findings shed light on the interplay between reactive astrocytes and neighboring neurons in the hypothalamus. This review summarizes recent discoveries related to the functions of hypothalamic reactive astrocytes in obesity and raises new potential therapeutic targets against obesity.

Effects of Mahwangpohang-tang on the Expression of Obesity-Related Genes and Cytokines in Obesity Mice (마황포황탕이 비만생쥐의 비만유전자 및 관련인자에 미치는 영향)

  • Song, In-Sun;Song, Tae-Won;Oh, Min-Suck
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.19 no.4
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    • pp.1055-1061
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    • 2005
  • In this study, the aim was to investigate the effect of Mahwangpohang-tang on the expression of obesity-related genes and cytokines in high fat diet induced obesity mice. In order to investigate the effects of Mahwangpohang-tang(MHPH) on the obesity-related genes and cytokines, C57BL/6 mice were fed with high fat diet. C57BL/6 mice were divided into three groups and fed for 13weeks. Body weight change, diet intake change, final increase of body weight, the ratio of the adipocyte in body weight, the expression of leptin gene in primary adipocytes, the expression of UCP-2 in primary adipocytes, the production change of $TNF-\alpha$ and leptin in primary adipocytes, the expression of leptin in adipocytes tissue. The body weight of Mahwangpohang-tang(MHPH) intake mice was significantly lower than high fat diet group. The amount of the adipocyte in body weight was decreased Significantly. In primary adipocytes, leptin gene expression and the expression of UCP-2 did not change significantly. In primary adipocytes, the amount of $TNF-\alpha$ was significantly decreased at dose of $100{\mu}/ml$ density. In adipocytes tissue, the expression of leptin did not change significantly. These results suggest that MHPH may inhibit the expression of obesity-related genes and cytokines in high fat diet induced obesity mice

Down-Regulation of Adipogenesis and Hyperglycemia in Diet-Induced Obesity Mouse Model by Aloe QDM

  • Kong, Hyun-Seok;Lee, Sung-Won;Shin, Seul-Mee;Kwon, Jeung-Hak;Jo, Tae-Hyung;Shin, Eun-Ju;Shim, Kyu-Suk;Park, Young-In;Lee, Chong-Kil;Kim, Kyung-Jae
    • Biomolecules & Therapeutics
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    • v.18 no.3
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    • pp.336-342
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    • 2010
  • Obesity-induced disorders contribute to the development of metabolic diseases such as insulin resistance, fatty liver diseases, and type 2 diabetes (T2D). In this study, we evaluated the hypoglycemic and hypolipidemic effects of aloe formula in high fat diet (HFD)-fed C57BL/6N mice. Male mice fed HFD for 28 weeks received a supplement of aloe formula, PAG, ALS, Aloe QDM, and an Aloe QDM complex for a further 8 weeks and were then compared with regular diet fed mice. After the experimental period, the blood glucose levels of the Aloe QDM complex-and PGZ-supplemented mice were significantly lower than those of the HFD-fed mice. Aloe formula, especially the Aloe QDM complex, and the PGZ treatment group profoundly affected the IPGTT and HOMA-IR. Immunochemistry was done for the morphological observation and the resulting sizes of adipocytes around the epididymis were significantly decreased when comparing the aloe formula-treated and HFD-fed groups. Further, aloe formula decreased mRNA expression of fatty acid synthesis enzymes and led to reduced hepatic steatosis in both liver and WAT. These results suggest that supplementation of Aloe QDM complex in the HFD-fed mice improved insulin resistance by lowering blood glucose levels and reducing adipocytes. Our data suggest that dietary aloe formula reduces obesity-induced glucose tolerance by suppressing fatty acid synthesis in the WAT and liver, both of which are important peripheral tissues affecting insulin resistance. The Aloe QDM complex could be used as a nutritional intervention against T2D.

Anti-obesity Effect of Crataegus pinnatifida through Gut Microbiota Modulation in High-fat-diet Induced Obese Mice (산사의 장내 미생물 조절을 통한 항비만 효과)

  • Kim, Min-Jee;Choi, Yura;Shin, Na Rae;Lee, Myeong-Jong;Kim, Hojun
    • Journal of Korean Medicine Rehabilitation
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    • v.29 no.4
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    • pp.15-27
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    • 2019
  • Objectives This study was performed to evaluate anti-obesity effects of Crataegus pinnatifida (CP) on high-fat-diet induced obese mice. Methods The experimental animals were divided into four groups: normal diet (NOR) group, high fat diet (HFD) group, HFD+Xenical (XEN) group, and HFD+CP (CP) group. NOR group was fed a normal diet and the other three groups were fed high fat diet during the experiment. After the first two weeks of diet, XEN group and CP group were administered with XEN or CP for seven weeks, respectively. After that, we measured body weight, liver weight, fat weight, food intake, and serum concentrations of lipids and liver enzymes. Also the liver, intestine, fat tissue was removed to estimate the obesity-related mRNA expressions and the stool sample was collected to analyze the gut microbiota. Results We found that body weight, fat weight, and triglyceride level were decreased significantly in CP group compared to HFD group. Also CP significantly suppressed gene expressions associated with lipogenesis and inflammation, and increased gene expressions of browning of white adipose tissue and mitochondrial biogenesis. Moreover, it shifted the microbial diversity closer to that of NOR group and increased Firmicutes/Bacteriodetes ratio. Conclusions These results suggest that CP decrease body weight, fat weight and serum triglyceride. Also it inhibit inflammation and adipogenesis, altering gut microbial diversity and abundance. In conclusion, CP could be used as a therapeutic drug for obesity via gut microbiota modulation.

Tschimganidine reduces lipid accumulation through AMPK activation and alleviates high-fat diet-induced metabolic diseases

  • Min-Seon Hwang;Jung-Hwan Baek;Jun-Kyu Song;In Hye Lee;Kyung-Hee Chun
    • BMB Reports
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    • v.56 no.4
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    • pp.246-251
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    • 2023
  • Obesity increases the risk of mortality and morbidity because it results in hypertension, heart disease, and type 2 diabetes. Therefore, there is an urgent need for pharmacotherapeutic drugs to treat obesity. We performed a screening assay using natural products with anti-adipogenic properties in 3T3-L1 cells and determined that tschimganidine, a terpenoid from the Umbelliferae family, inhibited adipogenesis. To evaluate the anti-obesity effects of tschimganidine in vivo. Mice were fed either a normal chow diet (NFD) or a high-fat chow diet (HFD) with or without tschimganidine for 12 weeks. Treatment with tschimganidine decreased lipid accumulation and adipogenesis, accompanied by reduced expression of adipogenesis and lipid accumulation-related factors. Tschimganidine significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and decreased that of AKT. Depletion of AMPK relieved the reduction in lipid accumulation resulting from tschimganidine treatment. Moreover, tschimganidine administration drastically reduced the weight and size of both gonadal white adipose tissue (WAT) and blood glucose levels in high-fat diet-induced obese mice. We suggest that tschimganidine is a potent anti-obesity agent, which impedes adipogenesis and improves glucose homeostasis. Tschimganidine can then be evaluated for clinical application as a therapeutic agent.