scholarly journals Addition of high load of lysophosphatidic acid to standard and high‐fat chows causes no significant changes of its circulating and peripheral tissue levels but affects body weight and visceral fat mass of mice

BioFactors ◽  
2018 ◽  
Vol 44 (6) ◽  
pp. 548-557 ◽  
Author(s):  
Manami Inoue ◽  
Yoko Okamoto ◽  
Yuta Atsumi ◽  
Masatoshi Shiojiri ◽  
Mayumi Hidaka ◽  
...  
Keyword(s):  
Body Weight ◽  
Fat Mass ◽  
Lysophosphatidic Acid ◽  
Visceral Fat ◽  
High Load ◽  
Peripheral Tissue ◽  
High Fat ◽  
Tissue Levels

Conjugated linoleic acid and chromium lower body weight and visceral fat mass in high-fat-diet-fed mice

Lipids ◽  
2006 ◽  
Vol 41 (5) ◽  
pp. 437-444 ◽  
Author(s):  
Arunabh Bhattacharya ◽  
M. Mizanur Rahman ◽  
Roger McCarter ◽  
Marianne O'Shea ◽  
Gabriel Fernandes
Keyword(s):  
Body Weight ◽  
Linoleic Acid ◽  
Conjugated Linoleic Acid ◽  
Fat Mass ◽  
Visceral Fat ◽  
High Fat Diet ◽  
Lower Body ◽  
High Fat ◽  
Lower Body Weight

Dietary d-Psicose Reduced Visceral Fat Mass in High-Fat Diet-Induced Obese Rats

2012 ◽  
Vol 77 (2) ◽  
pp. H53-H58 ◽  
Author(s):  
Young-Mee Chung ◽  
Joo Hyun Lee ◽  
Deuk Youl Kim ◽  
Se-Hee Hwang ◽  
Young-Ho Hong ◽  
...  
Keyword(s):  
Fat Mass ◽  
Visceral Fat ◽  
High Fat Diet ◽  
High Fat ◽  
Obese Rats

Abstract 17361: How Leptin Harms the Heart in High Fat Diet-Induced Obesity

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Maria Pini
Keyword(s):  
Body Weight ◽  
Mass Loss ◽  
Fat Mass ◽  
High Fat Diet ◽  
Cardiac Fibroblasts ◽  
High Fat ◽  
Wide Range ◽  
Plasma Leptin ◽  
Fat Mass Loss

Introduction: Sedentary lifestyle and excessive calorie intake are risk factors for CVD. We have demonstrated the cardioprotective effect of exercise in aged mice and the critical role of visceral adiposity and its profibrotic secretome in increasing cardiovascular risks in obesity and aging. The association between exercise, lowered plasma leptin and reduced inflammatory leukocytes has been recently shown in patients with atherosclerosis. It remains unclear whether elevated plasma leptin can preserve or alter cardiovascular function in obesity. Methods: We analyzed the effect of high fat diet (HFD) in C57BL/6J male mice on the heart in terms of function, structure, histology and key molecular markers. Two interventions were used: 1) active fat mass loss via exercise (daily swimming) during HFD; 2) passive fat mass loss via surgical removal of the visceral adipose tissue (VAT lipectomy) followed by HFD. Results: HFD increased body weight and adiposity, leading to higher plasma leptin, glucose and insulin levels, compared to control diet (CD) mice. HFD impaired left ventricle (LV) structure (hypertrophy, interstitial fibrosis) and cardiac function (echocardiography, in vivo hemodynamics). Atria of HFD mice had enhanced pro-inflammatory protein production. Exercise reduced circulating leptin levels in HFD mice by 50%, in line with fat mass loss. In contrast, lipectomy reduced visceral fat mass, but body weight, adiposity and plasma leptin did not change. Both exercise and VAT lipectomy improved cardiac contractility, reversed collagen deposition and oxidative stress in HFD mice. Both interventions downregulated LV pro-inflammatory markers. We proved the role of leptin in cardiac remodeling in vitro by incubating primary cardiac fibroblasts with hyperleptinemic plasma from HFD mice. Remarkably, plasma from HFD-EX (exercise) suppressed the fibro-proliferative and pro-inflammatory responses of cardiac fibroblasts. Conclusions: Leptin directly contribute to cardiac fibrosis in obesity via activation and proliferation of cardiac fibroblasts. Understanding how leptin signals to the heart might have implications in a wide range of CVD, potentially helping early stratification and personalized care.

Bisphenol A Promotes Adiposity and Inflammation in a Nonmonotonic Dose-response Way in 5-week-old Male and Female C57BL/6J Mice Fed a Low-calorie Diet

Endocrinology ◽  
2016 ◽  
Vol 157 (6) ◽  
pp. 2333-2345 ◽  
Author(s):  
Minglan Yang ◽  
Maopei Chen ◽  
Jiqiu Wang ◽  
Min Xu ◽  
Jichao Sun ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Body Weight ◽  
Bisphenol A ◽  
Body Mass ◽  
Fat Mass ◽  
High Fat Diet ◽  
Inflammatory Factors ◽  
Chow Diet ◽  
High Fat ◽  
Male And Female

A growing body of epidemiological research show that Bisphenol A (BPA) is positively correlated with obesity and metabolic disorders. However, the mechanisms of BPA on adiposity remain largely unknown. In this study, we found that 5-week-old male and female C57BL/6J mice exposed to four dosages of BPA (5, 50, 500, and 5000 μg/kg/d) by oral intake for 30 days showed significantly increased body weight and fat mass in a nonmonotonic dose-dependent manner when fed a chow diet. The effect occurred even at the lowest concentration (5μg/kg/d), lower than the tolerable daily intake of 50 μg/kg/day for BPA. However, no significant difference in body weight and fat mass was observed in either male or female mice fed a high-fat diet, suggesting that BPA may interact with diet in promoting obesity risk. In vitro study showed that BPA treatment drives the differentiation of white adipocyte progenitors from the stromal vascular fraction, partially through glucocorticoid receptor. BPA exposure increased circulating inflammatory factors and the local inflammation in white adipose tissues in both genders fed a chow diet, but not under high-fat diet. We further found that BPA concentration was associated with increased circulating inflammatory factors, including leptin and TNFα, in lean female subjects (body mass index < 23.0 kg/m2) but not in lean male subjects or in both sexes of overweight/obese subjects (body mass index > 25.0 kg/m2). In conclusion, we demonstrated the nonmonotonic dose effects of BPA on adiposity and chronic inflammation in 5-week-old mice, which is related to caloric uptake.

scholarly journals Energy homeostasis in apolipoprotein AIV and cholecystokinin-deficient mice

2017 ◽  
Vol 313 (5) ◽  
pp. R535-R548 ◽  
Author(s):  
Jonathan Weng ◽  
Danwen Lou ◽  
Stephen C. Benoit ◽  
Natalie Coschigano ◽  
Stephen C. Woods ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Expenditure ◽  
Fat Mass ◽  
High Fat Diet ◽  
Energy Homeostasis ◽  
Lipid Transport ◽  
Fat Absorption ◽  
High Fat ◽  
Reduced Body ◽  
Brown Adipose

Apolipoprotein AIV (ApoAIV) and cholecystokinin (CCK) are well-known satiating signals that are stimulated by fat consumption. Peripheral ApoAIV and CCK interact to prolong satiating signals. In the present study, we hypothesized that ApoAIV and CCK control energy homeostasis in response to high-fat diet feeding. To test this hypothesis, energy homeostasis in ApoAIV and CCK double knockout (ApoAIV/CCK-KO), ApoAIV knockout (ApoAIV-KO), and CCK knockout (CCK-KO) mice were monitored. When animals were maintained on a low-fat diet, ApoAIV/CCK-KO, ApoAIV-KO, and CCK-KO mice had comparable energy intake and expenditure, body weight, fat mass, fat absorption, and plasma parameters relative to the controls. In contrast, these KO mice exhibited impaired lipid transport to epididymal fat pads in response to intraduodenal infusion of dietary lipids. Furthermore, ApoAIV-KO mice had upregulated levels of CCK receptor 2 (CCK2R) in the small intestine while ApoAIV/CCK-KO mice had upregulated levels of CCK2R in the brown adipose tissue. After 20 wk of a high-fat diet, ApoAIV-KO and CCK-KO mice had comparable body weight and fat mass, as well as lower energy expenditure at some time points. However, ApoAIV/CCK-KO mice exhibited reduced body weight and adiposity relative to wild-type mice, despite having normal food intake. Furthermore, ApoAIV/CCK-KO mice displayed normal fat absorption and locomotor activity, as well as enhanced energy expenditure. These observations suggest that mice lacking ApoAIV and CCK have reduced body weight and adiposity, possibly due to impaired lipid transport and elevated energy expenditure.

scholarly journals Acetate rescues defective brain-adipose metabolic network in obese Wistar rats by modulation of peroxisome proliferator-activated receptor-γ

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kehinde Samuel Olaniyi ◽  
Morounkeji Nicole Owolabi ◽  
Chukwubueze Lucky Atuma ◽  
Toluwani Bosede Agunbiade ◽  
Bolanle Yemisi Alabi
Keyword(s):  
Body Weight ◽  
Fat Mass ◽  
Visceral Fat ◽  
Wistar Rats ◽  
Pyruvate Dehydrogenase Kinase ◽  
Peroxisome Proliferator ◽  
Elevated Plasma ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Glutamyl Transferase

AbstractWe investigated the hypothesis that acetate ameliorates brain-adipose metabolic dysfunction (BAMED) in high fat diet (HFD)-induced obesity, possibly by modulation of peroxisome proliferator-activated receptor-γ (PPAR-γ). Ten-week-old male Wistar rats were randomly assigned into four groups (n = 6/group): Control, acetate and obese with or without acetate groups received vehicle (distilled water; po), acetate (200 mg/kg, po) and 40% HFD with or without acetate respectively. The treatments lasted for 12 weeks. Obese animals showed increase in body weight, visceral fat mass, insulin and triglyceride-glucose index and a reduction in insulin sensitivity. In addition, obese animals also showed increase in plasma/hypothalamic and adipose pyruvate dehydrogenase kinase-4, lactate-pyruvate ratio, malondialdehyde, γ-glutamyl transferase, and a decrease in glucose-6-phosphate dehydrogenase, glutathione, nitric oxide and PPAR-γ. HFD also elevated plasma/hypothalamic lipid and decreased adipose lipid profile, increased hypothalamic and adipose tumor necrosis factor-α, interleukin-6 and histone deacetylase (HDAC), and elevated plasma/adipose leptin. These alterations were reversed by concomitant administration of acetate. The present results demonstrate that obesity is characterized by BAMED, which is accompanied by altered HDAC/PPAR-γ. The results in addition suggest that acetate, an HDAC inhibitor rescues BAMED with consequent normalization of body weight and visceral fat mass by modulation of PPAR-γ and suppression of oxidative stress.

scholarly journals Erchen Decoction Mitigates Lipid Metabolism Disorder by the Regulation of PPARγ and LPL Gene in a High-Fat Diet C57BL/6 Mice Model

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Mengting Zhang ◽  
Yanfei Shao ◽  
Bizhen Gao ◽  
Jicheng Chen ◽  
Ping Zhang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Lipid Metabolism ◽  
Visceral Fat ◽  
Protein Level ◽  
High Fat Diet ◽  
Blood Lipid ◽  
Abdominal Circumference ◽  
High Fat ◽  
Gene And Protein Expression

Erchen decoction (ECD) is a common treatment prescribed in traditional Chinese medicine (TCM) clinics, which has remarkable efficacy in the treatment of obesity, fatty liver, hyperlipidemia, diabetes, and other diseases caused by phlegm. In this study, we investigated the effect that ECD had on the lipid metabolism induced by high-fat diet in C57BL/6 mice. Body weight, body length, and abdominal circumference were detected. Blood lipid content was measured via biochemical assay kit. The gene and protein expression of PPARγ and LPL in visceral fat and skeletal muscle of mice was measured by real-time PCR and western blot. The research discovered that the phlegm-resolving effect that ECD had on high-fat diet mice was mainly manifested as reduced body weight, Lee’s index, abdominal circumference, and level of TG and TC. Meanwhile, we observed significantly increased PPARγ mRNA and protein level in visceral fat and PPARγ and LPL protein level in skeletal muscle in the ECD group. Contrarily, a decrease in PPARγ mRNA level in skeletal muscle in the ECD group was observed. Therefore, we speculate that ECD regulates the lipid metabolic disorder by decreasing the blood lipid level. Moreover, the potential molecular mechanism of ECD is to promote the expression of PPARγ in visceral fat and skeletal muscle and the expression of LPL in skeletal muscle.

scholarly journals Metabolic Burden of Erythropoietin Stimulated Erythropoiesis in Mice

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 2421-2421
Author(s):  
Constance Tom Noguchi ◽  
Heather Marie Rogers
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Fat Mass ◽  
High Fat Diet ◽  
Male Mice ◽  
Wild Type ◽  
Hematopoietic Tissue ◽  
High Fat ◽  
Epor Expression

Erythropoietin (EPO) promotes erythroid differentiation and increases glucose uptake in erythroid progenitor cells in culture. The metabolic burden associated with EPO treatment in adult mice is suggested by a decrease in body weight concomitant with increased hematocrit. Wild type male mice (C57Bl/6, age 8 months) treated with EPO showed the expected increase in hematocrit accompanied by a fall in blood glucose level and a decrease in body weight and fat mass. However, the decrease in body weight is even more evident in obese mice on a high fat diet and has also been linked to non-hematopoietic response, particularly with EPO receptor (EpoR) expression in white adipose tissue. We examined the metabolic burden of EPO treatment (3000U/kg for 3 weeks) in young, lean male mice (3 months) placed on high fat diet at the time of EPO administration. The increase in hematocrit was accompanied by decreased blood glucose level and improved glucose tolerance. However, no difference in body weight was observed between mice treated with EPO and the saline treated group, suggesting that the EPO stimulated decrease in body weight is evident primarily in older animals with greater fat mass. To determine the contribution of EpoR expression in non-hematopoietic tissue to the metabolic EPO response, young male mice with EpoR restricted to erythroid tissue (TgEpoR) were placed on high fat diet and treated with EPO. The expected increased hematocrit was also accompanied by decreased blood glucose level and improved glucose tolerance, and no change in body weight between EPO and saline treatment. The similar responses observed in young wild type and TgEpoR mice suggest that the EPO stimulated increase in glucose metabolism is associated with increased erythropoiesis rather than a direct EPO response in non-hematopoietic tissue. TgEpoR mice exhibit an age dependent increase in fat mass even greater than that observed in wild type mice, and by 8 months TgEpoR mice are obese, glucose intolerant and insulin resistant compared with wild type mice. At 8 months, TgEpoR mice treated with EPO show the increase in hematocrit and, despite the increase in fat mass, there is only a minimal decrease in body weight compared with wild type mice. These data provide evidence that in addition to the age dependent association of EPO stimulated decrease in body weight and fat mass, this decrease in body weight is due largely to EPO response related to EpoR expression in non-hematopoietic tissue. Interestingly, young male mice with targeted deletion of EpoR in adipose tissue placed on a high fat diet and treated with EPO show the increase in hematocrit and improvement in glucose tolerance, and at 8 months, the increase in hematocrit with EPO treatment is accompanied by minimal change in body weight. The similar metabolic response of these mice with targeted deletion of EpoR in adipose tissue to TgEpoR mice indicate the contribution of EpoR expression in adipose tissue to the loss of body weight and fat mass. Therefore, the metabolic burden associated with EPO stimulated erythropoiesis appears to be reflected in improved glucose metabolism and glucose tolerance with minimal or no effect on body weight, is evident in young, lean mice, and is independent of EpoR expression in non-hematopoietic tissue. In older mice, non-hematopoietic metabolic EPO response is more readily apparent as reflected in loss of body weight/fat mass, which overshadows the erythropoietic metabolic response. In combination, the metabolic response to EPO treatment results from EPO stimulated increased erythropoiesis, improved glucose metabolism and glucose tolerance, and an age dependent decrease in body weight and fat mass associated with EpoR expression in non-hematopoietic tissue, particularly in white adipose tissue. Disclosures No relevant conflicts of interest to declare.

DHEA protects against visceral obesity and muscle insulin resistance in rats fed a high-fat diet

1997 ◽  
Vol 273 (5) ◽  
pp. R1704-R1708 ◽  
Author(s):  
Polly A. Hansen ◽  
Dong Ho Han ◽  
Lorraine A. Nolte ◽  
May Chen ◽  
John O. Holloszy
Keyword(s):  
Insulin Resistance ◽  
Food Intake ◽  
Protective Effect ◽  
Fat Mass ◽  
Visceral Fat ◽  
High Fat Diet ◽  
Visceral Obesity ◽  
High Fat ◽  
Muscle Insulin Resistance

Visceral obesity is frequently associated with muscle insulin resistance. Rats fed a high-fat diet rapidly develop obesity and insulin resistance. Dehydroepiandrosterone (DHEA) has been reported to protect against the development of obesity. This study tested the hypothesis that DHEA protects against the increase in visceral fat and the development of muscle insulin resistance induced by a high-fat diet in rats. Feeding rats a diet providing 50% of the energy as fat for 4 wk resulted in a twofold greater visceral fat mass and a 50% lower rate of maximally insulin-stimulated muscle 2-deoxyglucose (2-DG) uptake compared with controls. Rats fed the high-fat diet plus 0.3% DHEA were largely protected against the increase in visceral fat (+11.3 g in high fat vs. +2.9 g in high fat plus DHEA, compared with controls) and against the decrease in insulin-stimulated muscle 2-DG uptake (0.94 ± 0.15 μmol ⋅ ml−1 ⋅ 20 min−1, controls; 0.46 ± 0.06 μmol ⋅ ml−1 ⋅ 20 min−1, high-fat diet; 0.78 ± 0.07 μmol ⋅ ml−1 ⋅ 20 min−1, high fat + DHEA). DHEA did not affect food intake. These results show that DHEA has a protective effect against accumulation of visceral fat and development of muscle insulin resistance in rats fed a high-fat diet.

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