scholarly journals A Low-Protein High-Fat Diet Leads to Loss of Body Weight and White Adipose Tissue Weight via Enhancing Energy Expenditure in Mice

Metabolites ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 301
Author(s):  
Yifeng Rang ◽  
Sihui Ma ◽  
Jiao Yang ◽  
Huan Liu ◽  
Katsuhiko Suzuki ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Acid Oxidation ◽  
High Fat ◽  
Plasma Biomarkers ◽  
Low Protein

Obesity has become a worldwide health problem over the past three decades. During obesity, metabolic dysfunction of white adipose tissue (WAT) is a key factor increasing the risk of type 2 diabetes. A variety of diet approaches have been proposed for the prevention and treatment of obesity. The low-protein high-fat diet (LPHF) is a special kind of high-fat diet, characterized by the intake of a low amount of protein, while compared to typical high-fat diet, may induce weight loss and browning of WAT. Physical activity is another effective intervention to treat obesity by reducing WAT mass, inducing browning of WAT. In order to determine whether an LPHF, along with exercise enhanced body weight loss and body fat loss as well as the synergistic effect of an LPHF and exercise on energy expenditure in a mice model, we combined a 10-week LPHF with an 8-week forced treadmill training. Meanwhile, a traditional high-fat diet (HPHF) containing the same fat and relatively more protein was introduced as a comparison. In the current study, we further analyzed energy metabolism-related gene expression, plasma biomarkers, and related physiological changes. When comparing to HPHF, which induced a dramatic increase in body weight and WAT weight, the LPHF led to considerable loss of body weight and WAT, without muscle mass and strength decline, while it exhibited a risk of liver and pancreas damage. The mechanism underlying the LPHF-induced loss of body weight and WAT may be attributed to the synergistically upregulated expression of Ucp1 in WAT and Fgf21 in the liver, which may enhance energy expenditure. The 8-week training did not further enhance weight loss and increased plasma biomarkers of muscle damage when combined with LPHF. Furthermore, LPHF reduced the expression of fatty acid oxidation-related genes in adipose tissues, muscle tissues, and liver. Our results indicated that an LPHF has potential for obesity treatment, while the physiological condition should be monitored during application.

scholarly journals Anti-Obesity and Anti-Diabetic Effects of Acacia Polyphenol in Obese Diabetic KKAy Mice Fed High-Fat Diet

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Nobutomo Ikarashi ◽  
Takahiro Toda ◽  
Takehiro Okaniwa ◽  
Kiyomi Ito ◽  
Wataru Ochiai ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Acid Synthesis ◽  
Diet Group ◽  
High Fat ◽  
Kkay Mice

Acacia polyphenol (AP) extracted from the bark of the black wattle tree (Acacia meansii) is rich in unique catechin-like flavan-3-ols, such as robinetinidol and fisetinidol. The present study investigated the anti-obesity/anti-diabetic effects of AP using obese diabetic KKAy mice. KKAy mice received either normal diet, high-fat diet or high-fat diet with additional AP for 7 weeks. After the end of administration, body weight, plasma glucose and insulin were measured. Furthermore, mRNA and protein expression of obesity/diabetic suppression-related genes were measured in skeletal muscle, liver and white adipose tissue. As a result, compared to the high-fat diet group, increases in body weight, plasma glucose and insulin were significantly suppressed for AP groups. Furthermore, compared to the high-fat diet group, mRNA expression of energy expenditure-related genes (PPARα, PPARδ, CPT1, ACO and UCP3) was significantly higher for AP groups in skeletal muscle. Protein expressions of CPT1, ACO and UCP3 for AP groups were also significantly higher when compared to the high-fat diet group. Moreover, AP lowered the expression of fat acid synthesis-related genes (SREBP-1c, ACC and FAS) in the liver. AP also increased mRNA expression of adiponectin and decreased expression of TNF-αin white adipose tissue. In conclusion, the anti-obesity actions of AP are considered attributable to increased expression of energy expenditure-related genes in skeletal muscle, and decreased fatty acid synthesis and fat intake in the liver. These results suggest that AP is expected to be a useful plant extract for alleviating metabolic syndrome.

Mice deleted for GPAT3 have reduced GPAT activity in white adipose tissue and altered energy and cholesterol homeostasis in diet-induced obesity

2014 ◽  
Vol 306 (10) ◽  
pp. E1176-E1187 ◽  
Author(s):  
Jingsong Cao ◽  
Sylvie Perez ◽  
Bryan Goodwin ◽  
Qingcong Lin ◽  
Haibing Peng ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Cholesterol Metabolism ◽  
Body Weight Gain ◽  
Cholesterol Homeostasis ◽  
High Fat

Glycerol-3-phosphate acyltransferases (GPATs) catalyze the first step in the synthesis of glycerolipids and glycerophospholipids. Microsomal GPAT, the major GPAT activity, is encoded by at least two closely related genes, GPAT3 and GPAT4. To investigate the in vivo functions of GPAT3, we generated Gpat3-deficient ( Gpat3 −/−) mice. Total GPAT activity in white adipose tissue of Gpat3 −/− mice was reduced by 80%, suggesting that GPAT3 is the predominant GPAT in this tissue. In liver, GPAT3 deletion had no impact on total GPAT activity but resulted in a 30% reduction in N-ethylmaleimide-sensitive GPAT activity. The Gpat3 −/− mice were viable and fertile and exhibited no obvious metabolic abnormalities on standard laboratory chow. However, when fed a high-fat diet, female Gpat3 −/− mice showed decreased body weight gain and adiposity and increased energy expenditure. Increased energy expenditure was also observed in male Gpat3 −/− mice, although it was not accompanied by a significant change in body weight. GPAT3 deficiency lowered fed, but not fasted, glucose levels and tended to improve glucose tolerance in diet-induced obese male and female mice. On a high-fat diet, Gpat3 −/− mice had enlarged livers and displayed a dysregulation in cholesterol metabolism. These data establish GPAT3 as the primary GPAT in white adipose tissue and reveal an important role of the enzyme in regulating energy, glucose, and lipid homeostasis.

scholarly journals Differential Protein Expression in White Adipose Tissue from Obesity-Prone and Obesity-Resistant Mice in Response to High Fat Diet and Anti-Obesity Herbal Medicines

2015 ◽  
Vol 35 (4) ◽  
pp. 1482-1498 ◽  
Author(s):  
Sang Woo Kim ◽  
Tae-Jun Park ◽  
Jae Heon Choi ◽  
Kanikkai Raja Aseer ◽  
Ji-Young Choi ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Proteomic Analysis ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Herbal Medicines ◽  
High Fat ◽  
Body Weight Reduction ◽  
Peptide Mass

Background: One of the most interesting issues in obesity research is why certain humans are obesity-prone (OP) while others are obesity-resistant (OR) upon exposure to a high-calorie diet. However, the pathways responsible for these phenotypic differences are still largely unknown. Methods: In order to discover marker molecules determining susceptibility and/or resistance to obesity in response to high fat diet (HFD) or anti-obesity herbal medicine (TH), we conducted comparative proteomic analysis of white adipose tissue (WAT) from OP, OR, as well as TH-treated mice. Results: OP mice fed HFD gained approximately 33% more body weight than OR mice, and TH significantly reduced body weight gain in HFD-fed mice by 30%. These mice were further subjected to proteomic analysis using two-dimensional electrophoresis (2-DE) combined with matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF-MS). Proteomic data revealed 59 spots that were differentially regulated from a total of 1,045 matched spots, and 57 spots of these were identified as altered WAT proteins between OP and OR mice by peptide mass finger printing. Interestingly, 45 proteins were similarly regulated in OR mice in response to TH treatment. Of these, 10 proteins have already been recognized in the context of obesity; however, other proteins involved in obesity susceptibility or resistance were identified for the first time in the present study. Conclusion: Our results suggest that TH actively contributed to body weight reduction in HFD-fed obese mice by altering protein regulation in WAT, and it was also found that TH-responsive proteins can be used as potent molecules for obesity treatment.

High-fat diet induces site-specific unresponsiveness to LPS-stimulated STAT3 activation in the hypothalamus

2014 ◽  
Vol 306 (1) ◽  
pp. R34-R44 ◽  
Author(s):  
Beatriz de Carvalho Borges ◽  
Rodrigo Rorato ◽  
Ernane Torres Uchoa ◽  
Paula Marangon ◽  
Glauber S. F. da Silva ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Brain Stem ◽  
High Fat Diet ◽  
Control Diet ◽  
Body Weight Loss ◽  
Hypothalamic Nucleus ◽  
High Fat

Hypophagia induced by inflammation is associated with Janus kinase (JAK)-2/signal transducer and activator of transcription (STAT) 3 signaling pathway, and leptin-mediated hypophagia is also mediated by JAK2-STAT3 pathway. We have previously reported that lipopolysaccharide (LPS) did not reduce food intake in leptin-resistant high-fat diet (HFD) rats but maintained body weight loss. We investigated whether changes in p-STAT3 expression in the hypothalamus and brain stem could account for the desensitization of hypophagia in HFD animals after a low LPS dose (100 μg/kg). Wistar rats fed standard diet (3.95 kcal/g) or HFD (6.3 kcal/g) for 8 wk were assigned into control diet-saline, control diet-LPS, HFD-saline, and HFD-LPS groups. LPS reduced feeding in the control diet but not HFD. This group showed no p-STAT3 expression in the paraventricular nucleus (PVN) and ventromedial hypothalamic nucleus (VMH), but sustained, though lower than control, p-STAT3 in the nucleus of the solitary tract (NTS) and raphe pallidus (RPa). LPS decreased body weight in HFD rats and increased Fos expression in the NTS. LPS increased body temperature, oxygen consumption, and energy expenditure in both control diet and HFD rats, and this response was more pronounced in HFD-LPS group. Brown adipose tissue (BAT) thermogenesis and increased energy expenditure seem to contribute to body weight loss in HFD-LPS. This response might be related with increased brain stem activation. In conclusion, LPS activates STAT3-mediated pathway in the hypothalamus and brain stem, leading to hypophagia, however, LPS effects on food intake, but not body weight loss, are abolished by leptin resistance induced by HFD. The preserved STAT3 phosphorylation in the brain stem suggests that unresponsiveness to LPS on STAT3 activation under HFD might be selective to the hypothalamus.

scholarly journals Cannabinoid Type 1 (CB1) Receptors on Sim1-Expressing Neurons Regulate Energy Expenditure in Male Mice

Endocrinology ◽  
2014 ◽  
Vol 156 (2) ◽  
pp. 411-418 ◽  
Author(s):  
Pierre Cardinal ◽  
Luigi Bellocchio ◽  
Omar Guzmán-Quevedo ◽  
Caroline André ◽  
Samantha Clark ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
Cb1 Receptor ◽  
Cb1 Receptors ◽  
High Fat ◽  
Brown Adipose

The paraventricular nucleus of the hypothalamus (PVN) regulates energy balance by modulating not only food intake, but also energy expenditure (EE) and brown adipose tissue thermogenesis. To test the hypothesis that cannabinoid type 1 (CB1) receptor in PVN neurons might control these processes, we used the Cre/loxP system to delete CB1 from single-minded 1 (Sim1) neurons, which account for the majority of PVN neurons. On standard chow, mice lacking CB1 receptor in Sim1 neurons (Sim1-CB1-knockout [KO]) had food intake, body weight, adiposity, glucose metabolism, and EE comparable with wild-type (WT) (Sim1-CB1-WT) littermates. However, maintenance on a high-fat diet revealed a gene-by-diet interaction whereby Sim1-CB1-KO mice had decreased adiposity, improved insulin sensitivity, and increased EE, whereas feeding behavior was similar to Sim1-CB1-WT mice. Additionally, high-fat diet-fed Sim1-CB1-KO mice had increased mRNA expression of the β3-adrenergic receptor, as well as of uncoupling protein-1, cytochrome-c oxidase subunit IV and mitochondrial transcription factor A in the brown adipose tissue, all molecular changes suggestive of increased thermogenesis. Pharmacological studies using β-blockers suggested that modulation of β-adrenergic transmission play an important role in determining EE changes observed in Sim1-CB1-KO. Finally, chemical sympathectomy abolished the obesity-resistant phenotype of Sim1-CB1-KO mice. Altogether, these findings reveal a diet-dependent dissociation in the CB1 receptor control of food intake and EE, likely mediated by the PVN, where CB1 receptors on Sim1-positive neurons do not impact food intake but hinder EE during dietary environmental challenges that promote body weight gain.

scholarly journals Body Composition Changes in Female APOE*3Leiden.CETP Transgenic Mice After 5-week Injection of Resveratrol-encapsulated Liposomes to Inguinal White Adipose Tissue (P21-041-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Zeynep Goktas ◽  
Md Shahjalal Hossain Khan ◽  
Yujiao Zu ◽  
Lei Hao ◽  
Shu Wang
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Transgenic Mice ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Saline Control ◽  
Control Group ◽  
High Fat

Abstract Objectives Many cell culture and animal studies have demonstrated that Trans-resveratrol (R) has the potential to induce beige cell formation and activity. Although human studies indicate that R can maintain metabolic health, evidence is inconclusive regarding its browning effectiveness mainly due to its low aqueous solubility and high hepatic metabolism in humans. To combat the shortcomings of R, we have successfully synthesized biocompatible and biodegradable R-encapsulated liposomes (Rlipo). We will directly inject Rlipo into inguinal white adipose tissue (iWAT) in this project. The purpose of this study to evaluate the anti-obesity effects of resveratrol-encapsulated liposomes in female APOE*3Leiden.CETP transgenic mice, which have human-like lipoprotein metabolism. Methods Rlipo was prepared using R and soy phosphatidylcholine (soy-PC) dissolved in ethanol. After mixing and drying with nitrogen, deionized water was added followed by a sonication step. Ultrafiltration was used to remove any unencapsulated R. The void liposomes (Vlipo) were prepared using only soy-PC. Female APOE*3Leiden.CETP mice (n = 40) were fed with a high fat diet (45% of calorie from fat) throughout the study. After 4 weeks of the high-fat diet administration, mice were randomly divided into 4 groups (n = 10) and received iWAT injections of Rlipo, Vlipo, free R and saline (control) once per week for 5 weeks. R concentration was 17.5 mg/kg body weight/week. Body weight and food intake were measured weekly. Body composition of mice was measured using an EchoMRITM every other week. Paired sample t-test and One-way ANOVA were used to analyze differences between means. Results After 5-weeks of treatment compared to baseline, fat percentage differences were 1.99 ± 0.93%, 1.85 ± 0.58%, 1.45 ± 0.67%, and 1.40 ± 0.68% in control, free R, Vlipo and Rlipo groups, respectively. Body weight and fat mass showed a similar trend of change. Although control group showed an increase in lean mass (0.25 ± 0.95 g), RLipo group showed a decrease (−0.14 ± 0.52 g). Food intake was similar among four groups. Conclusions Nanoencapsulation of R can enhance R's anti-obesity effects. However longer treatment time might be necessary to see more prominent results. Funding Sources NIH/NCCIH (Grant R15AT008733).

scholarly journals Emodin Improves Glucose and Lipid Metabolism Disorders in Obese Mice via Activating Brown Adipose Tissue and Inducing Browning of White Adipose Tissue

2020 ◽  
Author(s):  
Long Cheng ◽  
Shuofeng Zhang ◽  
Fei Shang ◽  
Jianning Sun ◽  
Shifen Dong
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Fasting Blood Glucose ◽  
Lipid Levels ◽  
High Fat ◽  
Brown Adipose ◽  
Lipid Metabolites ◽  
O 18

Abstract Background: Obesity has become a worldwide health threat related to type 2 diabetes, hypertension, cardiovascular disease, etc. Activating brown adipocytes and inducing browning of white adipocytes has been proposed as a potential molecular target for obesity treatment. In the present study, we investigated the effects of emodin on browning in mice with high-fat diet (HFD) and explore its underlying pharmacological mechanisms. Methods: The positive effects of emodin (40, 80 mg/kg/day, i.g. for 6 weeks) on lipid metabolism were evaluated in mice model of hyperlipidemia. Hyperlipidemia mice were induced by high-fat diet (60% of kilocalories from fat, 5.24 Kcal/kg) for 8 weeks. Body weight and food intake were monitored every week. After 6 weeks of treatment, fasting blood glucose, oral glucose tolerance, Lee's index, the ratio of fat weight to body weight, blood lipids, and adipose tissues morphology were assayed. Then uncoupling protein 1 (UCP1), CD36, fatty acid transporter 4 (FATP4), peroxisome proliferator activated receptor α (PPARα) and prohibitin (PHB) protein of subcutaneous white adipose tissue (scWAT) and brown adipose tissue (BAT) were analyzed. In addition, the lipid metabolites in adipose tissues were analyzed by ultra-high- performance liquid chromatography with electrospray ionization tandem mass spectrometry.Results: Emodin treatment decreased body weight gain, fasting blood glucose, Lee's index, the ratio of scWAT weight to body weight, and the levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-c) and Leptin in serum, and increased serum adiponectin content and improved glucose tolerance. Furthermore, emodin enhanced the expression of UCP1, CD36, FATP4, PPARα and PHB protein in scWAT and BAT. Meanwhile, emodin can significantly up-regulated lipid levels in scWAT of mice fed with HFD such as PC(O-18:2/22:5), PE(O-18:1/18:2), PE(O-18:2/20:4), PE(O-20:1/20:5), Cer(d14:1/20:0) and SM(d18:0/23:0), and reduced the lipid levels such as PC(O-18:0/20:0), PE(O-18:2/22:2), PE(O-18:0/22:5). In addition, emodin significantly up-regulate lipid levels in BAT of mice fed with HFD such as PC(14:0/16:0), PC(16:0/16:1), PC(16:1/16:1), PC(15:1/18:3), PC(18:0/20:0), LysoPC(20:0), LysoPC(22:0) and LysoPC(22:1), and reduced the lipid levels PC(12:0/20:4) and PC(17:0/22:5). Conclusions: These results indicated that hyperlipidemia could be alleviated by treatment of emodin via promoting browning of white adipose tissue. In addition, the disturbance of some small lipid metabolites in adipose also could be reversed by emodin.

scholarly journals Constitutive Activation of IKKβ in Adipose Tissue Prevents Diet-Induced Obesity in Mice

Endocrinology ◽  
2012 ◽  
Vol 153 (1) ◽  
pp. 154-165 ◽  
Author(s):  
Ping Jiao ◽  
Bin Feng ◽  
Jie Ma ◽  
Yaohui Nie ◽  
Erin Paul ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Energy Expenditure ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
High Fat ◽  
Fatty Acid Binding ◽  
Iκb Kinase ◽  
Age Related

The IκB kinase β (IKKβ) is a master kinase involved in obesity-related inflammation and insulin resistance through nuclear factor κB dependent and independent pathways. However, the effect of IKKβ activation in adipose tissue, the organ critical for storage of excessive energy and initiation of inflammatory responses in the context of obesity, on systemic insulin sensitivity and metabolism, has not been investigated. In our study, we found that mice overexpressing the constitutively active IKKβ in adipose tissue under the control of murine adipocyte fatty acid binding protein (aP2) promoter were protected from age-related and diet-induced body weight gains, despite increased food intake. The aP2-IKKβ SE mice have significantly reduced weights in all white adipose tissue depots and reduced triglyceride contents in adipose tissue, liver, and muscle. Despite increased systemic and tissue inflammation, aP2-IKKβ SE mice displayed decreased blood glucose levels, improved glucose, and insulin tolerance. This may be at least partially attributable to increased energy expenditure. Histological analysis revealed presence of many small adipocytes in white adipose tissue of aP2-IKKβ SE mice fed on high-fat diet. Furthermore, transgenic expression of IKKβ in adipose tissue improved high-fat diet-induced hepatosteatosis. Collectively, increased energy expenditure and reduced plasma free fatty acid levels may contribute to enhanced systemic insulin sensitivity in aP2-IKKβ SE mice. Our study demonstrates that presence of inflammation in adipose tissue before the development of obesity has beneficial effect on metabolism.

Sign in / Sign up

Export Citation Format

Share Document