scholarly journals Impact of Orexin-A Treatment on Food Intake, Energy Metabolism and Body Weight in Mice

PLoS ONE ◽  
2017 ◽  
Vol 12 (1) ◽  
pp. e0169908 ◽  
Author(s):  
Anne Blais ◽  
Gaëtan Drouin ◽  
Catherine Chaumontet ◽  
Thierry Voisin ◽  
Anne Couvelard ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Metabolism ◽  
Food Intake ◽  
Orexin A

scholarly journals The Effect of a 2-Week Red Ginseng Supplementation on Food Efficiency and Energy Metabolism in Mice

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1726
Author(s):  
Hyejung Hwang ◽  
Jisu Kim ◽  
Kiwon Lim
Keyword(s):  
Body Weight ◽  
Energy Metabolism ◽  
Food Intake ◽  
Weight Control ◽  
Fat Oxidation ◽  
Substrate Utilization ◽  
Mrna Levels ◽  
Red Ginseng ◽  
Energy Substrate ◽  
Metabolism Regulation

Red ginseng (RG) ingestion reportedly affects body weight, food intake, and fat accumulation reduction. It also induces changes in energy metabolism regulation and glycemic control. Previously, 2-week RG ingestion with endurance training was found to enhance fat oxidation during exercise. However, such effects on energy metabolism and the expression of mRNAs related to energy substrate utilization in resting mice (untrained mice) are still unclear. Here, we determined the effect of RG on energy metabolism and substrate utilization in untrained male mice. Twenty-four mice were separated into an RG group that received a daily dosage of 1 g/kg RG for 2 weeks, and a control (CON). Energy expenditure, blood and tissue glycogen levels, and expression of mRNAs related to energy substrate utilization in muscles were measured before and 2 weeks after treatment. Total food intake was significantly lower in the RG than in the CON group (p < 0.05), but final body weights did not differ. Carbohydrate and fat oxidation over 24 h did not change in either group. There were no significant differences in gastrocnemius GLUT4, MCT1, MCT4, FAT/CD36, and CPT1b mRNA levels between groups. Thus, the effects of RG ingested during rest differ from the effects of RG ingestion in combination with endurance exercise; administering RG to untrained mice for 2 weeks did not change body weight and energy metabolism. Therefore, future studies should consider examining the RG ingestion period and dosage for body weight control and improving energy metabolism.

scholarly journals Regulation of food intake and body weight by recombinant proghrelin

2009 ◽  
Vol 297 (6) ◽  
pp. E1269-E1275 ◽  
Author(s):  
Weizhen Zhang ◽  
Arundhati Majumder ◽  
Xiaobin Wu ◽  
Michael W. Mulholland
Keyword(s):  
Body Weight ◽  
Amino Acid ◽  
Energy Metabolism ◽  
Food Intake ◽  
Normal Saline ◽  
Biological Function ◽  
Intraperitoneal Administration ◽  
Fat Consumption ◽  
Regulate Food Intake ◽  
Cumulative Food Intake

Ghrelin is a 28-amino-acid hormone derived from the endoproteolytic processing of its prehormone proghrelin. Although ghrelin has been reported to regulate food intake and body weight, it is still unknown whether proghrelin exercises any biological function. Here we show that recombinant proghrelin alters food intake and energy metabolism in mice. After intraperitoneal administration of recombinant proghrelin (100 nmol/kg body wt), cumulative food intake was significantly increased at days 1, 2, and 3 (6 ± 0.3, 13 ± 0.5, and 20 ± 0.8 g vs. 5 ± 0.2, 10 ± 0.2, and 16 ± 0.3 g of the control mice receiving normal saline, respectively, n = 6, P < 0.05). Twelve-hour cumulative food intake in the light photo period in mice treated with proghrelin increased significantly relative to the control (2.1 ± 0.04 vs. 1.3 ± 0.2 g, n = 6, P < 0.05). No change in 12-h cumulative food intake in the dark photo period was observed between mice treated with proghrelin and vehicle (4.2 ± 0.6 vs. 4.3 ± 0.6 g, n = 6, P > 0.05). This is associated with a decrease in body weight (0.42 ± 0.04 g) for mice treated with proghrelin, whereas control animals gained body weight (0.31 ± 0.04 g). Mice treated with proghrelin demonstrate a significant decrease in respiratory quotient, indicating an increase in fat consumption. Recombinant proghrelin is functionally active with effects on food intake and energy metabolism.

scholarly journals Chronic Central Leptin Decreases Food Intake and Improves Glucose Tolerance in Diet-Induced Obese Mice Independent of Hypothalamic Malonyl CoA Levels and Skeletal Muscle Insulin Sensitivity

Endocrinology ◽  
2011 ◽  
Vol 152 (11) ◽  
pp. 4127-4137 ◽  
Author(s):  
Wendy Keung ◽  
Arivazhagan Palaniyappan ◽  
Gary D. Lopaschuk
Keyword(s):  
Body Weight ◽  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Food Intake ◽  
Glucose Tolerance ◽  
Tolerance Test ◽  
Acid Oxidation ◽  
Obese Mice ◽  
Malonyl Coa ◽  
Skeletal Muscle Insulin Sensitivity

Although acute leptin administration in the hypothalamus decreases food intake and increases peripheral energy metabolism, the peripheral actions of central chronic leptin administration are less understood. In this study, we investigated what effects chronic (7 d) intracerebroventricular (ICV) administration of leptin has on energy metabolism and insulin sensitivity in diet-induced obese mice. C57/BL mice were fed a low-fat diet (LFD; 10% total calories) or high-fat diet (HFD; 60% total calories) for 8 wk after which leptin was administered ICV for 7 consecutive days. Mice fed a HFD showed signs of insulin resistance, as evidenced by an impaired glucose tolerance test. Chronic leptin treatment resulted in a decrease in food intake and body weight and normalization of glucose clearance but no improvement in insulin sensitivity. Chronic ICV leptin increased hypothalamic signal transducer and activator of transcription-3 and AMP-activated protein kinase phosphorylation but did not change hypothalamic malonyl CoA levels in HFD fed and LFD-fed mice. In the gastrocnemius muscles, the levels of malonyl CoA in both leptin-treated groups were lower than their respective control groups, suggesting an increase in fatty acid oxidation. However, only in the muscles of ICV leptin-treated LFD mice was there a decrease in lipid metabolites including diacylglycerol, triacylglycerol, and ceramide. Our results suggest that chronic ICV leptin decreases food consumption and body weight via a mechanism different from acute ICV leptin administration. Although chronic ICV leptin treatment in HFD mice improves glucose tolerance, this occurs independent of changes in insulin sensitivity in the muscles of HFD mice.

scholarly journals The Ciji-Hua’ai-Baosheng II Formula Attenuates Chemotherapy-Induced Anorexia in Mice With H22 Hepatocellular Carcinoma

2021 ◽  
Vol 12 ◽  
Author(s):  
Shengyan Xi ◽  
Xiangyang Zhai ◽  
Yanan Wang ◽  
Yuewen Gong ◽  
Biqian Fu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Body Weight ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Inhibitory Effect ◽  
The Body ◽  
Untreated Group ◽  
Orexin A ◽  
Regulatory Factors ◽  
Group 5

Background: Ciji-Hua’ai-Baosheng II Formula (CHB-II-F) is a traditional Chinese medicine formula, which specifically targets different aspects of chemotherapy-induced adverse effects in patients with cancer. In our clinical application, CHB-II-F significantly alleviated chemotherapy-induced anorexia (loss of appetite) and improved the quality of life for patients with tumor during and after chemotherapy. However, the mechanism of CHB-II-F in alleviation of chemotherapy-induced anorexia remains to be further investigated.Aim of Study: To explore the therapeutic effect and mechanism of CHB-II-F on chemotherapy-induced anorexia in the mice model of H22 hepatoma.Materials and Methods: A total of 72 Kunming mice of SPF grade were inoculated subcutaneously with H22 hepatoma cells into the right anterior armpit of the mice. After 1 week of seeding, mice were injected intraperitoneally with a high dose of 5-fluorouracil (200 mg/kg 5-FU) to establish the model of chemotherapy. The mice were randomly divided into six groups: untreated group, 5-FU group, 5-FU plus Yangzheng Xiaoji capsule (YZXJC) group, and three groups of 5-FU plus different concentrations of CHB-II-F. All the mice in each group were treated for 14 days. The body weight, food intake, tumor volume, and tumor weight of mice were measured, and pathological examinations of tumor tissue, stomach, and duodenum were carried out. Expressions of serum Leptin, Neuropeptide Y (NPY), epidermal cell growth factor (EGF), Motilin (MTL), Orexin A (OXA), Gastrin (GAS), Ghrelin, Prostaglandin E2 (PGE2), and jejunum superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were examined. The protein and mRNA levels of proopiomelanocortin (POMC), Orexin receptor 1 (OX1R), neuropeptide Y (NPY), cocaine and amphetamine regulated transcript peptide (CART), Agouti gene-related protein (AgRP), Leptin receptor (Ob-R), and Ghrelin receptor (GHSR) were examined in hypothalamus, and the protein levels of substance P (SP) and 5-hydroxytryptamine (5-HT) in duodenum were measured.Results: The combination of CHB-II-F and 5-FU could enhance the inhibitory effect of 5-FU on tumor. The tumor inhibition rates of 5-FU group, YZXJC group, CHB-II-F(H) group, CHB-II-F(M) group, and CHB-II-F(L) group were 58.88, 28.08, 54.96, 37.69, and 28.61%, respectively. Compared with untreated group and 5-FU group, CHB-II-F significantly increased the body weight and food intake of tumor-bearing mice; increased the content of NPY, Orexin A, Ghrelin, GAS, MTL, EGF, and PGE2 in serum and the activity of SOD in jejunum; and decreased the content of Leptin in serum and the content of MDA in jejunum. Compared with untreated group and 5-FU group, CHB-II-F also enhanced the expression of OX1R, GHSR, NPY, and AgRP protein and gene and decreased the expression of Ob-R, POMC, and CART protein and gene in hypothalamus of mice, and the gene expression was consistent with the protein expression. In addition, CHB-II-F decreased the expression of 5-HT and SP protein in duodenum.Conclusion: In the murine model of H22 hepatocellular carcinoma (HCC) receiving chemotherapy, CHB-II-F enhances the inhibitory effect of 5-FU on tumor, significantly improves the pathological injury of gastrointestinal tract caused by chemotherapy, and regulates the secretion of gastrointestinal hormones. It may alleviate chemotherapy-induced anorexia by affecting appetite regulatory factors in the feeding area of hypothalamus central nervous system and peripheral appetite regulatory factors.

scholarly journals A novel traditional Chinese medicine ameliorates fatigue-induced cardiac hypertrophy and dysfunction via regulation of energy metabolism

2019 ◽  
Vol 316 (6) ◽  
pp. H1378-H1388 ◽  
Author(s):  
Rong Huang ◽  
Yuan-Chen Cui ◽  
Xiao-Hong Wei ◽  
Chun-Shui Pan ◽  
Quan Li ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Metabolism ◽  
Chinese Medicine ◽  
Food Intake ◽  
Traditional Chinese Medicine ◽  
Cardiac Hypertrophy ◽  
Western Blot ◽  
Prolonged Exercise ◽  
Heart Function ◽  
Heart Weight

Prolonged exercise and exercise training can adversely affect cardiac function in some individuals. QiShenYiQi Pills (QSYQ), which are a compound Chinese medicine, have been previously shown to improve pressure overload-induced cardiac hypertrophy. We hypothesized that QSYQ can ameliorate as well the fatigue-induced cardiac hypertrophy. This study was to test this hypothesis and underlying mechanism with a focus on its role in energy regulation. Male Sprague-Dawley rats were used to establish exercise adaptation and fatigue model on a motorized rodent treadmill. Echocardiographic analysis and heart function test were performed to assess heart systolic function. Food-intake weight/body weight and heart weight/body weight were assessed, and hematoxylin and eosin staining and immunofluorescence staining of myocardium sections were performed. ATP synthase expression and activity and ATP, ADP, and AMP levels were assessed using Western blot and ELISA. Expression of proteins related to energy metabolism and IGF-1R signaling was determined using Western blot. QSYQ attenuated the food-intake weight/body weight decrease, improved myocardial structure and heart function, and restored the expression and distribution of myocardial connexin 43 after fatigue, concomitant with an increased ATP production and a restoration of metabolism-related protein expression. QSYQ upgraded the expression of IGF-1R, P-AMPK/AMPK, peroxisome proliferator-activated receptor-γ coactivator-1α, nuclear respiratory factor-1, P-phosphatidylinositol 3-kinase (PI3K)/PI3K, and P-Akt/Akt thereby attenuated the dysregulation of IGF-1R signaling after fatigue. QSYQ relieved fatigue-induced cardiac hypertrophy and enhanced heart function, which is correlated with its potential to improve energy metabolism by regulating IGF-1R signaling. NEW & NOTEWORTHY Prolonged exercise may impact some people leading to pathological cardiac hypertrophy. This study using an animal model of fatigue-induced cardiac hypertrophy provides evidence showing the potential of QiShenYiQi Pills, a novel traditional Chinese medicine, to prevent the cardiac adaptive hypertrophy from development to pathological hypertrophy and demonstrates that this effect is correlated with its capacity for regulating energy metabolism through interacting with insulin-like growth factor-1 receptor.

scholarly journals The effect of Crocodile (Crocodylus Siamensis) Oil on Hepatic Energy Homeostasis Mechanism and Mitochondrial Function in Rats

2021 ◽  
Author(s):  
Wirasak Fungfuang ◽  
Kongphop Parunyakul ◽  
Krittika Srisuk ◽  
Pitchaya Santativongchai ◽  
Urai Pongchairerk ◽  
...  
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Energy Metabolism ◽  
Food Intake ◽  
Energy Intake ◽  
Tca Cycle ◽  
Liver Weight ◽  
Mitochondrial Morphology ◽  
Sterile Water ◽  
The Tca Cycle

Abstract Background: Fatty acid (FA) consumption can alter hepatic energy metabolism and liver mitochondrial functions. Crocodile oil (CO) is rich in both mono- and polyunsaturated fatty acids that contain natural anti-inflammatory and healing properties. We investigated the effect of CO on energy metabolism and mitochondrial morphology in rat liver.Methods: Twenty-one male Sprague–Dawley rats were randomly divided into three groups. Group 1: rats treated with sterile water (RO); group 2: rats treated with CO (3% v/w); and group 3: rats treated with palm oil (PO) (3 % v/w). Rats were orally administered sterile water, CO, and PO once daily for 7 weeks. Body weight, food intake, liver weight, energy intake, blood lipid profiles, and liver-targeted metabolites were evaluated. Histopathological study of the liver, mitochondrial architecture of liver cell, and HDHD3 protein expression in liver mitochondria were determined.Results: CO treatment had no effect on body weight, liver weight, liver index, dietary energy intake, and serum lipid profiles. The CO group exhibited significantly lower food intake than the RO group. The CO group also showed significantly higher oxaloacetate and malate levels, which encourage the TCA cycle imbalance, than the PO group. CO treatment significantly ameliorated hepatic steatosis as shown by a greater decrease of total surface area of lipid particles than that seen with PO treatment. CO administration maintained the liver’s mitochondrial morphology by upregulating the energetic maintenance protein—HDHD3. Moreover, the chemical-protein interaction also showed that the main fatty acid composition of CO preserved liver metabolism via the AMPK signaling pathway.Conclusion: Crocodile oil could support hepatic function through promoting the TCA cycle, maintaining hepatic mitochondrial architecture, and upregulating HDHD3.

scholarly journals Chronic intracerebroventricular administration of orexin-A to rats increases food intake in daytime, but has no effect on body weight

1999 ◽  
Vol 849 (1-2) ◽  
pp. 248-252 ◽  
Author(s):  
Akihiro Yamanaka ◽  
Takeshi Sakurai ◽  
Takuo Katsumoto ◽  
Masashi Yanagisawa ◽  
Katsutoshi Goto
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Intracerebroventricular Administration ◽  
Orexin A

scholarly journals Parabrachial Interleukin-6 Reduces Body Weight and Food Intake and Increases Thermogenesis to Regulate Energy Metabolism

Cell Reports ◽  
2019 ◽  
Vol 26 (11) ◽  
pp. 3011-3026.e5 ◽  
Author(s):  
Devesh Mishra ◽  
Jennifer E. Richard ◽  
Ivana Maric ◽  
Begona Porteiro ◽  
Martin Häring ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Metabolism ◽  
Food Intake ◽  
Interleukin 6 ◽  
Regulate Energy Metabolism

Tamoxifen antagonizes the effects of estradiol on energy balance and estrous behavior in Syrian hamsters

1993 ◽  
Vol 265 (3) ◽  
pp. R559-R562 ◽  
Author(s):  
G. N. Wade ◽  
J. B. Powers
Keyword(s):  
Body Weight ◽  
Energy Metabolism ◽  
Energy Balance ◽  
Food Intake ◽  
Potent Inhibitor ◽  
Estradiol Benzoate ◽  
Uterine Weight ◽  
Estradiol Treatment ◽  
Syrian Hamsters ◽  
Estrous Behavior

Ovariectomized Syrian hamsters were treated with estradiol benzoate (5 micrograms/day for 4 wk), tamoxifen (500 micrograms/day), an antiestrogen that competes with estradiol for central and peripheral estrogen receptors, or both estradiol benzoate and tamoxifen. As expected, estradiol treatment caused significant decreases in body weight and fat content without affecting food intake. Given alone, tamoxifen had no effect on body weight or composition, but when given concurrently, tamoxifen significantly attenuated the effects of estradiol. These results stand in contrast to findings in rats where nonsteroidal antiestrogens, including tamoxifen, mimic the effects of estradiol on body weight and energy metabolism and are completely devoid of any antiestrogenic actions. As in rats, tamoxifen was a potent inhibitor of estrous behavior, whether induced with estradiol alone or with sequential treatment with estradiol and progesterone. Again, as in rats, tamoxifen acted as an antagonist and a weak estrogen agonist on uterine weight. These findings support the notion that the relative agonistic and antagonistic actions of tamoxifen, and other antiestrogens, vary with species and with the estrogen-sensitive endpoint being investigated.

scholarly journals Single Head-Neck Irradiation Intervention Increases Thyroid Hormone Level and Enhances Energy Metabolism in High-Fat Diet Mice

2020 ◽  
Author(s):  
Qian Lin ◽  
Caishun Zhang ◽  
Manwen Li ◽  
Haidan Wang ◽  
Kaizhen Su ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Energy Metabolism ◽  
Food Intake ◽  
High Fat Diet ◽  
Chow Diet ◽  
High Fat ◽  
Brown Adipose ◽  
Neck Irradiation ◽  
Head Neck

Abstract Radiotherapy, an established treatment of malignant diseases of the head and neck, increases the risk of chronic metabolic disorders. However, the molecular mechanisms responsible for metabolic dysfunction after irradiation remain unknown. We aimed to determine whether single head-neck irradiation intervention changes the levels of thyroid hormones and affects energy metabolism in high-fat diet mice and in chow diet mice. C57BL/6 mice were treated with a single dose of 6 Gy X-ray head-neck irradiation and were fed a high-fat diet. Body weight, accumulated food intake, fasting blood glucose and glucose tolerance were measured during the study. Plasma, brown adipose tissue, thyroid, liver and white adipose tissue were collected for histological analysis. We found that head-neck irradiation significantly increased food intake and decreased body weight in high-fat diet mice. However, there were no obvious changes in chow diet mice. Further studies showed that head-neck irradiation significantly increased levels of 3,5,3’-triiodothyronine and thyroid-stimulating hormone, as well as expression of uncoupling protein 1 in brown adipose tissue and glucose transporter 2 in liver in high-fat diet mice. Our results suggest that single head-neck irradiation intervention increases thyroid hormones levels and enhances energy metabolism in high-fat diet mice.

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