scholarly journals Pyroglutamyl leucine, a peptide in fermented foods, attenuates dysbiosis by increasing host antimicrobial peptide

2019 ◽  
Vol 3 (1) ◽  
Author(s):  
Saki Shirako ◽  
Yumi Kojima ◽  
Naohiro Tomari ◽  
Yasushi Nakamura ◽  
Yasuki Matsumura ◽  
...  
Keyword(s):  
Body Weight ◽  
Oral Administration ◽  
Antimicrobial Peptide ◽  
High Fat Diet ◽  
Control Diet ◽  
Experimental Colitis ◽  
Fermented Foods ◽  
Food Protein ◽  
High Fat ◽  
Tryptic Fragment

Abstract PyroGlu-Leu is present in certain food protein hydrolysates and traditional Japanese fermented foods. Our previous study demonstrated that the oral administration of pyroGlu-Leu (0.1 mg/kg body weight) attenuates dysbiosis in mice with experimental colitis. The objective of this study was to elucidate why such a low dose of pyroGlu-Leu attenuates dysbiosis in different animal models. High fat diet extensively increased the ratio of Firmicutes/Bacteroidetes in feces of rats compared to control diet. Oral administration of pyroGlu-Leu (1 mg/kg body weight) significantly attenuated high fat diet-induced dysbiosis. By focusing on the production of intestinal antimicrobial peptides, we found that pyroGlu-Leu significantly increased the level of 4962 Da peptides, which identified as the propeptide of rattusin or defensin alpha 9, in ileum. We also observed increased tryptic fragment peptides from rattusin in the lumen. Here, we report that orally administered pyroGlu-Leu attenuates dysbiosis by increasing in the host antimicrobial peptide, rattusin.

scholarly journals Effect of selective expression of dominant-negative PPARγ in pro-opiomelanocortin neurons on the control of energy balance

2016 ◽  
Vol 48 (7) ◽  
pp. 491-501 ◽  
Author(s):  
Madeliene Stump ◽  
Deng-Fu Guo ◽  
Ko-Ting Lu ◽  
Masashi Mukohda ◽  
Xuebo Liu ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
High Fat Diet ◽  
Control Diet ◽  
Cre Recombinase ◽  
Dominant Negative ◽  
High Fat ◽  
Pparγ Agonist ◽  
The Brain

Peroxisome proliferator-activated receptor-γ (PPARγ), a master regulator of adipogenesis, was recently shown to affect energy homeostasis through its actions in the brain. Deletion of PPARγ in mouse brain, and specifically in the pro-opiomelanocortin (POMC) neurons, results in resistance to diet-induced obesity. To study the mechanisms by which PPARγ in POMC neurons controls energy balance, we constructed a Cre-recombinase-dependent conditionally activatable transgene expressing either wild-type (WT) or dominant-negative (P467L) PPARγ and the tdTomato reporter. Inducible expression of both forms of PPARγ was validated in cells in culture, in liver of mice infected with an adenovirus expressing Cre-recombinase (AdCre), and in the brain of mice expressing Cre-recombinase either in all neurons (NESCre/PPARγ-P467L) or selectively in POMC neurons (POMCCre/PPARγ-P467L). Whereas POMCCre/PPARγ-P467L mice exhibited a normal pattern of weight gain when fed 60% high-fat diet, they exhibited increased weight gain and fat mass accumulation in response to a 10% fat isocaloric-matched control diet. POMCCre/PPARγ-P467L mice were leptin sensitive on control diet but became leptin resistant when fed 60% high-fat diet. There was no difference in body weight between POMCCre/PPARγ-WT mice and controls in response to 60% high-fat diet. However, POMCCre/PPARγ-WT, but not POMCCre/PPARγ-P467L, mice increased body weight in response to rosiglitazone, a PPARγ agonist. These observations support the concept that alterations in PPARγ-driven mechanisms in POMC neurons can play a role in the regulation of metabolic homeostasis under certain dietary conditions.

scholarly journals Lactobacillus Rhamnosus Yoba Modulates Serum Cholesterol in Normo-Lipidemic Wistar Rats Fed a High Fat Diet (P20-013-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Adaku Iwueke ◽  
Conrad Miruka ◽  
John Ejekwumadu ◽  
Ronald Kiiza ◽  
Pius Theophilus
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Ldl Cholesterol ◽  
Lactobacillus Rhamnosus ◽  
Hdl Cholesterol ◽  
Male Rats ◽  
Fermented Foods ◽  
Distilled Water ◽  
High Fat

Abstract Objectives The study was aimed at assessing the effects of Lactobacillus rhamnosus yoba on the serum lipid profile and body weight of male Wistar rats fed a high fat diet. Methods 20 seven week old male rats weighing between 120 g and 180 g were used for the study and divided into 4 groups of 5 rats each. The control group was fed normal mice pellets and distilled water, while the other groups were fed mice pellets supplemented with 3% cholesterol and 2% saturated fat in addition to any of distilled water, Lactobacillus rhamnosus yoba or Norvastatin respectively. The body weight was measured at the start of the study and after 2 weeks while serum parameters were measured after 8 weeks. Data was analyzed using SPSS Version 20. ANOVA and Tukey's tests determined significant differences in means at 95% confidence interval. Results Lactobacillus rhamnosus yoba significantly (P < 0.005) modulated weight gain, serum total cholesterol and triglycerides when compared to the control. Similarly, LDL-cholesterol was significantly modulated (P < 0.005) while HDL-cholesterol was significantly enhanced (P < 0.005) when compared to the control. Conclusions The ability of Lactobacillus rhamnosus yoba to elevate HDL cholesterol and modulate LDL-cholesterol without the side effects of statins makes it a potential functional food. In line with the findings, the present study justifies the use of Lactobacillus rhamnosus yoba as a probiotic in fermented foods. Funding Sources NA.

Different Responses to a High-Fat Diet in IL-6 Conditional Knockout Mice Driven by Constitutive GFAP-Cre and Synapsin 1-Cre Expression

2019 ◽  
Vol 109 (2) ◽  
pp. 113-130 ◽  
Author(s):  
Olaya Fernández-Gayol ◽  
Paula Sanchis ◽  
Kevin Aguilar ◽  
Alicia Navarro-Sempere ◽  
Gemma Comes ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Control Diet ◽  
Conditional Knockout ◽  
Mrna Levels ◽  
High Fat ◽  
Significant Difference ◽  
Cellular Source ◽  
The Central Nervous System ◽  
Synapsin 1

Background/Aims: Interleukin-6 (IL-6) is a major cytokine controlling body weight and metabolism, at least in part through actions in the central nervous system (CNS) from local sources. Methods: We herewith report results obtained in conditional IL-6 KO mice for brain cells (Il6ΔGfap and Il6ΔSyn). Results: The reporter RiboTag mouse line demonstrated specific astrocytic expression of GFAP-dependent Cre in the hypothalamus but not in other brain areas, whereas that of synapsin 1-dependent Cre was specific for neurons. Feeding a high-fat diet (HFD) or a control diet showed that Il6ΔGfap and Il6ΔSyn mice were more prone and resistant, respectively, to HFD-induced obesity. Energy intake was not altered in HFD experiments, but it was reduced in Il6ΔSyn male mice following a 24-h fast. HFD increased circulating insulin, leptin, and cholesterol levels, decreased triglycerides, and caused impaired responses to the insulin and glucose tolerance tests. In Il6ΔGfap mice, the only significant difference observed was an increase in insulin levels of females, whereas in Il6ΔSyn mice the effects of HFD were decreased. Hypothalamic Agrp expression was significantly decreased by HFD, further decreased in Il6ΔGfap, and increased in Il6ΔSyn female mice. Hypothalamic Il-6 mRNA levels were not decreased in Il6ΔSyn mice and even increased in Il6ΔGfapmale mice. Microarray analysis of hypothalamic RNA showed that female Il6ΔGfap mice had increased interferon-related pathways and affected processes in behavior, modulation of chemical synaptic transmission, learning, and memory. Conclusion: The present results demonstrate that brain production of IL-6 regulates body weight in the context of caloric excess and that the cellular source is critical.

scholarly journals The Effects of Duodenojejunal Omega Switch in Combination with High-Fat Diet and Control Diet on Incretins, Body Weight, and Glucose Tolerance in Sprague-Dawley Rats

2017 ◽  
Vol 28 (3) ◽  
pp. 748-759 ◽  
Author(s):  
Dominika Stygar ◽  
Tomasz Sawczyn ◽  
Bronisława Skrzep-Poloczek ◽  
Aleksander J. Owczarek ◽  
Natalia Matysiak ◽  
...  
Keyword(s):  
Body Weight ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Control Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
And Control

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 Gynostemma Pentaphyllum Extract Ameliorates High-Fat Diet-Induced Obesity in C57BL/6N Mice by Upregulating SIRT1

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2475 ◽  
Author(s):  
Hyun Sook Lee ◽  
Su-Min Lim ◽  
Jae In Jung ◽  
So Mi Kim ◽  
Jae Kyoung Lee ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Fatty Acid Synthase ◽  
Binding Protein ◽  
Regulatory Element ◽  
Control Diet ◽  
Sirtuin 1 ◽  
Hormone Sensitive Lipase ◽  
High Fat ◽  
Gynostemma Pentaphyllum

Gynostemma pentaphyllum is widely used in Asia as a herbal medicine to treat type 2 diabetes, dyslipidemia, and inflammation. Here, we investigated the anti-obesity effect and underlying mechanism of G. pentaphyllum extract (GPE) enriched in gypenoside L, gypenoside LI, and ginsenoside Rg3 and obtained using a novel extraction method. Five-week-old male C57BL/6N mice were fed a control diet (CD), high-fat diet (HFD), HFD + 100 mg/kg body weight (BW)/day GPE (GPE 100), HFD + 300 mg/kg BW/day GPE (GPE 300), or HFD + 30 mg/kg BW/day Orlistat (Orlistat 30) for 8 weeks. The HFD-fed mice showed significant increases in body weight, fat mass, white adipose tissue, and adipocyte hypertrophy compared to the CD group; but GPE inhibited those increases. GPE reduced serum levels of triglyceride, total cholesterol, and LDL-cholesterol, without affecting HDL-cholesterol. GPE significantly increased AMPK activation and suppressed adipogenesis by decreasing the mRNA expression of CCAAT/enhancer binding protein-α (C/EBPα), peroxisome proliferator-activated receptor-γ (PPARγ), sterol regulatory element-binding protein-1c (SREBP1c), PPARγ coactivator-1α, fatty acid synthase (FAS), adipocyte protein 2 (AP2), and sirtuin 1 (SIRT1) and by increasing that of carnitine palmitoyltransferase (CPT1) and hormone- sensitive lipase (HSL). This study demonstrated the ameliorative effect of GPE on obesity and elucidated the underlying molecular mechanism.

scholarly journals Chronic administration of brain-derived neurotrophic factor in the hypothalamic paraventricular nucleus reverses obesity induced by high-fat diet

2010 ◽  
Vol 298 (5) ◽  
pp. R1320-R1332 ◽  
Author(s):  
ChuanFeng Wang ◽  
Rebecca J. Godar ◽  
Charles J. Billington ◽  
Catherine M. Kotz
Keyword(s):  
Body Weight ◽  
Body Fat ◽  
Paraventricular Nucleus ◽  
Neurotrophic Factor ◽  
High Fat Diet ◽  
Control Diet ◽  
Brain Derived Neurotrophic Factor ◽  
Hypothalamic Paraventricular Nucleus ◽  
High Fat ◽  
Metabolic Indices

An acute injection of brain-derived neurotrophic factor (BDNF) in the hypothalamic paraventricular nucleus (PVN) reduces body weight by decreasing feeding and increasing energy expenditure (EE), in animals on standard laboratory chow. Animals have divergent responses to a high-fat diet (HFD) exposure, with some developing obesity and others remaining lean. In the current study, we tested two hypotheses: 1) BDNF in the PVN reverses HFD-induced obesity, and 2) animals with higher body fat have a greater physiological response to BDNF than those with less body fat. Eighty-four 10-wk old rats were allowed HFD ad libitum for 9 wk and then prepared with bilateral PVN cannulas. Animals were then divided into tertiles based on their body fat rank: high, intermediate, and low (H, I, and L). Each group was further divided into 2 subgroups and then PVN injected with BDNF or control (artificial cerebrospinal fluid, aCSF) every other day for 3 wk. Energy intake (EI), body weight, and body composition were measured. At study's end, rats were killed to allow measurement of other metabolic indices. In parallel, another 12 rats were fed control diet (CD), PVN-cannulated and injected with aCSF. HFD exposure induced obesity, particularly in the H body fat group, with a significant increase in EI, body weight, fat mass, liver size, and serum glucose, triglycerides, insulin, and leptin. BDNF significantly reduced EI, body weight, body fat, lean mass, and serum metabolic indices. These BDNF effects were greatest in the H body fat group. These data indicate that BDNF reduced HFD-induced obesity and metabolic syndrome-like measures, and the animals with the most body fat had the most significant response to BDNF.

scholarly journals Melatonin counteracts changes in hypothalamic gene expression of signals regulating feeding behavior in high-fat fed rats

2015 ◽  
Vol 21 (3) ◽  
Author(s):  
María J. Ríos-Lugo ◽  
Vanesa Jiménez-Ortega ◽  
Pilar Cano-Barquilla ◽  
Pilar Fernández Mateos ◽  
Eduardo J. Spinedi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Feeding Behavior ◽  
High Fat Diet ◽  
Control Diet ◽  
Male Rats ◽  
Mrna Levels ◽  
High Fat ◽  
Medial Basal Hypothalamus ◽  
Group I

AbstractPrevious studies indicate that the administration of melatonin caused body weight and abdominal visceral fat reductions in rodent models of hyperadiposity. The objective of the present study performed in high-fat fed rats was to evaluate the activity of melatonin on gene expression of some medial basal hypothalamus (MBH) signals involved in feeding behavior regulation, including neuropeptide Y (NPY), proopiomelanocortin (POMC), prolactin-releasing peptide (PrRP), leptin- and insulin-receptors (R) and insulin-R substrate (IRS)-1 and -2. Blood levels of leptin and adiponectin were also measured.Adult Wistar male rats were divided into four groups (n=16 per group): (i) control diet (3% fat); (ii) high-fat (35%) diet; (iii) high-fat diet+melatonin; (iv) control diet+melatonin. Rats had free access to high-fat or control chow and one of the following drinking solutions: (a) tap water; (b) 25 μg/mL of melatonin.After 10 weeks, the high-fat fed rats showed augmented MBH mRNA levels of NPY, leptin-R, PrRP, insulin-R, IRS-1 and IRS-2. The concomitant administration of melatonin counteracted this increase. Feeding of rats with a high-fat diet augmented expression of the MBH POMC gene through an effect insensitive to melatonin treatment. The augmented levels of circulating leptin and adiponectin seen in high-fat fed rats were counteracted by melatonin as was the augmented body weight: melatonin significantly attenuated a body weight increase in high-fat fed rats without affecting chow or water consumption. Melatonin augmented plasma leptin and adiponectin in control rats.The results indicate that an effect on gene expression of feeding behavior signals at the central nervous system (CNS) may complement a peripheral rise of the energy expenditure produced by melatonin to decrease body weight in high-fat fed rats.

scholarly journals Different Doses of Curcumin Supplementation Did Not Improve Biochemical Profile and Weight in C57BL/6 Male Mice Receiving High-Fat Diet

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 699-699
Author(s):  
Caroline Silva ◽  
Priscila Fassini ◽  
Leandra Ramalho ◽  
Daniela Sartori ◽  
Vivian Suen
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Statistical Significance ◽  
Control Diet ◽  
Standard Diet ◽  
Biochemical Profile ◽  
Male Mice ◽  
High Fat ◽  
Pancreatic Steatosis ◽  
Different Doses

Abstract Objectives Curcuma supplementation has been investigated to prevent or treat obesity. However, evidence suggests development of pancreatic steatosis as well. In this context, the aim of this study was to investigate the effect of different doses of curcumin supplementation on weight, biochemical profile, and histological analysis of the pancreas and liver of mice fed a high-fat diet. Methods This was an experimental, longitudinal and randomized study. Fifty C57BL/6 male mice, thirty days age, were separated into five groups: 1. Standard diet (n = 10); 2. High-fat diet (n = 10); 3. High-fat diet plus 50 mg of curcumin/kg of body weight (n = 10); 4. High-fat diet plus 250 mg of curcumin/kg of body weight (n = 10); 5. High-fat diet plus 500 mg of curcumin/kg of body weight (n = 10). Group 1 was fed a standard control diet (AIN 93 G), group 2 was fed a purified high-fat diet (AIN 93 HF 60%) and both groups received only the vehicle (carboxymethyl cellulose - CMC 1%) by gavage. Mice from groups 3, 4 and 5 were fed a purified high-fat diet (AIN 93 HF 60%) plus curcumin at different doses (50, 250 and 500 mg/kg of body weight diluted in 1% CMC) by gavage for twelve weeks. All groups received food and water ad libitum. At the end of the experimental period, we analysed lipid profile, blood glucose, insulin, histology of the pancreas and liver. ANOVA one way and Kruskal-Wallis analysis were performed and a value of P ˂ 0.05 was used to denote statistical significance. Results Curcumin supplementation did not improve weight and biochemical profile. Additionally, histological changes were not observed at any dose of supplementation. Pancreatic or hepatic steatosis was not evidenced in high-fat diet groups and also in the groups who received curcumin, suggesting no toxic effects at the different doses of supplementation provided. Conclusions Our results suggest that curcumin supplementation has no beneficial effect on weight gain prevention and biochemical profile, regardless of the dose administered. Funding Sources FAPESP (São Paulo Research Foundation).

scholarly journals Maternal and postnatal high-fat diet consumption programs energy balance and hypothalamic melanocortin signaling in nonhuman primate offspring

2017 ◽  
Vol 313 (2) ◽  
pp. R169-R179 ◽  
Author(s):  
Elinor L. Sullivan ◽  
Heidi M. Rivera ◽  
Cadence A. True ◽  
Juliana G. Franco ◽  
Karalee Baquero ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Nonhuman Primate ◽  
High Fat Diet ◽  
Control Diet ◽  
High Fat ◽  
Melanocortin System ◽  
Juvenile Period ◽  
Primate Model ◽  
Related Peptide

Maternal high-fat-diet (HFD) consumption during pregnancy decreased fetal body weight and impacted development of hypothalamic melanocortin neural circuitry in nonhuman primate offspring. We investigated whether these impairments during gestation persisted in juvenile offspring and examined the interaction between maternal and early postnatal HFD consumption. Adult dams consumed either a control diet (CTR; 15% calories from fat) or a high-saturated-fat diet (HFD; 37% calories from fat) during pregnancy. Offspring were weaned onto a CTR or HFD at ~8 mo of age. Offspring from HFD-fed dams displayed early catch-up growth and elevated body weight at 6 and 13 mo of age. Maternal and postnatal HFD exposure reduced the amount of agouti-related peptide fibers in the paraventricular nucleus of the hypothalamus. Postnatal HFD consumption also decreased the amount of agouti-related peptide fibers in the arcuate nucleus of the hypothalamus. Postnatal HFD was associated with decreased food intake and increased activity. These results support and extend our previous findings of maternal diet effects on fetal development and reveal, for the first time in a nonhuman primate model, that maternal HFD-induced disturbances in offspring body weight regulation extended past gestation into the juvenile period. Maternal HFD consumption increases the risk for offspring developing obesity, with the developmental timing of HFD exposure differentially impacting the melanocortin system and energy balance regulation. The present findings provide translational insight into human clinical populations, suggesting that profound health consequences may await individuals later in life following intrauterine and postnatal HFD exposure.

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