Browse
Submit Data
Databases
API
Help

Dataset Information

16 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dataset on mice body weights and food intake following treatment with PG545.

ABSTRACT: This data article contains analysis of data observed in E₀ mice placed on high fat diet, and treated by intraperitoneal injections of either normal saline (control) or the heparanase inhibitor PG545, in two different doses. Mice body weights and food intake were measured weekly and analyzed data are presented in graphs. Data will be of value for further understanding the role of the enzyme heparanase in controlling food intake and body weight. For further interpretations, see please "Heparanase inhibition attenuates atherosclerosis progression and liver steatosis in E₀ mice" (Muhammad et al. 2018).

SUBMITTER: Kinaneh S

PROVIDER: S-EPMC6143748 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Dataset on mice body weights and food intake following treatment with PG545.

Kinaneh Safa S Agbaria Mohammad M Abu-Saleh Niroz N Hamoud Shadi S

Data in brief 20180906

This data article contains analysis of data observed in E<sub>0</sub> mice placed on high fat diet, and treated by intraperitoneal injections of either normal saline (control) or the heparanase inhibitor PG545, in two different doses. Mice body weights and food intake were measured weekly and analyzed data are presented in graphs. Data will be of value for further understanding the role of the enzyme heparanase in controlling food intake and body weight. For further interpretations, see please " ...[more]

PMID: 30238043

Similar Datasets

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

Project description:Orexin-A and -B are hypothalamic neuropeptides of 33 and 28-amino acids, which regulate many homeostatic systems including sleep/wakefulness states, energy balance, energy homeostasis, reward seeking and drug addiction. Orexin-A treatment was also shown to reduce tumor development in xenografted nude mice and is thus a potential treatment for carcinogenesis. The aim of this work was to explore in healthy mice the consequences on energy expenditure components of an orexin-A treatment at a dose previously shown to be efficient to reduce tumor development. Physiological approaches were used to evaluate the effect of orexin-A on food intake pattern, energy metabolism body weight and body adiposity. Modulation of the expression of brain neuropeptides and receptors including NPY, POMC, AgRP, cocaine- and amphetamine related transcript (CART), corticotropin-releasing hormone (CRH) and prepro-orexin (HCRT), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored. Our results show that orexin-A treatment does not significantly affect the components of energy expenditure, and glucose metabolism but reduces intraperitoneal fat deposit, adiposity and the expression of several brain neuropeptide receptors suggesting that peripheral orexin-A was able to reach the central nervous system. These findings establish that orexin-A treatment which is known for its activity as an inducer of tumor cell death, do have minor parallel consequence on energy homeostasis control.

| S-EPMC5235373 | biostudies-literature

Inadequate food and water intake determine mortality following stroke in mice.

Project description:Experimental stroke models producing clinically relevant functional deficits are often associated with high mortality. Because the mechanisms that underlie post-stroke mortality are largely unknown, results obtained using these models are often difficult to interpret, thereby limiting their translational potential. Given that specific forms of post-stroke care reduce mortality in patients, we hypothesized that inadequate food and water intake may underlie mortality following experimental stroke. C57BL/6 mice were subjected to 1?h of intraluminal filament middle cerebral artery occlusion. Nutritional support beginning on the second day after filament middle cerebral artery occlusion reduced the 14-day mortality rate from 59% to 15%. The surviving mice in the post-stroke support group had the same infarct size as non-surviving control mice, suggesting that post-stroke care was not neuroprotective and that inadequate food and/or water intake are the main reasons for filament middle cerebral artery occlusion-induced mortality. This notion was supported by the presence of significant hypoglycemia, ketonemia, and dehydration in control mice. Taken together, these data suggest that post-filament middle cerebral artery occlusion mortality in mice is not primarily caused by ischemic brain damage, but secondarily by inadequate food and/or water intake. Thus, providing nutritional support following filament middle cerebral artery occlusion greatly minimizes mortality bias and allows the study of long-term morphological and functional sequelae of stroke in mice.

| S-EPMC5464703 | biostudies-other

LEAP2 changes with body mass and food intake in humans and mice.

Project description:Acyl-ghrelin administration increases food intake, body weight, and blood glucose. In contrast, mice lacking ghrelin or ghrelin receptors (GHSRs) exhibit life-threatening hypoglycemia during starvation-like conditions, but do not consistently exhibit overt metabolic phenotypes when given ad libitum food access. These results, and findings of ghrelin resistance in obese states, imply nutritional state dependence of ghrelin's metabolic actions. Here, we hypothesized that liver-enriched antimicrobial peptide-2 (LEAP2), a recently characterized endogenous GHSR antagonist, blunts ghrelin action during obese states and postprandially. To test this hypothesis, we determined changes in plasma LEAP2 and acyl-ghrelin due to fasting, eating, obesity, Roux-en-Y gastric bypass (RYGB), vertical sleeve gastrectomy (VSG), oral glucose administration, and type 1 diabetes mellitus (T1DM) using humans and/or mice. Our results suggest that plasma LEAP2 is regulated by metabolic status: its levels increased with body mass and blood glucose and decreased with fasting, RYGB, and in postprandial states following VSG. These changes were mostly opposite of those of acyl-ghrelin. Furthermore, using electrophysiology, we showed that LEAP2 both hyperpolarizes and prevents acyl-ghrelin from activating arcuate NPY neurons. We predict that the plasma LEAP2/acyl-ghrelin molar ratio may be a key determinant modulating acyl-ghrelin activity in response to body mass, feeding status, and blood glucose.

| S-EPMC6715358 | biostudies-literature

IL-37 Expression Reduces Lean Body Mass in Mice by Reducing Food Intake.

Project description:The human cytokine interleukin (IL)-37 is an anti-inflammatory member of the IL-1 family of cytokines. Transgenic expression of IL-37 in mice protects them from diet-induced obesity and associated metabolic complications including dyslipidemia, inflammation and insulin resistance. The precise mechanism of action leading to these beneficial metabolic effects is not entirely known. Therefore, we aimed to assess in detail the effect of transgenic IL-37 expression on energy balance, including food intake and energy expenditure. Feeding homozygous IL-37 transgenic mice and wild-type (WT) control mice a high-fat diet (HFD; 45% kcal palm fat) for 6 weeks showed that IL-37 reduced body weight related to a marked decrease in food intake. Subsequent mechanistic studies in mice with heterozygous IL-37 expression versus WT littermates, fed the HFD for 18 weeks, confirmed that IL-37 reduces food intake, which led to a decrease in lean body mass, but did not reduce fat mass and plasma lipid levels or alterations in energy expenditure independent of lean body mass. Taken together, this suggests that IL-37 reduces lean body mass by reducing food intake.

| S-EPMC6121375 | biostudies-literature

Targeting Clic1 for the Treatment of Obesity: A Novel Therapeutic Strategy to Reduce Food Intake and Body Weight

Project description:Overconsumption of energy-rich food is a key driver of the obesity epidemic. However, the neural circuits that regulate food overconsumption are highly complex and many molecular components of these circuits remain unknown. Our recent studies attribute a novel role of Clic1 as a driver of food intake and overconsumption. Clic1 is expressed in the arcuate nucleus of the hypothalamus and expression specifically increases in Agrp/Npy neurons in the fasted state. Importantly, Clic1 exists in two forms and fasting induces a transformation from the predominant soluble enzymatic form to the membrane-associated ion channel form. Clic1KO mice eat significantly less and have a lower body weight than WT littermates when either fed chow or high fat diet. Furthermore, pharmacological inhibition of Clic1 inhibition results in suppression of food intake and promotes highly efficacious weight loss in obese mice.

2023-07-31 | GSE229799 | GEO

Immediate increase in food intake following exercise messages.

Project description:Communications to stimulate weight loss include exercise-promotion messages that often produce unsatisfactory results due to compensatory behavioral and metabolic mechanisms triggered by physical activity. This research investigated potential automatic facilitation of eating immediately after exercise messages in the absence of actual exercise. Two controlled experiments demonstrated greater than control food intake following exposure to print messages typical of exercise campaigns as well as subliminal presentation of action words associated with exercise (e.g., "active"). These inadvertent effects may explain the limited efficacy of exercise-promotion programs for weight loss, particularly when systematic dietary guidelines are absent.

| S-EPMC4807735 | biostudies-literature

Variations in body weight, food intake and body composition after long-term high-fat diet feeding in C57BL/6J mice.

Project description:To investigate the variations in body weight, food intake, and body composition of both male and female C57BL/6J mice during a diet-induced obesity model with high-fat diet (HFD) feeding.Mice were individually housed and fed ad libitum either a low-fat diet (LFD, 10% calories from fat; n?=?15 male, n?=?15 female) or HFD (45% calories from fat; n?=?277 male, n?=?278 female) from 8 to 43 weeks of age. Body weight, food intake, and body composition were routinely measured.Body weight was significantly increased with HFD (vs. LFD) in males from week 14 (P?=?0.0221) and in females from week 27 (P?=?0.0076). Fat mass and fat-free mass of all groups were significantly increased over time (all P?<?0.0001), with a large variation observed in fat mass. Baseline fat mass, fat-free mass, and daily energy intake were significant predictors of future body weight for both sexes (P?<?0.0001). Baseline fat mass was a significant predictor of future body fat (P?<?0.0001).Both males and females have large variations in fat mass, and this variability increases over time, while that of fat-free mass remains relatively stable. Sex differences exist in HFD responses and multivariate predicting models of body weight.

| S-EPMC4180788 | biostudies-literature

Reduced food intake and body weight in mice deficient for the G protein-coupled receptor GPR82.

Project description:G protein-coupled receptors (GPCR) are involved in the regulation of numerous physiological functions. Therefore, GPCR variants may have conferred important selective advantages during periods of human evolution. Indeed, several genomic loci with signatures of recent selection in humans contain GPCR genes among them the X-chromosomally located gene for GPR82. This gene encodes a so-called orphan GPCR with unknown function. To address the functional relevance of GPR82 gene-deficient mice were characterized. GPR82-deficient mice were viable, reproduced normally, and showed no gross anatomical abnormalities. However, GPR82-deficient mice have a reduced body weight and body fat content associated with a lower food intake. Moreover, GPR82-deficient mice showed decreased serum triacylglyceride levels, increased insulin sensitivity and glucose tolerance, most pronounced under Western diet. Because there were no differences in respiratory and metabolic rates between wild-type and GPR82-deficient mice our data suggest that GPR82 function influences food intake and, therefore, energy and body weight balance. GPR82 may represent a thrifty gene most probably representing an advantage during human expansion into new environments.

| S-EPMC3247265 | biostudies-literature

Peripheral Spexin Inhibited Food Intake in Mice.

Project description:Spexin (SPX, NPQ), a novel endogenous neuropeptide, was firstly identified by bioinformatics. Spexin gene and protein widely distributed in the central nervous system and peripheral tissues, such as the hypothalamus and digestive tract. The role of spexin in appetite regulation in mammalian is still unclear. The present study was designed to investigate the mechanism and effect of peripheral spexin on food intake in mice. During the light period, an intraperitoneal (i.p.) injection of spexin (10 nmol/mouse) significantly inhibited cumulative food intake at 2, 4, and 6 h after treatment in fasted mice. During the dark period, spexin (1 and 10 nmol/mouse, i.p.) significantly suppressed cumulative food intake at 4 and 6 h after treatment in freely feeding mice. The GALR3 antagonist SNAP37889, not GALR2 antagonist, significantly antagonized the inhibitory effect on cumulative food intake (0-6 h) induced by spexin. Spexin significantly reduced the mRNA level of Npy mRNA, not Agrp, Pomc, Cart, Crh, Orexin, or Mch, in the hypothalamus. Spexin (10 nmol/mouse, i.p.) increased the number of c-Fos positive neurons in hypothalamic AHA and SCN, but not in ARC, DMN, LHA, PVN, SON, or VMH. The hypothalamic p-CaMK2 protein expression was upregulated by spexin. This study indicated that acute peripheral injection of spexin inhibited mouse food intake. The anorectic effect may be mediated by GALR3, and inhibiting neuropeptide Y (NPY) via p-CaMK2 and c-Fos in the hypothalamus.

| S-EPMC7426757 | biostudies-literature

Peripheral administration of prokineticin 2 potently reduces food intake and body weight in mice via the brainstem.

Project description:Background and purposeProkineticin 2 (PK2) has recently been shown to acutely reduce food intake in rodents. We aimed to determine the CNS sites and receptors that mediate the anorectic effects of peripherally administered PK2 and its chronic effects on glucose and energy homeostasis.Experimental approachWe investigated neuronal activation following i.p. administration of PK2 using c-Fos-like immunoreactivity (CFL-IR). The anorectic effect of PK2 was examined in mice with targeted deletion of either prokineticin receptor 1 (PKR1) or prokineticin receptor 2 (PKR2), and in wild-type mice following administration of the PKR1 antagonist, PC1. The effect of IP PK2 administration on glucose homeostasis was investigated. Finally, the effect of long-term administration of PK2 on glucose and energy homeostasis in diet-induced obese (DIO) mice was determined.Key resultsI.p. PK2 administration significantly increased CFL-IR in the dorsal motor vagal nucleus of the brainstem. The anorectic effect of PK2 was maintained in mice lacking the PKR2 but abolished in mice lacking PKR1 and in wild-type mice pre-treated with PC1. DIO mice treated chronically with PK2 had no changes in glucose levels but significantly reduced food intake and body weight compared to controls.Conclusions and implicationsTogether, our data suggest that the anorectic effects of peripherally administered PK2 are mediated via the brainstem and this effect requires PKR1 but not PKR2 signalling. Chronic administration of PK2 reduces food intake and body weight in a mouse model of human obesity, suggesting that PKR1-selective agonists have potential to be novel therapeutics for the treatment of obesity.

| S-EPMC3572566 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data