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Ghrelin

Ghrelin is a 28-amino acid peptide hormone produced primarily in the stomach and pancreas.
It functions as a potent stimulator of growth hormone release and plays a key role in regulating appetite, energy balance, and glucose homeostasis.
Ghrelin levels are influenced by fasting and feeding states, and dysregulation of ghrelin signaling has been implicated in various metabolic and endocrine disorders, includeing obesity, diabetes, and cachexia.
Studying ghrelin and its related pathways is crucial for understanding the complex mechanisms governing energy homeostasis and developing potential therapuetic interventions.

Most cited protocols related to «Ghrelin»

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Publication 2015
A Fibers Arachis hypogaea Butter Cacao Diet Flavor Enhancers Fluorescence Food Ghrelin Hormones Infrared Rays Injections, Intraperitoneal Lighting Mus Photometry Rubber Vanilla
One of the most important features of an evidence map is the cataloging of the large number and variety of outcomes reported in the published literature. This step typically occurs after data extraction since the scope of an evidence-map database is large. Thus, it is often difficult to pre-define all outcome categories of interest. The research team worked with the stakeholder panel to classify outcomes into clinically and biologically meaningful outcome categories that could be used in evidence-map analyses. The research team recorded outcomes reported in each publication and took the first attempt in identifying clinically and biologically relevant groups. Standardized coding was then developed for each outcome category. Feedback was sought from the stakeholder panel, and the outcome categories and coding were modified based on the final consensus of the stakeholder panel. Table 2 shows the final list of outcomes for each outcome category that are reported in the studies included in the LCS evidence-map database. Specifically, outcomes related to appetite or satiety ratings such as hunger score and desire to eat were often rated by a visual analog scale (VAS) and were classified under the ‘Appetite’ category. Outcomes focused on neurological measurements and sensing signals by the brain were classified under the ‘Energy Sensing’ category. Body weight, body composition and changes in weight-related outcomes were classified under the ‘Body Weight or Composition’ category. The ‘Dietary Intake’ category included outcomes such as energy intake, dietary intake, food intake and carbohydrate intake, and finally the ‘Glycemic’ category included glucose, insulin and gastric hormones. Our stakeholder panel did not identify additional outcomes that were not reported in the literature. Both outcome categories and full outcome lists were included in the evidence-map database, which can be used in future analyses with current or new outcome category coding.

Outcomes of interest by outcome groups in the LCS evidence-map database

Outcome groupsOutcomes of interest
AppetiteAppetite ratings using a visual analog scale (VAS), hunger, desire to eat, fullness, prospective consumption, thirst, motivational and behavioral factors reported through questionnaire
Energy sensing by brainNeurological measurements (fMRI, EEG), sensory rating (sweetness, intensity, pleasantness, sensory specific satiation), taste, perception and preference, taste reaction time
Body weight or body compositionBody weight, body composition, BMI, waist circumferences, weight or BMI changes
Dietary intakeEnergy intake, dietary intake, food intake, carbohydrate intake, sugar intake, salt intake, water intake
GlycemicGlucose, Hemoglobin A1c (HbA1c), insulin concentration, insulin sensitivity, hypoglycemia, glucagon, glucose-dependent insulinotropic peptide (GIP), glucagon-like peptide-1 (GLP-1), peptide tyrosine tyrosine (PYY), cholecystokinin (CCK), enterostatin, ghrelin, leptin, somatostatin, oxyntomodulin
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Publication 2016
Body Composition Brain Carbohydrates Cholecystokinin Eating fMRI Gastric Inhibitory Polypeptide Ghrelin Glucagon Glucagon-Like Peptide 1 Glucose Hemoglobin A, Glycosylated Hormones Hunger Hypoglycemia Insulin Insulin Sensitivity Leptin Motivation Oxyntomodulin procolipase Sodium Chloride, Dietary Somatostatin Stomach Taste Thirst tyrosyltyrosine Visual Analog Pain Scale Waist Circumference
Animal numbers required for the dietary challenge were estimated using a priori power analyses [G*Power v3.1.5]. Based on our preliminary data, differences in fat content between TBT-exposed and control males when maintained with the HFD are ≥ 23% with SEM within groups of ≤ 10%. Hence, setting type I and II errors (α and β) at 0.05 and the effect size d = 1.47, the minimum sample size required for a Power (1−β) of 0.8 was calculated to be ≥ 7 animals per group.
Animals from F0-F4 were maintained on a standard diet (SD–Rodent Diet 20 5053*; PicoLab) throughout the experiment. F4 males and females (avoiding siblings within the same gender) were maintained on a higher fat diet (HFD–Mouse Diet 20 5058*; PicoLab) between weeks 19 and 25. Mice were subsequently returned to the SD for 8 more weeks prior to euthanasia at 33 weeks of age (Supplementary Fig. 1B). Body weight and body composition were measured weekly using EchoMRITM Whole Body Composition Analyzer, which provides lean, fat and water content information. Total water weight includes free water mainly from the bladder and water contained in lean tissue. For the fasting challenge, animals were fasted for 16 H at week 32. Body weight and body composition were measured before and after fasting and percentage of body weight and fat and lean weight loss was calculated. At week 33 animals were euthanized by isofluorane exposure followed by cardiac exsanguination after 4 H fasting. Blood was drawn into a heparinized syringe and centrifuged for 15 min at 5000 rpm at 4 °C. Plasma was transferred to a clean tube and preserved at −80 °C. Leptin levels from males and females were analyzed using the Mouse Leptin ELISA kit (Crystal Chem). Seven metabolic hormones in plasma were analyzed using Luminex® multiplexing technology (Bio-Plex ProTM Diabetes kit, Bio-Rad, Supplementary Table 4) following manufacture´s protocol in eight non-sibling randomly selected F4 males from each group. Adiponectin levels in plasma were measured using Adiponectin (mouse) EIA Kit (Cayman Chemical). Hormone level changes range from 25% (glucagon) to 220% (ghrelin) with SEM within groups of ≤ 15%. Setting the conditions as described above with an effect size d = 3.47, the minimum sample size was calculated to be 3 animals per group.
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Publication 2017
Adiponectin Animals BLOOD Body Composition Body Weight Caimans Diabetes Mellitus Diet Diet, High-Fat Enzyme-Linked Immunosorbent Assay Euthanasia Exsanguination Females Ghrelin Glucagon Heart Hormones Leptin Males Mice, House Plasma Rodent Syringes Therapy, Diet Tissues Urinary Bladder
Data are expressed as means ± SEM. The incremental areas under the curve (iAUC) for blood glucose, serum insulin, subjective satiety and in vitro rate of starch hydrolysis as well as the negative area under the curve for glucose (neg AUC), were calculated using the trapezoid model. The glycaemic and insulinaemic indexes (GI and II) were calculated from the 120 min incremental post-prandial area for blood glucose and serum insulin by using WWB as a reference (GI and II = 100). In addition, the course of glycaemia was analyzed by calculation a glycaemic profile (GP); The time (min) during which the blood glucose was above fasting concentration was divided with the incremental peak value (mM) of blood glucose for each subject and test meal (Graph Pad Prism, version 4.03, Graph Pad Software, San Diego, CA, USA). In the cases where the blood glucose concentration remained above fasting for the entire 180 min, the duration value was set to 180 min. A GP index was calculated from the GP by using WWB as a reference (GP Index = 100). HI was calculated from the 180 min incremental area for starch hydrolysis in vitro by using WWB as a reference. Relative changes (%) from fasting concentration to the nadir and to the concentration at 180 min after commencing breakfast were calculated for plasma ghrelin.
The data were analyzed with a general linear model (ANOVA) followed by Tukey's multiple comparison test (MINITAB, release 14.13, Minitab Inc, State College, PA). In the cases of unevenly distributed residuals (tested with Anderson-Darling and considered unevenly distributed when p < 0.05), Box Cox transformation were performed on the data prior to the ANOVA.
Significant difference between the products at different time points where evaluated using a mixed model (PROC MIXED in SAS release 8.01, SAS Institute Inc, Cary, NC) with repeated measures and an autoregressive covariance structure. When significant interactions between treatment and time were found, Tukey's multiple comparison test were performed for each time point (MINITAB, release 14.13, Minitab Inc).
Correlation analysis was conducted to evaluate the relation among dependent measures with the use of Spearman's partial coefficients controlling for subjects (two-tailed test), (SPSS software, version 16.0; SPSS Inc, Chicago, IL, USA).
Due to problems drawing capillary blood samples from one subject, the blood glucose statistics was analyzed with n = 11. One subject failed to ingest the WGRP meal according to instructions and data from this product for that subject was therefore excluded from the statistical analysis.
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Publication 2009
Blood Glucose Capillaries Ghrelin Glucose Hydrolysis Insulin neuro-oncological ventral antigen 2, human Plasma prisma Satiation Serum Starch Trapezoid Bones
All analyses were cross-sectional and performed using SAS/STAT 8.2. Leptin, ghrelin, and adiponectin were square-root transformed and insulin log transformed based on the distribution of residuals from the multivariate regression models. We evaluated the relationship of age, sex, BMI, and time of storage of blood sample on hormones using multiple regression. Partial correlations adjusted for age, sex, and BMI were calculated for hormones and QUICKI, with and without control of other potential confounders. The relationships between hormones and sleep were evaluated using multiple linear regression after control for potential confounders including age, sex, BMI, SDB, and morningness tendencies (as measured using the Horne-Ostberg questionnaire, an indirect surrogate of earlier rising time). In all analyses involving insulin, glucose, and QUICKI (but not leptin, ghrelin, and adiponectin), participants with diabetes (self-reported diagnosis, or currently taking insulin or diabetic medications, or with glucose >300 mg/dl) were excluded. Participants with SDB were not removed from the analyses shown. When controlling for AHI in models, participants who used continuous positive airway pressure or who had inadequate sleep were excluded. Because controlling for AHI did not significantly change the sleep-hormone regression coefficients, these analyses are not shown. The relationship of BMI with average nightly sleep was evaluated using a quadratic fit. This was examined using multiple visits (n = 1,828) from 1,040 participants with sleep diary data available. Mixed modeling techniques were used to account for within-subject correlation for participants with multiple visits. SAS procedure mixed was used for modeling and hypothesis testing using robust standard errors and a compound symmetric within-subject correlation structure. All reported p values are two-sided. For illustrative purposes, changes in leptin, ghrelin, and BMI for different sleep amounts were calculated at the average values and sex distribution of the relevant sample.
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Publication 2004
11-dehydrocorticosterone Adiponectin BLOOD Continuous Positive Airway Pressure Diabetes Mellitus Diagnosis Ghrelin Glucose Hormones Insulin Leptin Pharmaceutical Preparations Plant Roots Sleep

Most recents protocols related to «Ghrelin»

The primary outcome was glucose iAUC. Secondary outcomes were iAUC for insulin, glucagon-like peptide 1 (GLP-1), gastric inhibitory polypeptide (GIP), peptide YY (PYY), ghrelin, leptin, and glucagon.
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Publication 2023
Gastric Inhibitory Polypeptide Ghrelin Glucagon Glucagon-Like Peptide 1 Glucose Insulin Leptin Peptide YY
The chemical analysis was performed as previously described [21 (link)]. Appetite-related hormones, including insulin, glucagon-like peptide (GLP-1), peptide YY3–36 (PYY3–36), cholecystokinin-8 (CCK-8), and ghrelin, were assayed using an enzyme-linked immunosorbent kit (Jiangsu Meimian Industrial Co., Ltd, Yancheng, China), while the blood glucose was measured with a biochemical kit (Shanghai Rongsheng Biotech Co., Ltd., Shanghai, China).
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Publication 2023
Blood Glucose cholecystokinin 8 Enzymes Ghrelin Glucagon-Like Peptides Hormones Immunosorbents Insulin peptide YY (3-36)
Blood samples were collected in EDTA tubes and a DPPIV inhibitor (Millipore) and protease inhibitor cocktail (Sigma) was immediately added, according to the manufacturer’s instructions. Samples were centrifuged at 1000× g for 10 min and the plasma was aliquoted and stored at −30 °C. A Human Metabolic Hormone Magnetic Bead Panel (HMHEMAG-34K, Milliplex, Merck, Santiago, Chile) [19 (link)] was used to simultaneously determine plasma concentrations of ghrelin, leptin, gastric inhibitory polypeptide (GIP), glucagon-like peptide 1 (GLP-1), peptide YY (PYY), pancreatic polypeptide (PP), glucagon, amylin, insulin, and C-peptide, using a Luminex 200 System (Merck, Santiago, Chile), according to the manufacturers’ instructions.
Post-prandial glucose concentrations were measured at 0, 30, 60, and 120 min with a glucometer (Accu-Check, Roche, Santiago, Chile) and plasma 7α-hydroxy-4-cholesten-3-one (7α-HC) was determined by liquid chromatography coupled mass spectrometry (LC-MS/MS) by the Clinical Laboratory of the Pontificia Universidad Católica (Santiago, Chile) (intra-assay coefficient of variation = 5.6%) [20 (link)].
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Publication 2023
Amylin Biological Assay BLOOD C-Peptide Clinical Laboratory Services Dipeptidyl-Peptidase IV Inhibitors Edetic Acid Gastric Inhibitory Polypeptide Ghrelin Glucagon Glucagon-Like Peptide 1 Glucose Homo sapiens Hormones Insulin Leptin Liquid Chromatography Mass Spectrometry Pancreatic Polypeptide Peptide YY Plasma Protease Inhibitors
The studied group consisted of 60 patients (group termed urolithiasis patients—UP), which: (1) reported to the urology office and were qualified for the treatment due to the need for extracorporeal shockwave lithotripsy—(ESWL); (2) showed hyperuricemia (in men and post-menopausal women above 7 mg/dL (416.4 µmol/L), in premenopausal women above 6 mg/dL (356.9 µmol/L)) and did not take before any medications lowering UA; (3) had abnormal blood pressure values (>130/85 mmHg) or received antihypertensive treatment, and (4) showed an abnormal waist circumference > 94 cm in male(M), > 80 cm in female(F).
After the initial examination in the form of determining the level of serum glucose, high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) and performing morphology, samples were selected, leaving only those patients who showed at least 3 out of 5 features of MetS ((1) incorrect waist size—for Caucasian, Middle East, and Mediterranean population: 94 cm (M), 80 cm (F); (2) TG = 150 mg/dL or appropriate therapy; (3) High-density lipoprotein cholesterol (HDL-C) 40 mg/dL (M), 50 mg/dL (F), or appropriate therapy; (4) blood pressure: 130/85 mmHg or appropriate therapy, and (5) fasting blood glucose 100 mg/dL or using appropriate therapy) and did not show features of other acute or chronic inflammatory conditions. Finally, 57 patients aged 27–60 met the qualification criteria and were included in this study.
The control group (CG) comprised 30 healthy volunteers who reported to the laboratory for their check-ups. The conditions for participation in the study were age (18–60 years) and the absence of acute and chronic inflammation, pregnancy, and diagnosed diseases. After the initial examination in the form of determining the levels of glucose, HDL-C, and TG and performing morphology, samples were selected, leaving those patients who did not show signs of MetS and did not show signs of other acute or chronic inflammatory conditions. Finally, 29 patients aged 22–60 were qualified for the study.
The structure of the study group is shown in Figure 2.
After qualification, all eligible participants had their UA, ghrelin, leptin, IL-6, TNF-α, and CRP serum levels measured. Next, in both studied groups, urinalysis assessments were made. The full research model is presented in Figure 3.
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Publication 2023
Antihypertensive Agents Blood Glucose Blood Pressure Chronic Condition Extracorporeal Shockwave Lithotripsy Ghrelin Glucose Healthy Volunteers High Density Lipoprotein Cholesterol Hyperuricemia Inflammation Leptin Males Patients Pharmaceutical Preparations Postmenopause Pregnancy Serum Therapeutics Triglycerides Tumor Necrosis Factor-alpha Urinalysis Urolithiasis Waist Circumference White Person Woman

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Publication 2023
Acclimatization Animals Axon Diploid Cell Eye Fibrosis Food Ghrelin Gossypium Hormones Lens, Crystalline Light Mus Neurons Operative Surgical Procedures Photometry Plexiglas Saline Solution Satiation Virus

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More about "Ghrelin"

Ghrelin is a 28-amino acid peptide hormone primarily produced in the stomach and pancreas.
It functions as a potent stimulator of growth hormone (GH) release and plays a crucial role in regulating appetite, energy balance, and glucose homeostasis.
This appetite-stimulating hormone, also known as the 'hunger hormone,' is influenced by fasting and feeding states.
Dysregulation of ghrelin signaling has been implicated in various metabolic and endocrine disorders, including obesity, diabetes, and cachexia (wasting syndrome).
Studying ghrelin and its related pathways, such as DPP4 inhibitors, is essential for understanding the complex mechanisms governing energy homeostasis.
Researchers can leverage tools like the Bio-Plex 200 system, Diprotinin-A, and Pefabloc to accurately measure ghrelin levels and its interactions with other metabolic hormones using assays like the Bio-Plex Pro Mouse Diabetes Assay and the MILLIPLEX MAP Human Metabolic Hormone Magnetic Bead Panel.
These techniques, combined with the use of Sigma protease inhibitors, help ensure the integrity and reliability of ghrelin research.
PubCompare.ai revolutionizes ghrelin research by helping users locate the most robust and reliable protocols from literature, pre-prints, and patents.
Its AI-driven comparisons ensure researchers identify the best protocols and products, enhancing reproducibility and accuracy in their ghrelin studies.
By utilizing PubCompare.ai, scientists can experience the power of optimized ghrelin research and contribute to the deeper understanding of this crucial hormone's role in energy homeostasis and related metabolic conditions.