Serum Ghrelin Levels Research Articles

Regulatory Effects of Copper on Ghrelin Secretion in Rat Fundic Glands.

Copper (Cu) is an effective additive in feed for promoting growth. Growth dan axis comprising growth hormone (GH), somatostatin (SS) and GH-releasing hormone (GHRH), with ghrelin regulating their release. The growth-promoting effects of Cu are closely related to ghrelin, but the specific mechanism behind the relationship remains unknown. We investigated the adjustment of ghrelin synthesis and secretion by Cu. Sprague-Dawley rats were fed basal diets with an addition of 0, 120 or 240 mg/kg Cu sulfate for 28 day to establish a growth-promoting model. Signalling molecules relevant to ghrelin synthesis and secretion were detected and mechanistically explored using enzyme-linked immunosorbent assay, quantitative reverse-transcription polymerase chain reaction and Western blot analysis. The 120 mg/kg supplement improved growth performance; significantly increased the serum levels of ghrelin, ghrelin O-acyltransferase (GOAT), acylated ghrelin (AG), GH, and reactive oxygen species (ROS) and decreased those of SS; significantly increased the mRNA and protein expression of ghrelin, GOAT, ghrelin receptor (GHS-R1α), and activator protein 1 (AP-1); increased the phosphorylation ratio of JNK and p38 MAPK; and inhibited the mRNA and protein expression of SS and SS receptor subtype 2 (SSTR2) in gastric fundic gland tissues. Thus, Cu may affect gastric ghrelin synthesis at the transcriptional level by activating the JNK/p38 MAPK pathway through increased ROS levels and regulating the activation of the downstream redox-sensitive transcription factor AP-1. SS plays a crucial determinant role in ghrelin regulation via intragastric Cu. Cu promotes GOAT activity and ghrelin secretion by inhibiting SS secretion, affecting AG levels, and promoting ghrelin acylation through ghrelin/GOAT/GHS-R1α system, modulating ghrelin secretion.

Delphinidin or α-amyrin attenuated liver steatosis and metabolic disarrangement in rats fed a high-fat diet.

Non-alcoholic fatty liver disease (NAFLD) is a liver pathology concomitant with metabolic disarrangement. This study assessed the therapeutic impacts of delphinidin, an anthocyanin, or α-amyrin, a pentacyclic triterpenoid, on NAFLD in rats and the underlying mechanisms involved. NAFLD was established by feeding a high-fat diet (HFD) for 10 weeks, either alone or in combination with delphinidin (40 mg/kg, oral) or α-amyrin (20 mg/kg, oral). Delphinidin or α-amyrin ameliorated the metabolic and histopathological perturbations induced by HFD. These compounds markedly attenuated NAFLD-induced hepatic steatosis, as evidenced by a substantial decrease in body weight, insulin resistance, and liver and adipose tissue indices. Alongside normalization of the atherogenic index, both improved HFD-mediated abnormalities in serum lipids, liver enzymes, leptin, and ghrelin levels. Moreover, their intervention activated the NFE2 like bZIP transcription factor 2 and heme oxygenase 1 pathways and abrogated HFD-triggered activation of mitogen-activated protein kinase 1 signaling. These remedies inhibited hepatic apoptosis and modulated the gene expression of lipogenic enzymes. Furthermore, histological analysis corroborated the suppression of lipid accumulation and amelioration of hepatic architecture in the treated rats. Our findings highlight the hepatoprotective value of delphinidin or α-amyrin against NAFLD and related metabolic diseases through their insulin-sensitizing, anti-inflammatory, antioxidant, and antiapoptotic effects.

Hesperidin facilitating gastrointestinal motility by “Gut-brain axis” and “SCF/C-Kit signaling pathways”

Hesperidin shows promising results as a potential feed additive for enhancing gastrointestinal motility in animals. Gastrointestinal function plays a pivotal role in animal growth and the digestibility of dietary nutrients, with gastrointestinal motor function serving as a crucial component. However, limited research has been conducted on the application of hesperidin as a feed additive to promote gastrointestinal motility. The present study aims to assess the efficacy of Hesperidin as a feed additive in promoting gastrointestinal motility and elucidating its underlying mechanism. A total of 200 newly hatched (1-day-old) broilers with similar body weight were randomly allocated into 4 groups as follows: the control group receiving only the basal diet, and the other 3 groups supplemented with 50, 100, and 150 mg of hesperidin per kg of the basal diet, respectively. Each group consisted of 5 replicates with ten broilers per replicate, and the feeding trial lasted for a duration of 21 d. At 21 d of age, a 5% w/v Evans Blue solution in distilled water was utilized to measure intestinal transit rates (ITR). Gastric emptying (GE) was evaluated by administering a phenol red solution at a concentration of 0.05% w/v (1 mL/broiler). Fifteen broilers from each group were euthanized and immediately dissected to obtain gizzard, hypothalamus, duodenum, and jugular blood samples. Jugular blood samples were collected for brain-gut peptide content analysis, while gizzard, hypothalamus, and duodenum samples were used for immunohistochemical analysis. Real-time qPCR was performed on gizzard samples. The results demonstrated a significant improvement in the GE and ITR of broilers in all treatment groups compared to the control group (P < 0.05), particularly in the 100mg/Kg and 150mg/Kg hesperidin group. Incorporation of hesperidin into the broilers' diet significantly enhances serum levels of ghrelin, encompassing serotonin (5-HT), motilin (MTL), cholecystokinin (CCK), and Stem Cell Factor (SCF) as well as substance P (SP) in the gizzard and duodenal tissues while reducing vasoactive intestinal peptide (VIP) levels (P < 0.05). The group administered a dosage of 150mg/Kg exhibited the most pronounced effect.Immunohistochemistry analysis revealed that hesperidin supplementation up-regulated SP protein content and down-regulated VIP protein content in the hypothalamus, gizzard, and duodenum of broilers (P < 0.05), with the most pronounced effect illustrated in the 150mg/Kg hesperidin group. Furthermore, addition of hesperidin to broiler feed resulted in a significant up-regulation of protein expression and gene expression related to SCF and The protein expression of Receptor tyrosine kinase (C-Kit) was significantly upregulated in the 150mg/Kg group, while the gene expression of C-Kit was significantly upregulated in the 50 mg/Kg group (P < 0.05). In conclusion, hesperidin exhibits promising potential as a feed additive for broilers, as its dietary supplementation of hesperidin improves gastrointestinal motility through modulation of both "gut-brain axis" signaling pathways and "SCF/C-Kit signaling pathways" within broiler chicken's digestive system. Notably, basal diet supplemented with 150mg/Kg hesperidin demonstrates superior efficacy.

Lindera aggregata improves intestinal function and alleviates depressive behaviors through the BDNF/TrkB/CREB signaling pathway induced by CUMS in mice

Depression is a common mental illness, which is highly related to intestinal motor dysfunction and causes a global burden of disease. Lindera aggregata (LA), a traditional medicinal herb, has been used to treat gastrointestinal disorders; however, the effect of LA on depression remains unclear. Here, we assessed the impact of LA on chronic unpredictable mild stress (CUMS)-induced depression in mice and explored the related mechanisms. The results showed that LA ameliorated depressive behaviors in mice exposed to CUMS, as evidenced by improved performance in the sucrose preference test, force swimming test, and open field test, as well as increased serum levels of adrenocorticotropic hormone and 5-hydroxytryptamine. In addition, LA increased the serum levels of D-xylose and ghrelin, indicating that LA can promote gastrointestinal motility. Additional studies revealed that LA relieved CUMS-induced hippocampal tissue damage, as shown by hematoxylin and eosin and Nissl staining. LA increased the expression levels of brain-derived neurotrophic factor (BDNF) and promoted the activation of tropomyosin receptor kinase B (TrkB) and cAMP response element-binding (CREB) in the hippocampus of CUMS-exposed mice or in corticosterone-injured HT22 cells. In conclusion, LA can improve CUMS-induced depressive behavior in mice, potentially through hippocampal neuroprotection mediated by the BDNF/TrkB/CREB signaling pathway, which also contributes to improved intestinal function.

Evaluating the impact of metabolic and cognitive stress on ghrelin and nesfatin-1 hormones in patients with diabetes and diabetic depression.

Nesfatin-1 and ghrelin, initially recognised as hormones involved in regulating energy, have emerged as crucial players with vital functions in various human body systems. In this study, we conducted a comparative assessment of nesfatin-1 and ghrelin responses in individuals experiencing metabolic stress due to diabetes, those with depressive diabetes characterised by both metabolic and mental stress, and healthy controls. We collected blood samples from a total of 90 participants, consisting of 30 people with type II diabetes mellitus (DM), 30 people with type II DM and major depressive disorders, and 30 healthy individuals. Diabetes was diagnosed based on glycated haemoglobin (HbA1c) levels, while depression was assessed using DSM-V criteria. Insulin resistance (HOMA-IR) was calculated, and serum ghrelin and nesfatin-1 levels were measured using ELISA kits. We observed statistically significant decreases in nesfatin-1 and ghrelin levels in the diabetic group (p<0.0001). However, in the depressive diabetic group, nesfatin-1 levels increased significantly, while ghrelin levels decreased further. The nesfatin-1 to ghrelin ratio decreased in the diabetic group but increased significantly in the depressive diabetic group (p<0.0001). Nesfatin-1 and ghrelin hormones exhibit parallel impacts in response to metabolic stress, but nesfatin-1 demonstrates contrasting actions compared to ghrelin when mental stress is added to metabolic stress. The findings of this study suggest that nesfatin-1 and ghrelin hormones may play active roles as protective, prognostic, and even etiological factors in various stress situations, particularly those involving mental stress, in addition to their known functions in regulating energy.

Genetic Variations and Serum Levels of Leptin and Ghrelin in Autism Spectrum Disorder.

This study aims to examine leptin and ghrelin gene polymorphisms and serum levels in children with autism spectrum disorder (ASD). The study comprised a case group of 40 children aged 2-7 diagnosed with ASD and a control group of 40 healthy children. The severity of ASD symptoms was assessed using the Childhood Autism Rating Scale and the Autism Behavior Checklist. Leptin and ghrelin gene variants were genotyped using polymerase chain reaction (PCR) restriction fragment length polymorphism (RFLP) methods. Serum ghrelin and leptin levels were measured using enzyme-linked immunosorbent assay kits. In this study, gene polymorphisms and allele frequencies were examined, and no significant difference was found (P > .05 for all). Our findings indicated no significant difference in leptin serum levels between the groups (P = .584). However, ghrelin serum levels were significantly lower in the ASD group (P = .027). Receiver operating curve analysis to determine the cutoff value of serum ghrelin level as a diagnostic indicator for ASD resulted in a cutoff value of 885.7 pg/mL with 42.50% sensitivity and 85% specificity (P = .021). No significant relationship was found between leptin and ghrelin serum levels and the severity of ASD (P > .05 for all). Our study is the first to evaluate leptin and ghrelin gene polymorphisms in ASD. Our findings indicate no association between leptin and ghrelin gene polymorphisms and ASD. However, our study suggests that ghrelin serum levels may potentially contribute to the etiology of ASD. More research is needed to understand the role of leptin and ghrelin in ASD.

Adipokines in Neuroendocrine Tumors: An Evaluation of the Serum Levels of Ghrelin and Leptin.

Neuroendocrine tumors (NETs) are a heterogeneous group of tumors that are characteristically different from other malignancies. The difference is not only in the prognosis, which is usually more favorable in such patients, but also in the high clinical progression of the disease, where NET patients do not experience the cachexia typical of other malignancies. The purposes of this study were to evaluate the ghrelin and leptin levels in a group of patients diagnosed with gastroenteropancreatic neuroendocrine tumors (GEP-NETs) and bronchopulmonary neuroendocrine tumors (BP-NETs) and to analyze the relationship between the body mass index (BMI), cachexia and selected NET markers. The study group comprised 52 patients with GEP-NETs and BP-NETs, while the controls comprised 67 healthy volunteers. The ghrelin and leptin concentrations were determined in both groups. The concentrations of chromogranin A, serotonin, 5-hydroxyindoleacetic acid (5-HIAA), total cholesterol, triglycerides and glucose were determined in the study group. Characteristics of the study group and of the controls were defined by age, sex and BMI, and the effects of these factors on the ghrelin and leptin concentrations were assessed. The data obtained were subject to statistical analysis. The study cohort showed higher levels of ghrelin as compared to the controls (142.31 ± 26.00 vs. 121.49 ± 35.45, p = 0.016), and no statistical difference in the levels of leptin (11.15 ± 9.6 vs. 12.94 ± 20.30, p = 0.439) were observed. Significantly lower levels of leptin were found in patients with the small intestine primary location, as compared to individuals with primary locations in the lungs and the pancreas (4.9 ± 6.49 vs. 16.97 ± 15.76, p = 0.045, and 4.9 ± 6.49 vs. 12.89 ± 8.56, p = 0.016, respectively). A positive correlation was observed between the leptin levels and the BMIs in both the study group (rS = 0.33, p = 0.016) and the controls (rS = 0.41, p = 0.001). The study group showed a negative correlation between the leptin levels and 5-HIAA (rS = -0.32, p = 0.026) and a negative correlation between the leptin levels and Ki-67 (rS = -0.33, p = 0.018). The control group showed negative correlations between the ghrelin and the volunteer age (rS = -0.41, p = 0.008), the leptin and the volunteer age (rS = -0.44, p < 0.001), the leptin and total cholesterol (rS = -0.24, p < 0.049) as well as the leptin and triglycerides (rS = -0.33, p < 0.006). The current study emphasized the importance of the markers' determination, where ghrelin appears as a valuable diagnostic biomarker in NETs, probably responsible for maintaining a normal BMI, despite the progression of the disease.

Changes in serum ghrelin and resistin levels after sleeve gastrectomy versus one anastomosis gastric bypass: prospective cohort study.

Humoral factors and neural mechanisms play a central role in the pathogenesis of obesity and in weight loss following bariatric surgery. Although various hormones and adipokines, including ghrelin and resistin, are linked to obesity, studies analyzing the changes in fasting ghrelin and resistin levels in patients following one anastomosis gastric bypass (OAGB) are lacking. The authors aimed to investigate resistin and ghrelin levels before and after two commonly used bariatric procedures with different mechanisms of action: sleeve gastrectomy (SG) and OAGB. Fasting serum ghrelin and resistin levels were evaluated by using ELISA in a nonrandomized, prospective cohort study for the pattern of changes in the preoperative period and 1 week, 1 month, 3 months and, 12 months after surgery in age and sex-matched patients with BMI ≥40kg/m 2 undergoing either SG ( n =40) or OAGB ( n =40). Their relationships with demographic parameters such as body weight, BMI, presence of T2DM, HbA 1 C, and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) index were also evaluated. OAGB was superior in weight control compared to the SG group. There were significant differences in resistin and ghrelin levels between the OAGB and SG groups. Ghrelin decreased more in the SG group than the preoperative values. This change in ghrelin levels was more significant at 1 year after SG [preoperative mean (range) level of 334.2 (36.6-972.1) pg/ml decreased to 84 (9.1-227) pg/ml at 1 year] whereas in the OAGB group no significant change was observed [preoperative mean (range) level of 310 (146-548) pg/ml decreased to 264 (112-418) pg/ml at 1 year]. Resistin levels decreased in both groups, especially after 3 months and onward following both operations [the mean (range) resistin levels were 2.6 (0.87-5.4) ng/ml and decreased to 1.1 (0.5-2.4) ng/ml in the SG group vs 2.48 (0.89-6.43) ng/ml decreased to 0.72 (0.35-1.8) ng/ml in OAGB group at 1 year], which was in parallel with changes in HOMA-IR index, body weight, and BMI changes at 1st year. HOMA-IR index changes were similar, but more prominent after OAGB. OAGB was als3 three months and onward), and HOMA-IR changes. This is the first study to compare fasting ghrelin and resistin levels after OAGB and SG. Although similar changes were observed, ghrelin changes were more prominent after SG, whereas resistin were observed after OAGB. OAGB was superior in T2DM control, which was in parallel with weight loss, fasting resistin levels, and HOMA-IR changes suggesting a possible effect of resistin after OAGB in glucose metabolism and insulin resistance.

Does gastric tissue Ghrelin and Leptin correlate with serum values? A pilot study of the Indian Obese population

BackgroundWhile serum Ghrelin and leptin has been studied over the last decades, there are very few human studies correlating the serum levels with the presence of the ghrelin and leptin cells in gastric tissue. MethodsWe have assessed the presence of leptin and ghrelin cells in the resected sleeve of stomach following Laparoscopic Sleeve Gastrectomy (LSG) and correlated the same with serum levels of ghrelin and leptin hormones before and after 6 months of surgery. The study was conducted at department of gastro-intestinal (GI) surgery of a tertiary care hospital from 2017–2019. ResultsForty-five patients participated in the study. Thirty-five of the specimens were negative for ghrelin cells and 29 were negative for leptin cells. While the levels of serum ghrelin in the ghrelin-negative specimen group were lower than normal, the levels in the ghrelin-positive specimen group were significantly higher, which reduced following LSG. In the leptin group, while the leptin-positive group had higher serum levels that dropped after surgery, the leptin-negative group also showed raised serum leptin levels, which further increased after surgery. Serum ghrelin levels showed a positive correlation with serum insulin levels but did not translate to statistically significant increased number of diabetic patients. ConclusionGhrelin and leptin cells are not universally present in the stomach in Indian population. Serum values of leptin and ghrelin correlates positively to the presence of their secreting cells in the Gastric sleeve. This study gives scope to evaluate the presence and distribution of these cells in the gastric sleeve.

Sleep quality in patients with chronic spontaneous urticaria and relation with Orexin-A, leptin, and ghrelin.

Background: Sleep can be affected in patients with chronic spontaneous urticaria (CSU). The mechanisms of sleep regulation remain poorly understood. Orexin-A, a neuroexcitatory peptide, plays a role in coordinating sleep-wake states. Ghrelin and leptin are involved in sleep regulation through the orexin system. Objective: The effects of orexin-A, ghrelin, and leptin on sleep quality in patients with CSU have not been investigated. We aimed to determine the effects of CSU on sleep quality and the association between serum orexin-A, ghrelin, and leptin levels, and sleep quality in patients with CSU. Methods: Thirty-three patients with CSU and 34 sex- and age-matched controls were included in the study. Serum orexin-A, leptin, and ghrelin levels, and the Pittsburgh Sleep Quality Index (PSQI) and the Epworth Sleepiness Scale (ESS) scores were measured in patients with CSU and in the controls; also used were the chronic urticaria quality-of-life questionnaire score and the urticaria activity score used for 7 consecutive days. Results: Median (minimum-maximum) orexin-A, leptin, and ghrelin levels in patients were 385 pg/mL (90-495 pg/mL), 3.1 ng/mL (0-21.2 ng/mL), and 701.8 pg/mL (101.9-827.7 pg/mL), respectively. Median serum orexin-A and leptin levels were higher in the patients compared with the controls (p < 0.001 and p = 0.012, respectively), whereas the median serum ghrelin levels were similar to the controls (p = 0.616). The serum orexin-A level was positively correlated with ghrelin (r = 0.298, p = 0.014), PSQI sleep quality (r = 0.356, p = 0.003), and ESS (r = 0.357, p = 0.003). Conclusion: Serum orexin-A is associated with sleep quality in patients with CSU. Further studies are needed to elucidate the role of ghrelin and leptin on sleep quality in patients with CSU.

Activation of bitter taste receptors (TAS2R) protects against rotenone-induced neurotoxicity: Could ghrelin have a role?

AimsBitter taste receptors (TAS2Rs) and their downstream signaling pathways are expressed not only in the oral tissues but also in extraoral tissues. Emerging data has demonstrated the beneficial effect of ghrelin in neurodegenerative diseases. Gaining more insight into the interaction between TAS2Rs and gut hormones may expand their therapeutic applications. Herein, we aimed to assess the possible effect of TAS2R activation by denatonium benzoate (DB) in modulating functional and neurobiochemical alterations in a model of Parkinson’s disease (PD). Main methodsPD model was induced by daily injection of rotenone (2 mg/kg). Rats received DB (5 mg/kg), atenolol (10 mg/kg), or both concomitantly with rotenone, daily for 28 days. Evaluation of the motor abnormalities and histological examination of brain tissues were conducted. In addition, striatal dopamine contents, immunohistochemical expression of tyrosine hydroxylase, plasma ghrelin level, and biochemical analysis of markers of inflammation and oxidative stress were assessed. Key findingsTreatment with DB increased serum levels of ghrelin and striatal dopamine contents with consequent amelioration of oxidative stress and attenuation of inflammatory cytokines. Moreover, DB treatment significantly ameliorated motor disturbance and histological abnormalities compared to untreated rats. Atenolol inhibited ghrelin release and abolished the positive effect of DB suggesting the involvement of ghrelin on such effects. SignificanceThe current study suggests that TAS2Rs agonists are promising candidates for ameliorating rotenone-induced PD pathology in rats, an action that could be linked to the enhancement of ghrelin release with consequent antioxidant and anti-inflammatory activities.

Serum Ghrelin and Glucagon-like Peptide 1 Levels in Children with Prader-Willi and Bardet-Biedl Syndromes

Prader-Willi syndrome (PWS) and Bardet-Biedl syndrome (BBS) are causes of pediatric syndromic obesity. We aimed to investigate a possible role for ghrelin and glucagon-like peptide-1 (GLP-1) in the pathophysiology of PWS and BBS. The study included 12 children with PWS, 12 children with BBS, 13 pediatric obese controls (OC) and 12 pediatric lean controls (LC). Fasting serum ghrelin and GLP-1 levels were measured by ELISA. In the PWS group, no significant difference was detected for median ghrelin levels when compared with OC and LC, which were 0.96 (0.69-1.15), 0.92 (0.72-1.20) and 1.13 (0.84-1.29) ng/mL, respectively. Similarly, there was no difference in PWS median GLP-1 levels when compared with OC and LC; 1.86 (1.5-2.94), 2.24 (1.62-2.78) and 2.06 (1.8-3.41) ng/mL, respectively. In the BBS group, there was no difference in median ghrelin levels when compared with OC and LC; 1.05 (0.87-1.51), 0.92 (0.72-1.20) and 1.13 (0.84-1.29) ng/mL, respectively. Neither was there a significant difference in median GLP-1 levels; 2.46 (1.91-4.17), 2.24 (1.62-2.78) and 2.06 (1.8-3.41) ng/mL for BBS, OC and LC, respectively. There were no differences in median fasting ghrelin or GLP-1 levels when comparing patients with PWS and BBS with obese or lean peers. However, similar studies with larger series are needed.

Exploring the Role of Metabolic Hormones in Amyotrophic Lateral Sclerosis.

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by progressive loss of motor neurons. Emerging evidence suggests a potential link between metabolic dysregulation and ALS pathogenesis. This study aimed to investigate the relationship between metabolic hormones and disease progression in ALS patients. A cross-sectional study was conducted involving 44 ALS patients recruited from a tertiary care center. Serum levels of insulin, total amylin, C-peptide, active ghrelin, GIP (gastric inhibitory peptide), GLP-1 active (glucagon-like peptide-1), glucagon, PYY (peptide YY), PP (pancreatic polypeptide), leptin, interleukin-6, MCP-1 (monocyte chemoattractant protein-1), and TNFα (tumor necrosis factor alpha) were measured, and correlations with ALSFRS-R, evolution scores, and biomarkers were analyzed using Spearman correlation coefficients. Subgroup analyses based on ALS subtypes, progression pattern of disease, and disease progression rate patterns were performed. Significant correlations were observed between metabolic hormones and ALS evolution scores. Insulin and amylin exhibited strong correlations with disease progression and clinical functional outcomes, with insulin showing particularly robust associations. Other hormones such as C-peptide, leptin, and GLP-1 also showed correlations with ALS progression and functional status. Subgroup analyses revealed differences in hormone levels based on sex and disease evolution patterns, with male patients showing higher amylin and glucagon levels. ALS patients with slower disease progression exhibited elevated levels of amylin and insulin. Our findings suggest a potential role for metabolic hormones in modulating ALS progression and functional outcomes. Further research is needed to elucidate the underlying mechanisms and explore the therapeutic implications of targeting metabolic pathways in ALS management.

Endoscopic transoral outlet reduction induces enterohormonal changes in patients with weight regain after Roux-en-Y gastric bypass

Abstract Background and study aims Transoral outlet reduction (TORe) has long been employed in treating weight regain after Roux-en-Y gastric bypass. However, its impact on gut hormones and their relationship with weight loss remains unknown. Patients and methods This was a substudy of a previous randomized clinical trial. Adults with significant weight regain and dilated gastrojejunostomy underwent TORe with argon plasma coagulation (APC) alone or APC plus endoscopic suturing (APC-suture). Serum levels of ghrelin, GLP-1, and PYY were assessed at fasting, 30, 60, 90, and 120 minutes after a standardized liquid meal. Results were compared according to allocation group, clinical success, and history of cholecystectomy. Results Thirty-six patients (19 APC vs. 17 APC-suture) were enrolled. There were no significant baseline differences between groups. In all analyses, the typical postprandial decrease in ghrelin levels was delayed by 30 minutes, but no other changes were noted. GLP-1 levels significantly decreased at 12 months in both allocation groups. Similar findings were noted after dividing groups according to the history of cholecystectomy and clinical success. The APC cohort presented an increase in PYY levels at 90 minutes, while the APC-suture group did not. Naïve patients had significantly lower PYY levels at baseline (P = 0.01) compared with cholecystectomized individuals. This latter group experienced a significant increase in area under the curve (AUC) for PYY levels, while naïve patients did not, leading to a higher AUC at 12 months (P = 0.0001). Conclusions TORe interferes with the dynamics of gut hormones. APC triggers a more pronounced enteroendocrine response than APC-suture, especially in cholecystectomized patients.

Effect of valproic acid monotherapy on serum leptin and ghrelin levels in epileptic children (literature review)

The incidence of epilepsy varies between industrialized countries and developing ones. Anti-epileptic drugs are the standard of care for epilepsy management with sodium valproate being the most commonly prescribed anti-epileptic drug in children with epilepsy. Valproic acid (VPA) is a first generation anti-epileptic drug used widely as a monotherapy or part of polytherapy for a variety of seizures in children more than two years of age. It is stated that long-term treatment with VPA is associated with risks such as weight gain, hyperinsulinemia, metabolic syndrome, and cardiovascular disease. However,the exact pathogenesis of weight gain has not been clearly identified pathogenetically. Studying the effect of VPA monotherapy on possible causative factors (leptin and ghrelin levels) of weight gain would help in undertaking appropriate preventive actions alongside VPA therapy. We review the available literature on the research carried out on this subject in the following sections.

TUMOR NECROSIS FACTOR-Α AND INTERLEUKIN-6 IN BLOOD SERUM OF INFANTS AND CHILDREN WITH CONGENITAL HEART DISEASES

The aim of the study was to evaluate the levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in infants and children with congenital heart defects (CHD) in comparison with the levels in the control groups. Materials and methods. The volume study included 56 patients, including 35 cyanotic and 21 cyanotic with congenital heart disease, as well as 20 control subjects. We used a specific immunoassay to measure serum ghrelin, TNF-a and IL-6 levels. All patients' cardiac diagnoses were based on clinical examination, laboratory tests, electrocardiography and echocardiography; and none of the patients had pulmonary hypertension. The body mass index (BMI) was calculated as the ratio of body weight (kg) and height squared (m). The study also included 20 healthy infants and children corresponding to age and gender as a control group. Informed consent was obtained from the parents. Results. The results of the analysis indicate a significant increase in IL-6 and TNF-a levels in cyanotic and acyanotic patients with congenital heart defects compared with the control group (P &lt; 0.0001). The findings highlight the importance of cytokines in the pathophysiology of congenital heart defects and their effect on patient growth. It is suggested that elevated levels of IL-6 and TNF-a may stimulate the process of apoptosis, which may play a key role in growth retardation. These data indicate the presence of growth disorders in a significant proportion of patients with congenital heart defects. These results provide additional details about the nature of growth disorders in patients with congenital heart defects and highlight the importance of further research to better understand the molecular and immunological mechanisms associated with this condition. Conclusion. The findings of this study support the hypothesis of the effect of cytokines on growth in congenital heart defects. Elevated levels of IL-6 and TNF-a are likely associated with chronic congestive heart failure and hypoxia. Further research is needed to confirm these results and develop therapeutic strategies for managing growth retardation in children with congenital heart defects.

Study of the relationship between ghrel in hormone and nitric oxide in patients with chronic kidney disease in thi-qar governorate – IRAQ

Objective: When abnormalities in kidney structure or function are evident for more than three months, it is referred to as chronic kidney disease (CKD), a complicated and progressive chronic disorder that can have devastating health effects. Either reduced glomerular filtration rate or indicators of renal injury could be evident. End-stage renal disease (ESRD) patients are increasingly choosing PD, HD, and kidney transplantation as treatments to extend their lives because of the development of renal replacement therapies, such as kidney transplantation, hemodialysis (HD), peritoneal dialysis (PD), and continuous renal replacement therapy (which is frequently used for acute renal failure). Loss of muscle mass may result from dialysis treatments that increase protein breakdown and decrease protein synthesis. These reactions continue after dialysis. The purpose of this research is to look into the connection between the ghrelin. Materials and Method: In order to determine the blood lipid profile and Ghrelin hormone levels, 90 individuals with Chronic Kidney Disease (CKD) on dialysis were divided into 45 males, 45 females, and 90 healthy subjects. The Ghrelin hormone concentration was compared with the other biochemical parameters, and the relationship between the hormones Ghrelin and Nitric Oxide was also found. Results: Ninety healthy subjects and ninety chronic kidney disease (CKD) patients with dialysis had their blood lipid profiles and Ghrelin hormone and nitric oxide levels measured. The results included a comparison of the hormone's concentration with other biochemical parameters and the identification of the hormone's relationship with nitric oxide. Results: When compared to the control group, dialysis patients' nitric oxide levels significantly decreased (p≤0.05). There were no discernible variations in the levels of serum nitric oxide between the sexes. (p &lt; 0.05).Ghrelin levels in the blood serum of dialysis patients were significantly lower than those in the control group (p≤0.05). Additionally, it was demonstrated that the level of the hormone Ghrelin was significantly lower in females than in males (p≤0.05). Conclusion: When comparing dialysis patients to the control group, we detect a significant drop in the levels of Ghrelin Hormone and Nitric Oxide in patients with chronic kidney disease.It follows that low nitric oxide and ghrelin levels in chronic renal disease patients can cause kidney failure to progress to an advanced degree and eventually require dialysis.

Changes in Circulating Acylated Ghrelin and Neutrophil Elastase in Diabetic Retinopathy.

Background and Objectives: The role and the levels of ghrelin in diabetes-induced retinal damage have not yet been explored. The present study aimed to measure the serum levels of total ghrelin (TG), and its acylated (AG) and des-acylated (DAG) forms in patients with the two stages of diabetic retinopathy (DR), non-proliferative (NPDR) and proliferative (PDR). Moreover, the correlation between serum ghrelin and neutrophil elastase (NE) levels was investigated. Materials and Methods: The serum markers were determined via enzyme-linked immunosorbent assays in 12 non-diabetic subjects (CTRL), 15 diabetic patients without DR (Diabetic), 15 patients with NPDR, and 15 patients with PDR. Results: TG and AG serum levels were significantly decreased in Diabetic (respectively, p < 0.05 and p < 0.01 vs. CTRL), NPDR (p < 0.01 vs. Diabetic), and in PDR patients (p < 0.01 vs. NPDR). AG serum levels were inversely associated with DR abnormalities (microhemorrhages, microaneurysms, and exudates) progression (r = -0.83, p < 0.01), serum neutrophil percentage (r = -0.74, p < 0.01), and serum NE levels (r = -0.73, p < 0.01). The latter were significantly increased in the Diabetic (p < 0.05 vs. CTRL), NPDR (p < 0.01 vs. Diabetic), and PDR (p < 0.01 vs. PDR) groups. Conclusions: The two DR stages were characterized by decreased AG and increased NE levels. In particular, serum AG levels were lower in PDR compared to NPDR patients, and serum NE levels were higher in the PDR vs. the NPDR group. Together with the greater presence of retinal abnormalities, this could underline a distinctive role of AG in PDR compared to NPDR.

Evaluation of serum levels of leptin and ghrelin in patients with celiac disease before and after treatment with a gluten-free diet

Background and Objective. Celiac disease (CeD) is an autoimmune condition characterized by specific serological and tissue characteristics resulting from gluten consumption in genetically predisposed individuals. The only currently treatment available for CeD is strict lifelong adherence to a gluten-free diet (GFD), which leads to remission. This study aimed to evaluate leptin and ghrelin serum levels in celiac patients before and after treatment with a gluten-free diet. Patients and Methods. Thirty patients aged 3 to 50 years with CeD and 30 age- and gender-matched healthy controls were included in the study. Serum levels of leptin and ghrelin in patients before GFD and after four months of GFD treatment were measured using ELISA kits. Results. The mean serum ghrelin concentration in celiac cases decreased from 653.6 pg/ml to 483.2 pg/ml after GFD treatment (p &lt; 0.001). Although the mean serum ghrelin concentration before treatment was not significantly different between the case and control groups, it was significantly lower in celiac patients than in the control group after treatment (p &lt; 0.001). The average concentration of serum leptin in the control group was significantly higher than before and after the treatment of celiac patients, but the average concentration of serum leptin in celiac patients did not change significantly after GFD treatment (p = 0.298). Conclusion. In conclusion, this study suggests that a GFD can positively affect the levels of leptin and ghrelin hormones in celiac patients. Key words: celiac disease, leptin, ghrelin, gluten-free diet

Correlation between Helicobacter pylori and serum levels of ghrelin, obestatin, leptin and motilin in hyperemesis gravidarum

Correlation between Helicobacter pylori and serum levels of ghrelin, obestatin, leptin and motilin in hyperemesis gravidarum