The Gestational Effects of Maternal Appetite Axis Molecules on Fetal Growth, Metabolism and Long-Term Metabolic Health: A Systematic Review

Increased maternal food intake is considered a normal pregnancy adjustment. However, the overavailability of nutrients may lead to dysregulated fetal development and increased adiposity, with long-lasting effects on offspring in later life. Several gut-hormone molecules regulate maternal appetite, with both their orexigenic and anorectic effects being in a state of sensitive equilibrium. The aim of this manuscript is to systematically review literature on the effects of maternal gut-hormone molecules on fetal growth and metabolism, birth weight and the later metabolic health of offspring. Maternal serum ghrelin, leptin, IGF-1 and GLP-1 appear to influence fetal growth; however, a lack of consistent and strong correlations of maternal appetite axis hormones with birth weight and the concomitant correlation with fetal and birth waist circumference may suggest that these molecules primarily mediate fetal energy deposition mechanisms, preparing the fetus for survival after birth. Dysregulated intrauterine environments seem to have detrimental, sex-dependent effects on fetal energy stores, affecting not only fetal growth, fat mass deposition and birth weight, but also future metabolic and endocrine wellbeing of offspring.

Study of serum ghrelin and resistin levels and their correlation with zinc and magnesium in men with type 2 diabetes

Introduction: The objectives of our work were to compare the serum concentrations of lipid parameters,insulin, resistin, ghrelin, zinc and magnesium between two groups of men with obese type 2 diabetes and a control group and to study possible correlations between these differentparameters. Material and methods: This was a monocentric case-control study during the period 19 October 2015 to 18 November 2015. It included biological parameters from two separate samples: a group of 41 male, obese, type 2 diabetic patients and a group of 34 diabetes-free controls. Results: Mean plasma ghrelin concentrations were significantly lower in patients with type 2 diabetes compared to those in the control group: (14.05 ± 2.35 pg/mL) versus (45.45 ± 13.59 pg/mL). Mean resistance was significantly higher in diabetics (10.09 ± 2.63 ng/mL) compared to healthy subjects (2.22 ± 0.58 ng/mL). In multivariate analysis, body mass index (BMI) and insulin levels were factors that could influence zincemia variability, while BMI and ghrelinaemia appeared to be predictors of magnesium variability. Discussion: Most correlation studies are based on serum zinc concentration. The different possible correlations between resistin, zinc, magnesium and ghrelin require an increase in the size of the study population, as well as an increase in nutritional surveys during the different stages of type 2 diabetes and obesity. Conclusion: It would be interesting to evaluate, according to the stages of obesity, serum levels of magnesium and ghrelin, on the one hand, and serum levels of zinc and insulin, on the other hand.

Investigating Helicobacter pylori-related pyloric hypomotility; Functional, histological and molecular alterations

Multiple theories have been proposed describing the pathogenic mechanisms of Helicobacter pylori (H. pylori)-associated gastric motility disorders. We assessed ex-vivo pyloric activity in h.pylori infected rats, and tried to explore the associated ghrelin hormone alteration and pyloric fibrogenesis. In addition, miR-1 was assessed in pyloric tissue samples, being recently accused of having a role in smooth muscle dysfunction. Ninety adult male Wistar albino rats were assigned into 9 groups: 1)Control group, 2)Sterile broth (vehicle group), 3)amoxicillin control, 4) omeperazole control, 5)clarithromycin control, 6)triple therapy control, 7)H. pylori- group, 8)H. pylori-clarithromycin group, and 9)H.pylori-triple therapy group. Urease enzyme activity was applied as an indicator of H. pylori infection. Ex-vivo pyloric contractility was evaluated. Serum ghrelin was assessed, and histological tissue evaluation was performed. Besides, pyloric muscle miR-1 expression was measured. The immunological epithelial to mesenchymal transition (EMT) markers; transforming growth factor β (TGFβ), alpha-smooth muscle actin (α-SMA) and E-cadherin-3 were also evaluated. By H. pylori infection, a significant (P<0.001) reduced pyloric contractility index was recorded. The miR-1 expression was decreased (P<0.001) in the H. pylori-infected group, associated with reduced serum ghrelin, elevated TGFβ, and α-SMA levels and reduced E-cadherin levels. Decreased miR-1 and disturbed molecular pattern were improved by treatment. In conclusion: H. pylori infection was associated with reduced miR-1, epithelial to mesenchymal transition, and pyloric hypomotility. The miR-1 may be a target for further studies to assess its possible involvement in H.pylori associated pyloric dysfunction, which might help in management of human H. pylori manifestations and complications.

Serum Ghrelin in Mild Cognitive Impairment and Alzheimer's Disease A Systematic Review and Meta-analysis

Background Serum ghrelin levels have been reported to be altered in Alzheimer’s disease (AD) patients and individuals with Mild cognitive impairment (MCI). However, whether serum ghrelin can be used as a biomarker of AD is inconsistent and conflicting. Methods We carried out a systematic review and meta-analysis to examine the serum levels of ghrelin and acylated ghrelin (AG) in patients with AD or MCI, in comparison with normal controls (NC). We searched PubMed, The Cochrane Library, Web of Science and Chinese National Knowledge Infrastructure (CNKI) from 1999 to March 2021. Results 10 relevant studies were included for this study. 8 studies reported serum levels of ghrelin (417 AD or MCI patients and 382 controls) and 5 studies reported serum levels of AG (142 AD or MCI patients and 152 controls). We found that AD and MCI patients had a tendency toward a decrease in the serum levels of ghrelin (SMD=-1.04; 95%CI (-2.30, 0.23); P = 0.11; significant heterogeneity: I2 = 98%), but no statistical significance was found. AG levels in the serum level of AD and MCI patients were significantly higher than NC subjects (SMD = 0.99; 95%CI (0.21, 1.77); P = 0.01; significant heterogeneity: I2 = 87%). Conclusion This meta-analysis suggested that AG may be a potential MCI or early AD biomarker and confirmed previous findings that ghrelin became desensitized in AD patients. This meta-analysis was limited to small sample sizes and lacked of stratifying the level of heterogeneity in AD and MCI patients. More and large sample, multi-center case-control studies on the relationship between serum AG and AD or MCI patients are still needed in the future.