Plasma Concentrations Of Hormones Research Articles

Assessing the effects of ex vivo hormonal exposure on oxidative responses in equine leukocytes: A preliminary study

Breed differences exist between horses and ponies in circulating concentrations of several hormones, notably ACTH and insulin. These hormones regulate stress and metabolic responses, but in other species, they also impact leukocyte oxidant responses. The effects of these hormones on equine leukocytes have not been evaluated to date. If equine leukocytes are similarly regulated, breed differences in increased plasma hormone concentrations or altered sensitivity to them at the leukocyte level could result in breed-related differences in oxidant responses or oxidative status. The objective of this study was therefore to determine the effects of ex vivo exposure to adrenocorticotropic hormone (ACTH), α-melanocyte stimulating hormone (α-MSH), insulin, or leptin on reactive oxygen species (ROS) production from leukocytes isolated from horses and ponies. We hypothesized that ACTH, α-MSH, insulin, and leptin would alter oxidant responses from equine leukocytes in a breed specific manner. Blood was collected from 10 apparently healthy Quarter horses and seven Welsh ponies for isolation of neutrophils and peripheral blood mononuclear cells (PBMCs) via density gradient centrifugation. Cells were incubated with media (negative control), microbial antigens (positive control), or ACTH, α-MSH, leptin, or insulin for two hours. Induced ROS production was quantified with a previously validated fluorometric assay. Data was compared within groups by comparing a stimulant within a group (horses or ponies) to baseline, between groups by comparing horse response to pony response, and among stimulants using one- and two-way, repeated measures ANOVA (P<0.05). There was no significant effect of breed on basal, microbial-induced, or hormone-induced ROS production from neutrophils (P=0.465) or PBMCs (P=0.749), but in neutrophils, a significant interaction between breed and stimulant was present (P=0.037). ROS production from PBMCs from horses after hormone exposure did not differ from cells exposed to media only (P=0.1520–0.8180). Similarly, neither leptin nor insulin exposure significantly induced ROS production from PBMCs from ponies (P= 0.2645 and 0.4678 respectively), but exposure to ACTH or α-MSH induced a significant increase in ROS production (P=0.0441 and 0.0440 respectively) compared to unstimulated cells. Hormones that vary in availability among breeds may induce ex vivo pro-oxidant responses in equine leukocytes, but specific effects are breed-, leukocyte type-, and hormone-dependent. Breed differences in hormonally induced leukocyte ROS production may warrant further investigation in the context of circulating oxidative stress and how this might relate to future disease risk.

Sex-Linked Changes in Biotransformation of Phenol in Brook Trout (Salvelinus fontinalis) over an Annual Reproductive Cycle

The microsomal metabolism of phenol (11 °C) over an annual reproductive cycle from June to December was studied using fall spawning adult brook trout (Salvelinus fontinalis). Hepatic microsomes were isolated from three male and three female fish each month. Incubations were optimized for time, cofactor concentration, pH, and microsomal protein concentration. The formation of phase I ring-hydroxylation metabolites, i.e., hydroquinone (HQ) and catechol (CAT), was quantified by HPLC with dual-channel electrochemical detection. Sample preparation and chromatographic conditions were optimized to achieve the separation and sensitivity required for the analysis of these labile products. Biotransformation of phenol over a range of substrate concentrations (1 to 150 mM) was quantified for the calculation of Michaelis–Menten constants (Km and Vmax) for each month. Results indicate a nearly equal production of HQ and CAT among males and females in late June. At the peak of maturity in October, there was an approximate ten-fold greater production of ring-hydroxylation metabolites noted in females in comparison with males on a total liver basis. In vitro phase II biotransformation of phenol glucuronidation was assessed by determining the Michaelis–Menten constants (Km, Vmax) using brook trout hepatic microsomes over a range of substrate concentrations (1 to 60 mM). Initially, there were no significant differences in the glucuronide rate of formation (pmol/min/mg protein) or total capacity (nmol/min/liver) between females and males. At the peak of maturation, the maximum rate of glucuronide formation was 4-fold less in females; however, the total capacity was 2-fold less in females due to the increased liver size in the females. The alterations in biotransformation coincided with increases in the hepatic and gonadal somatic indices and with changes in plasma hormone concentrations. These experiments provide insight into the metabolic deactivation of xenobiotics and to provide data for the prediction of altered hepatic biotransformation rates and pathways during the reproductive cycle.

The pathophysiology of estrogen in perinatal depression: conceptual update.

Estrogen levels fall sharply after parturition and have long been considered an etiologic contributor to postpartum depression (PPD); however, no differences have been reported in plasma hormone concentrations in people who develop PPD. We examine the question: What is the current view of estrogen and the neurophysiologic processes it impacts in the development and treatment of PPD? A literature review of the role of estrogen on candidate hormonal and epigenetic systems in the peripartum period was performed, including landmark historical studies and recent publications on estrogen-related research. The authors reviewed these papers and participated in reaching consensus on a conceptual framework of estrogen activity within the complexity of pregnancy physiology to examine its potential role for driving novel interventions. Estrogen fluctuations must be conceptualized in the context of multiple dramatic and interacting changes inherent in pregnancy and after birth, including progesterone, corticosteroids, inflammation, circadian biology and psychosocial challenges. Individuals who develop PPD have increased sensitivity to epigenetic alteration at estrogen-responsive genes, and these changes are highly predictive of PPD. An effective estrogen-based treatment for PPD has yet to be found, but interventions focused on associated inflammation and circadian rhythms are promising. Our understanding of the biological basis of PPD, one of the most common morbidities of the perinatal period, is expanding beyond changes in gynecologic hormone concentrations to include their impact on other systems. This growing understanding of the many processes influencing PPD will allow for the development of novel prevention and treatment strategies.

Taurine drives body protein renewal and accretion in beef steers

The aims of the present study were to investigate the effects of dietary supplementation with rumen-protected taurine (RPT) on whole-body protein turnover, plasma metabolomics, and whole blood cell transcriptomics in steers. Eight steers, averaging 220 ± 3.26 (mean ± SD) kg of liveweight, were allocated in a replicate 4 × 4 Latin square design. The experimental treatments consisted of four levels of RPT supplementation: 0, 25, 50, and 75 g RPT per day, added to a basal diet. The results showed that supplementation with RPT linearly decreased the fecal nitrogen (N) excretion (P = 0.001) and the 15N fractional recovery rate (P = 0.047), while it linearly increased the urinary excretion of taurine (P = 0.045) as well as the average daily weight gain (P = 0.003), protein synthesis (P < 0.001), protein degradation (P < 0.001) and the whole-body protein turnover (P < 0.001). Supplementation with RPT linearly increased the plasma concentrations of growth hormone (P = 0.005) and quadratically affected the plasma concentration of insulin-like growth factor-1 (P = 0.013), and it linearly decreased the plasma concentration of albumin (P = 0.022). Supplementation with RPT altered the whole blood cell mRNA expression and upregulated the expressions of the marker genes, including RPS6KB1, PRSS42, COL1A2, ENSBTAG00000013055 and ENSBTAG00000038159 which are related to protein metabolism. The plasma metabolome profiling indicated that supplementation with RPT upregulated the plasma concentrations of taurine, lysine and methionine. The experiment revealed the impact and the mechanisms of taurine on driving whole-body protein turnover and protein accretion in steers. Two novel marker genes which could be related to body protein degradation in steers were identified.

The incretin effect in type 2 diabetes in a Sub-Saharan African population

AimType 2 diabetes is increasing in Sub-Saharan Africa, but the pathophysiology in this population is poorly investigated. In Western populations, the incretin effect is reduced in type 2 diabetes, leading to lowered insulin secretion. The aim of this study was to investigate the incretin effect in a group of Sub-Saharan Africans with type 2 diabetes.MethodsTwenty adults diagnosed with type 2 diabetes, based on either an oral glucose tolerance test (n = 10) or on glycated hemoglobin A1c (n = 10), and 10 non-diabetic controls were included in an interventional study in Tanzania. We investigated the incretin effect as the difference between the plasma insulin area under the curve during an oral glucose tolerance test and that obtained during an intravenous glucose infusion. Differences between diabetes groups were analyzed by Kruskal–Wallis one-way analysis of variance.ResultsThe incretin effect did not differ between groups (p = 0.45), and there was no difference in plasma concentrations of the incretin hormones during the OGTT.ConclusionA reduced incretin effect appears not to contribute to hyperglycemia in type 2 diabetes in this Tanzanian population. More research is needed to explain the diabetes phenotype often seen in Sub-Saharan Africa.Trial registrationClinicaltrials.gov: NCT03106480, date of registration: 04/10/2017.

Intraduodenal calcium enhances the effects of L-tryptophan to stimulate gut hormone secretion and suppress energy intake in healthy males: a randomized, crossover, clinical trial

BackgroundIn humans, intraduodenal infusion of L-tryptophan (Trp) increases plasma concentrations of gastrointestinal hormones and stimulates pyloric pressures, both key determinants of gastric emptying and associated with potent suppression of energy intake. The stimulation of gastrointestinal hormones by Trp has been shown, in preclinical studies, to be enhanced by extracellular calcium and mediated in part by the calcium-sensing receptor. ObjectivesThis study aim was to determine whether intraduodenal calcium can enhance the effects of Trp to stimulate gastrointestinal hormones and pyloric pressures and, if so, whether it is associated with greater suppression of energy intake, in healthy males. MethodsFifteen males with normal weight (mean ± standard deviation; age: 26 ± 7 years; body mass index: 22 ± 2 kg/m2), received on 3 separate occasions, 150-min intraduodenal infusions of 0, 500, or 1000 mg calcium (Ca), each combined with Trp (load: 0.1 kcal/min, with submaximal energy intake-suppressant effects) from t = 75–150 min, in a randomized, double-blind, crossover study. Plasma concentrations of GI hormones [gastrin, cholecystokinin, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide (GLP)-1, and peptide tyrosine-tyrosine (PYY)], and Trp and antropyloroduodenal pressures were measured throughout. Immediately postinfusions (t = 150–180 min), energy intake at a standardized buffet-style meal was quantified. ResultsIn response to calcium alone, both 500- and 1000-mg doses stimulated PYY, while only the 1000-mg dose stimulated GLP-1 and pyloric pressures (all P < 0.05). The 1000-mg dose also enhanced the effects of Trp to stimulate cholecystokinin and GLP-1, and both doses stimulated PYY but, surprisingly, reduced the stimulation of GIP (all P < 0.05). Both doses substantially and dose dependently enhanced the effects of Trp to suppress energy intake (Ca-0+Trp: 1108 ± 70 kcal; Ca-500+Trp: 961 ± 90 kcal; and Ca-1000+Trp: 922 ± 96 kcal; P < 0.05). ConclusionsIntraduodenal administration of calcium enhances the effect of Trp to stimulate plasma cholecystokinin, GLP-1, and PYY and suppress energy intake in healthy males. These findings have potential implications for novel nutrient-based approaches to energy intake regulation in obesity.The trial was registered at the Australian New Zealand Clinical Trial Registry (www.anzctr.org.au) as ACTRN12620001294943).

Mechanisms contributing to lactose and sucrose-induced postprandial lipaemia

Fructose-containing sugars can exaggerate postprandial lipaemia and stimulate hepatic de novo lipogenesis (DNL) when compared to glucose-based carbohydrates(1). Galactose has recently been shown to increase postprandial lipaemia compared to glucose(2), but mechanisms remain uncharacterised. The aim of this study was to assess the effect and mechanisms of lactose-induced lipaemia.Twenty-four non-obese adults (12 male and 12 female) completed three trials in a randomised, crossover design (28 ± 7-day washout). During trials, participants consumed test drinks containing 50 g fat with 100 g of carbohydrate. The control carbohydrate was a glucose polymer (maltodextrin), the experimental carbohydrate was galactose-containing carbohydrate (lactose) and the active comparator was fructose-containing carbohydrate (sucrose). Hepatic DNL was assessed by the 2H2O method and [U-13C]-palmitate was added to the test drink to trace the fate of the ingested fat. Blood and breath samples were taken to determine plasma metabolite and hormone concentrations, in addition to plasma and breath 2H and 13C enrichments. Data were converted into incremental under the curve (iAUC) and were checked for normality by visual inspection of residuals. Differences between trials were assessed by one-way ANOVA. Where a main effect of trial was detected, post- hoc t-tests were performed to determine which trials differed from lactose according to the principle of closed-loop testing.The plasma triacylglycerol iAUC (mean ± SD) in response to maltodextrin was 51 ± 68 mmol/L*360 min. Following lactose ingestion, plasma triacylglycerol iAUC increased to 98 ± 88 mmol/L*360 min (p&lt;0.001 vs maltodextrin), which was comparable to sucrose [90 ± 95 mmol/L*360 min (p=0.41 vs lactose)]. Hepatic DNL in response to maltodextrin was 6.6 ± 3.0%. Following ingestion of lactose, hepatic DNL increased to 12.4 ± 6.9% (p=0.02 vs maltodextrin), which was comparable to sucrose [12.2 ± 6.9% (p=0.96 vs lactose)]. Exhaled 13CO2 in response to maltodextrin was 10.4 ± 4.1 mmol/kgFFM*360 min. Following ingestion of lactose, exhaled 13CO2 was 8.8 ± 4.9 mmol/kgFFM*360 min (p=0.09 vs maltodextrin), which was lower than sucrose [11.1 ± 3.9 mmol/kgFFM*360 min (p=0.01 vs lactose)].These data are consistent with the hypothesis that hepatic de novo lipogenesis contributes to both lactose and sucrose-induced lipaemia and provide a rationale to investigate the longer-term effects of lactose and sucrose on metabolism.

Diagnostic utility of clinicodemographic, biochemical and metabolite variables to identify viable pregnancies in a symptomatic cohort during early gestation

A significant number of pregnancies are lost in the first trimester and 1–2% are ectopic pregnancies (EPs). Early pregnancy loss in general can cause significant morbidity with bleeding or infection, while EPs are the leading cause of maternal mortality in the first trimester. Symptoms of pregnancy loss and EP are very similar (including pain and bleeding); however, these symptoms are also common in live normally sited pregnancies (LNSP). To date, no biomarkers have been identified to differentiate LNSP from pregnancies that will not progress beyond early gestation (non-viable or EPs), defined together as combined adverse outcomes (CAO). In this study, we present a novel machine learning pipeline to create prediction models that identify a composite biomarker to differentiate LNSP from CAO in symptomatic women. This prospective cohort study included 370 participants. A single blood sample was prospectively collected from participants on first emergency presentation prior to final clinical diagnosis of pregnancy outcome: LNSP, miscarriage, pregnancy of unknown location (PUL) or tubal EP (tEP). Miscarriage, PUL and tEP were grouped together into a CAO group. Human chorionic gonadotrophin β (β-hCG) and progesterone concentrations were measured in plasma. Serum samples were subjected to untargeted metabolomic profiling. The cohort was randomly split into train and validation data sets, with the train data set subjected to variable selection. Nine metabolite signals were identified as key discriminators of LNSP versus CAO. Random forest models were constructed using stable metabolite signals alone, or in combination with plasma hormone concentrations and demographic data. When comparing LNSP with CAO, a model with stable metabolite signals only demonstrated a modest predictive accuracy (0.68), which was comparable to a model of β-hCG and progesterone (0.71). The best model for LNSP prediction comprised stable metabolite signals and hormone concentrations (accuracy = 0.79). In conclusion, serum metabolite levels and biochemical markers from a single blood sample possess modest predictive utility in differentiating LNSP from CAO pregnancies upon first presentation, which is improved by variable selection and combination using machine learning. A diagnostic test to confirm LNSP and thus exclude pregnancies affecting maternal morbidity and potentially life-threatening outcomes would be invaluable in emergency situations.

Food temperature altered macronutrients induced changes in satiety hormones; glucagon - like peptide -1 and cholecystokinin and their correlation with subjective satiety.

The benefits of dietary macronutrients for weight management depend on the integrity of gut hormones. The role of food temperature in the release of satiety hormones and satiety needs elucidation. We aimed to determine the impact of different food temperatures with varying macronutrient compositions on satiety-related gut hormones glucagon-like peptide-1 (GLP-1) and cholecystokinin (CCK) and find the correlation of satiety hormones with appetite scores and remainder-day food (energy) intake. Thirteen healthy participants (eight males and five females) aged 25-35 years with body mass index 18.5-24.9 kg/m2 with no medical illnesses or eating disorders consumed three compositions of meals (high carbohydrate, high fat, and high protein meals) each at three temperatures (cold, warm, and hot) in a randomized, double-blinded, controlled crossover design. Plasma concentrations of peptide hormones were determined at 0, 30, and 240 minutes by enzyme-linked immunosorbent assay, and 24-hours food recall was used for remainder-day food intake (remainder energy). Data were analyzed using SPSS version 27.0. The change in plasma levels of gut hormones with time was assessed using Friedman test; Kruskal-Wallis test was employed to compare GLP-1 and CCK hormonal levels across nine meals. A comparison of the three meals at the three temperatures (total of nine groups), showed that the GLP-1 and CCK plasma concentrations were significantly different (P < 0.001). GLP-1 and CCK responses increased more after hot meals than cold meals. Overall, high-fat meals had more effective gut hormone secretions. The area under the curve was increased for GLP-1 in high-fat meals and for CCK in hot meals. The peptide hormones (GLP-1 and CCK) were positively correlated with satiety scores and inversely with remainder food intake. The temperature of food was found to be an effective stimulus for the regulation of CCK and GLP-1 secretion. Hot food temperature increased satiety hormones (CCK and GLP-1), independent of food macronutrient composition.

Adaptive thermogenesis, at the level of resting energy expenditure, after diet alone or diet plus bariatric surgery.

The objective of this study was to compare the magnitude of adaptive thermogenesis (AT), at the level of resting energy expenditure (REE), after a very low-energy diet alone or combined with Roux-en-Y gastric bypass or sleeve gastrectomy, as well as to investigate the association between AT and changes in appetite. A total of 44 participants with severe obesity underwent 10 weeks of a very low-energy diet alone or combined with Roux-en-Y gastric bypass or sleeve gastrectomy. Body weight and composition, REE, subjective appetite feelings, and plasma concentrations of gastrointestinal hormones were measured at baseline and week 11. AT, at the level of REE, was defined as a significantly lower measured versus predicted (using a regression model with baseline data) REE. Participants lost 18.4 ± 3.9 kg of body weight and experienced AT, at the level of REE (-121 ± 188 kcal/day; p < 0.001), with no differences among groups. The larger the AT, at the level of REE, the greater the reduction in fasting ghrelin concentrations and the smaller the reduction in feelings of hunger and desire to eat in the postprandial state. Weight-loss modality does not seem to modulate the magnitude of AT, at the level of REE. The greater the AT, at the level of REE, the greater the drive to eat following weight loss.

Glucose-regulatory hormones and growth in very preterm infants fed fortified human milk

BackgroundBovine colostrum (BC) contains a range of milk bioactive components, and it is unknown how human milk fortification with BC affects glucose-regulatory hormones in very preterm infants (VPIs). This study aimed to investigate the associations between hormone concentrations and fortification type, birth weight (appropriate/small for gestational age, AGA/SGA), milk intake, postnatal age, and body growth.Methods225 VPIs were randomized to fortification with BC or conventional fortifier (CF). Plasma hormones were measured before, one and two weeks after start of fortification. ΔZ-scores from birth to 35 weeks postmenstrual age were calculated.ResultsCompared with CF, infants fortified with BC had higher plasma GLP-1, GIP, glucagon, and leptin concentrations after start of fortification. Prior to fortification, leptin concentrations were negatively associated with growth, while IGF-1 concentrations associated positively with growth during fortification. In AGA infants, hormone concentrations generally increased after one week of fortification. Relative to AGA infants, SGA infants showed reduced IGF-1 and leptin concentrations.ConclusionFortification with BC increased the plasma concentrations of several glucose-regulatory hormones. Concentrations of IGF-1 were positively, and leptin negatively, associated with growth. Glucose-regulatory hormone levels were affected by birth weight, milk intake and postnatal age, but not closely associated with growth in VPIs.ImpactLittle is known about the variation in glucose-regulatory hormones in the early life of very preterm infants (VPIs).This study shows that the levels of glucose-regulatory hormones in plasma of VPIs are highly variable and modified by birth weight (appropriate or small for gestational age, AGA or SGA), the type of fortifier, enteral nutritional intake, and advancing postnatal age.The results confirm that IGF-1 levels are positively associated with early postnatal growth in VPIs, yet the levels of both IGF-1 and other glucose-regulatory hormones appeared to explain only a small part of the overall variation in growth rates.

Environmental Effect of High-voltage Towers on the Cerebellum and Cognitive Impairments in the Monkey.

Today, high-voltage (HV) lines create a pernicious environment for humans living or working in the vicinity and even under these lines. The male rhesus monkey is used to investigate the effects of fields produced by HV towers. This study examines the function and level of impact in rhesus monkeys' brains from the cerebellum's cognitive, biological, and structural perspective. Two monkeys have been used, one as a control and the second as a test. The monkey under test was subjected to a simulated HV electrical field of 3 kV/m, 4 hours a day, for 1 month. Behavioral tests were performed using a device designed and built for this purpose. Concentration analysis of adrenocorticotropic hormones (ACTH) and inspection of glucocorticoid receptor gene's (GR) expression were performed by the reverse transcription polymerase chain reaction method. Changes in cerebellar anatomy were examined with magnetic resonance imaging (MRI). All tests were performed before and after the study period and compared with the control monkey. Cognitive tests showed a significant reduction for the monkey exposed to the HV electrical field in the first week after imposition compared with the same time before. Also, the expression of the GR gene decreased, and the concentration of ACTH hormone in plasma increased. Surveying the level of cerebral MRI images did not show any difference, but hemorrhage was evident in a part of the cerebellum. The tested monkey's cognitive, biological, and MRI results showed a decrease in visual learning and memory indices.

Effect of feeding calf starter with calcium salts of medium-chain fatty acids on the growth and metabolic hormones in calves.

We investigated the effects of a calf starter supplemented with calcium salts of medium-chain fatty acids (MCFA-Ca) on growth and plasma hormone concentration in calves. Twelve Holstein calves were randomly assigned to two dietary groups (without supplementation [CON] and supplemented with MCFA-Ca [MCFA]) from 4 d of age. Calves were fed 1.0kg/d of milk replacer until 5wk of age and were completely weaned at 7wk of age. Calves in the MCFA group received a calf starter containing 1% MCFA-Ca. dry matter intake (DMI) was measured daily, and body weight was measured weekly. Rumen fluid was collected at 13wk of age to measure pH and volatile fatty acid concentration. Preprandial blood samples were collected weekly to measure the basal plasma hormone and metabolite concentrations. At 4, 8, and 13wk of age, peri-prandial blood samples were collected every 30min, from 60min before feeding to 120min after feeding, to observe metabolic responses to feeding. In addition, insulin sensitivity was assessed using euglycemic-hyperinsulinemic clamps at 4, 8, and 13wk of age in three calves from each treatment. There were no differences in starter and hay DMI between the treatments. However, the average daily gain (ADG) after weaning was higher in the MCFA group than in the CON group. Weekly changes in plasma parameters did not differ between the treatments. Plasma concentrations of preprandial ghrelin and postprandial total ketone bodies at 13wk of age were higher in the MCFA group than in the CON group. At 8wk of age, peri-prandial plasma insulin concentrations were lower in the MCFA group than in the CON group. There were no differences between the treatments in terms of insulin sensitivity. The present study suggested that feeding weaning calves MCFA-Ca increases the ADG during the postweaning period, which may be mediated by endocrine signals, such as enhanced ghrelin secretion and decreased insulin secretion, without altering insulin sensitivity.

Suboptimal Weight Loss 13 Years After Roux-en-Y Gastric Bypass Is Associated with Blunted Appetite Response

PurposeBariatric surgery remains the most efficient treatment to achieve a sustained weight loss. However, a large proportion of patients experience suboptimal weight loss (SWL). The exact mechanisms involved remain to be fully elucidated, but the homeostatic appetite control system seems to be involved. The aim of this study was, therefore, to compare the plasma concentration of gastrointestinal hormones, and appetite ratings, between those experiencing SWL and optimal weight loss (OWL) after Roux-en-Y gastric bypass (RYGB).Materials and MethodsFifty participants from the Bariatric Surgery Observation Study (BAROBS) experiencing either SWL or OWL (< or ≥ 50% of excess weight loss (EWL), respectively) > 13 years post-RYGB were compared to 25 non-surgical controls. Plasma concentrations of acylated ghrelin (AG), total glucagon-like peptide-1 (GLP-1), total peptide YY (PYY), cholecystokinin (CCK), and subjective ratings of hunger, fullness, desire to eat (DTE), and prospective food consumption (PFC) were assessed in the fasting and postprandial (area under the curve (AUC)) states.ResultsThose experiencing OWL presented with higher basal AG and GLP-1 iAUC, and lower AG iAUC compared with SWL and controls. Additionally, both bariatric groups presented with higher PYY and CCK iAUC compared to controls. PFC tAUC was also lower in OWL compared to the SWL group. Total weight loss was positively correlated with GLP-1 tAUC and negatively correlated with fasting and tAUC DTE and PFC tAUC.ConclusionsSWL > 13 years post-RYGB is associated with lower basal ghrelin, as well as a weaker satiety response to a meal. Future studies should investigate the causality of these associations.Graphical

Improvement Prospects of Lycopene Supplementation in the L-NAME Toxicity on the Male Wistar Rat Reproductive System

Non-selective nitric oxide synthase inhibitors, such as N (G)-nitro-L-arginine Methyl Ester (L-NAME), are typically prescribed to treat spinal injuries and hypotension. Many physiological processes, including the regulation of reproductive hormones, are ty pically linked to it. Bioactivity in physiological systems is influenced by the antioxidant lycopene. This study sought to determine the imp act of lycopene supplementation and L-NAME administration on gonadal hormones and sperm parameters. Twenty male Wistar rats were used for this study and were divided into four groups containing 5 rats each. L-NAME (5mg/kg) was administered through drinking water and Lycopene (5mg/kg) was supplemented through oral gavage for four weeks. Using established protocols with Elisa Kits, plasma hormone levels were ascertained. Estradiol did not differ substantially across all groups, however, the group that received L-NAME had lower plasma concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone, and nitric oxide (NO). Lycopene supplements raised testosterone, FSH, LH, and NO levels while not affecting estradiol. The sperm profile was altered with L-NAME but ameliorated in Lycopene supplementation. We conclude that lycopene has the potential to protect against hormonal imbalance and male infertility resulting from Nitric oxide synthase (NOS) inhibition.

The effect of maternal organic manganese supplementation on performance, immunological status, blood biochemicaland antioxidant status of Afshari ewes and their newborn lambs in transition period.

It has been documented that adequate maternal manganese (Mn) status is vital for performance and health of ewes and their newborn lambs. However, required level and form of dietary Mn in ruminants are not well defined. The current study was conducted to evaluate the effect of maternal organic Mn supplementation on performance, immunological status, blood biochemicaland antioxidant status of Afshari ewes and their newborn lambs in transition period. For this purpose, various organic Mn concentrations were utilized as a supplementary ingredient in formulating the diets of ewes. The ewes were randomly allocated into three groups, fed with 0, and 80 mg/kg organic Mn supplemented diet. At the end of the experiment, the parameters including the performance of newborn lambs, as well as biochemical factors, immune statusand antioxidant status in ewes and their newborn lambs were evaluated. The results showed a significant increase in the plasma concentrations of Mn, glucose, insulin, thyroid hormones (T3 , T4 )and enzymatic antioxidants (SOD, GPX , CAT) in ewes and their newborn lambs that were treated with maternal organic Mn. Moreover, inorganic Mn treatments, the concentration of IgG in newborn lamb's plasma, and colostrum of ewes increased. According to this research, organic Mn acts as a valuable and safe supplementary material that could be exploited for enhancing health of ewes and their newborn lambs.

Metabolic adaptation is associated with a greater increase in appetite following weight loss: a longitudinal study

BackgroundWeight loss is associated with a disproportionate reduction in energy expenditure, along with increases in hunger feelings and ghrelin concentrations. These changes are presumed to be homeostatic mechanisms to counteract the energy deficit. The possibility that these 2 components of the energy balance equation are mechanistically linked has never been examined. ObjectiveThis study aimed to determine if the disproportionate reduction in resting metabolic rate (RMR) seen with weight loss is associated with changes in the plasma concentration of gastrointestinal hormones involved in appetite regulation and subjective appetite ratings. MethodsThis was a longitudinal study with repeated measurements. Fifty-six individuals with obesity (body mass index [BMI]: 34.5±0.5 kg/m2; age: 47±1 y; 26 males) underwent an 8 wk low-energy diet, followed by 4 wk of refeeding and weight stabilization. The RMR, respiratory quotient (RQ), body composition, plasma concentrations of ghrelin, glucagon-like peptide 1, peptide YY, cholecystokinin, insulin, and appetite ratings in the fasting and postprandial states were measured at baseline, Wk9 and 13. Metabolic adaptation was defined as significantly lower when measured versus the predicted RMR (pRMR) (from own regression model using baseline data). ResultsA 14.2±0.6 kg weight loss was seen at Wk9 and maintained at Wk13. RQ was significantly reduced at Wk9 (0.82±0.06 vs. 0.76±0.05, P< 0.001) but returned to baseline at Wk13. Metabolic adaptation was seen at Wk9, but not Wk13 (-341±58, P <0.001 and -75±72 kJ/d, P = 0.305, respectively). The larger the difference between measured and predicted RMR at both timepoints, the greater the increase in hunger, desire to eat, and composite appetite score (fasting and postprandial at Wk9, postprandial only at Wk13), even after adjusting for weight loss and RQ. ConclusionA larger metabolic adaptation during weight loss is accompanied by a greater drive to eat. This might help explain the interindividual differences in weight loss outcomes to dietary interventions.

Environmental stress during adolescence promotes depression-like behavior and endocrine abnormalities in rats

ObjectiveTo assess the ability of environmental stress (ES) during adolescence on depression-like behaviors and endocrinology in rats. MethodsMale and female Sprague-Dawley rats before or during puberty were divided into three groups: control group (CON), low-frequency ES group (LF), and high-frequency ES group (HF). ES included water/food deprivation and reversal of day and night. After 4 weeks of ES, the behavioral tests were performed. Plasma concentrations of hormones and peptides were determined by enzyme-linked immunosorbent assay (ELISA). ResultsES induced a significant decrease in sucrose preference value in female adolescent rats but not males. In prepubertal rats, the reductions in sucrose preference upon ES were observed without a sex-specific effect. Compared with the CON group, female adolescent rats showed a significant increase, while male adolescent rats showed a significant decrease in plasma corticosterone (CORT) after ES. Also, ES significantly increased plasma leptin in female and male adolescent rats. Moreover, ES significantly increased plasma cholecystokinin (CCK), neuropeptide Y (NPY), and testosterone (TS) levels in adolescent female rats but not in males. No significant differences were found in plasma progesterone and E2 among adolescent rats. The prepubertal male rats showed significant plasma E2 and TS increase after ES, while there were no significant differences between groups in plasma CORT, leptin, CCK, NPY, and progesterone. ConclusionsES may cause depression-like behaviors in adolescent female rats. Our findings supplement the scientific basis for formulating strategies to treat and prevent adolescent depression.

Exposure to ecologically relevant estrogen levels do not influence morphology or immune parameters in hatchling American alligators (Alligator mississippiensis)

Human activity has increased concentrations of endocrine-disrupting contaminants (EDCs) in many ecological systems. Many EDCs are xenoestrogens, which imitate naturally derived estrogen like estradiol 17-β (E2). These pollutants can critically affect a broad range of biological functions, particularly in organisms inhabiting aquatic environments. E2 and associated receptors are involved in regulating innate immune responses, where documentation of exogenous E2 on immune parameters is important for understanding health consequences. In this study, we explore the impact of environmentally relevant concentrations of E2 on circulating glucocorticoid levels and several innate immune parameters in hatchling American alligators (Alligator mississippiensis). Twenty-three hatchling alligators were randomly placed in one of three groups that differed in dietary E2 concentration: control (no E2 exposure), low E2 (0.5 μg/kg E2), or high E2 (1 μg/kg E2) for 10 weeks. Following this period, several biomarkers were quantified to monitor the impact of E2: growth, change in body condition, white blood cell (WBC) counts, glucocorticoid levels, and general antibody response. Blood E2 concentrations were greater in individuals exposed to E2, but plasma corticosterone levels were reduced among the experimental groups. Morphology, growth, and immune parameters of E2 exposed animals did not differ from controls. These results suggest that acute exposure to increased environmental estrogen concentrations may alter plasma hormone concentrations but have little to no impact on immediate morphology or immune responses. Future studies may expand on this by monitoring biomarkers in wild populations across time, which will provide insight into how different ontogenetic stages are impacted by environmental contaminants.

Unbiased multitissue transcriptomic analysis reveals complex neuroendocrine regulatory networks mediated by spinal cord injury-induced immunodeficiency

BackgroundSpinal cord injury (SCI), which causes loss of sensory and motor function in the body below the level of injury, is a devastating disease of the central nervous system. SCI leads to severe secondary immunosuppression, called SCI-induced immunodeficiency syndrome (SCI-IDS), which is characterized by increased susceptibility to infection and further exacerbates neurological dysfunction. Several studies have suggested that SCI-IDS is an independent risk factor for poor neurological prognosis. SCI-IDS predominantly occurs following injury above the T5 levels and eventually leads to systemic immune failure, possibly via the sympathetic–adrenal medullary axis and the hypothalamic‒pituitary‒adrenal (HPA) axis. However, the mechanism remains unclear.Methods and objectivesThe concentrations of adrenocorticotropic hormone and cortisol in plasma, as well as changes in sympathetic activity (blood pressure and catecholamine levels in plasma), were assessed in rats in the high-level (T3) spinal cord injury (T3-SCI) group and the low-level (T10) spinal cord injury (T10-SCI) group. Second, the differential regulation of the gene network between the sympathetic–adrenal medullary axis and the HPA axis was explored by histology and multitissue transcriptomics, and the neuroendocrine–immune network associated with SCI-IDS was further elucidated.ResultsThe spleen and thymus gland, which are secondary immune organs, were significantly atrophied in rats in the T3-SCI group, and the white pulp of the spleen was significantly atrophied. The level of cortisol, which is mediated by the adrenal glands, was markedly elevated, but norepinephrine levels were markedly decreased. There was no difference in adrenocorticotropic hormone expression between any of the groups. The transcriptome analysis results showed that the downregulated differentially expressed genes (DEGs) in the T3-SCI group were enriched in the GO term immunoregulation, indicating that splenic immune function was markedly impaired after high-level SCI. The upregulated DEGs in the hypothalamus (hub genes: Nod2, Serpine1, Cebpb, Nfkbil1, Ripk2, Zfp36, Traf6, Akap8, Gfer, Cxcl10, Tnfaip3, Icam1, Fcgr2b, Ager, Dusp10, and Mapkapk2) were significantly enriched in inflammatory pathways, and the downregulated genes (hub genes: Grm4, Nmu, P2ry12, rt1-bb1, Oprm1, Zfhx2, Gpr83, and Chrm2) were enriched in pathways related to inhibitory Gi-mediated G protein-coupled receptor (Gi-GPCR) neurons and neuropeptide changes. The upregulated genes in the adrenal glands (hub genes: Ciart, per2, per3, cry1, and cry2) were enriched in cortisol secretion and circadian rhythm changes, and the downregulated genes (hub genes: IL7r, rt1-bb, rt1-bb1, rt1-da, rt1-ba, cd74, cxcr3, vcam1, ccl5, bin1, and IL8) were significantly enriched in MHC-mediated immune responses.ConclusionsTo explore the possible mechanism underlying SCI-IDS, this study assessed the differential regulation of the gene network associated with neuroendocrine immunity after SCI. Progressive neuroinflammation spreads after injury, and neurotransmission through Gi-mediated G protein-coupled receptors in the HPA axis and neuropeptide production by the hypothalamus are inhibited. Disruption of the connection between the hypothalamus and the adrenal glands causes autonomous regulation of the adrenal glands, disturbance of circadian rhythm and finally hypercortisolemia, leading to general suppression of peripheral adaptive immunity. Neuraxial nerve inflammation caused by SCI persists indefinitely, blocking nerve repair; persistent system-wide immunosuppression in the periphery results in increased susceptibility to infection, leading to poor neurological prognosis.