Meal Initiation Research Articles

#655 Warm meal after a haemodialysis session saves the day (and lives?)

Abstract Background and Aims The haemodialysis (HD) process leads to chronic nutrient deficiency, particularly of proteins and amino acids. About 6-12 grams of amino acids loss and 7-8 grams of protein loss occurring during each dialysis session may contribute to hypoalbuminemia, a strong predictor of malnutrition and mortality [1]. Optimal dietary protein intake (DPI) may replenish low plasma amino acids, but DPI inadequacy is a common issue in HD patients, as well as malnutrition due to comorbidities. COVID-19 has made dramatic changes in dialysis centers’ procedures, including the transition from warm meals to cold sandwiches for patients to eat after the session. After the end of COVID-19 pandemic warm meals (meat dish included) were reintroduced. Our aim was to quantify the effect of one to three warm meals per week after the HD session (depending on the regime) on the patients’ protein status. Method Data of 68 patients (24 females and 44 males) on chronic HD were collected after signing the ICF consisting of total protein and albumin values measured two months apart. The first measurement was done while patients were on the long-term sandwich diet after every HD session. The second measurement was done 45 days after the warm meal diet was initiated after every session. Serum total protein and serum albumin were measured, with normal intervals for total serum protein and albumin being 66–81 g/L and 45–51 g/L respectively. The values were compared using Wilcoxon signed-rank test. Results The average albumin value with dry food was 35.9 g/L and for total protein 63.6 g/L, with just 6 patients having normal albumin levels (8.8%) and 21 patients having normal total protein levels (30.9%). The average albumin value after 45 days of HD with warm meals was 39.8 g/L and 66.6 g/L for total protein, with 28 patients having normal albumin levels (41.2%) and 36 patients having normal total protein levels (52.9%). This marks an increase of 4.7% in average value of total protein (3 g/L) and statistically significant increase in albumin value of 10.8% (3.9 g/L, p < 0.001). Greater number of patients had normal total protein and albumin values (4.7 times more patients had a normal albumin level after the initiation of warm meals, and 1.7 times more patients had normal total protein levels). There is a difference regarding male and female patients with a greater impact on males. Male patients had an average total proteins value increase of 5.3% (3.37 g/L) while female patients had 3.5% (2.29 g/L). There was a statistically significant increase in albumin value both for male (p < 0.001) and female patients (p = 0.002). In male patients the average increase was 12% (4.33 g/L), while in female patients it was 8.5% (3.04 g/L). After the introduction of warm meals, 50% of male patients had normal albumin values (vs. 9% before), while 25% of female patients reached normal albumin values (vs. 8.3% before). Conclusion Patients on chronic HD suffer from malnutrition which could lead to significantly higher mortality. Adequate nutrition is crucial for their wellbeing. This study has shown that having a warm meal (protein based) can lead to an increase of total plasma protein and albumin with a higher impact on male patients. In this way we could increase DPI of HD patients, reduce the chance of malnutrition and reduce the cardiovascular risk and mortality.

Abstract A072: Ghrelin deletion reduces mammary tumor growth and enhances response to immunotherapy

Abstract Ghrelin is a peptide hormone, primarily produced in the stomach, best known for its role as a regulator of nutrient sensing, appetite, and meal initiation. However, increasing evidence supports a more complex and nuanced role for ghrelin in a diverse array of biological processes, including cancer. Ghrelin’s effects on breast cancer development and progression are not clear, as the literature detailing its effects is conflicting. Several studies in breast cancer survivors have concluded that higher expression of ghrelin is correlated with better recurrence-free and breast cancer-specific survival. However, additional clinical and foundational science studies have suggested greater complexity for ghrelin’s role in breast cancer development as a splice variant of ghrelin, namely In1-ghrelin, is associated with increased tumor proliferation and reduced disease-free survival of breast cancer patients. Thus, the current study sought to determine the effects of ghrelin deletion within mammary tumor cells (67NR) on subsequent tumor growth. Specifically, we hypothesized that ghrelin deletion would significantly alter tumor growth. Adult female mice received bilateral orthotopic injections of the nonmetastatic murine breast carcinoma cell line 67NR or one of two CRISPR generated ghrelin deleted cell lines 1G9 or 2G2 (derived from the 67NR cell line). Ghrelin deletion significantly reduced tumor volume and tumor mass by ~60% and ~55%, respectively. Additionally, ghrelin deletion significantly increased median survival duration by ~30%. When examining changes within the tumor microenvironment we observed a significant increase in macrophage colonization in ghrelin knockouts relative to the parental 67NR tumors. Notably, the percent F4/80 staining within the tumor positively correlated with length of survival. To determine the role of these F4/80 cells on tumor progression, we ablated these macrophages by feeding chow containing the colony stimulating factor receptor 1 inhibitor, PLX5622, for the entirety of the study. Ablating macrophages significantly increased tumor volume and tumor mass and rendered the previous beneficial effects of ghrelin deletion null, suggesting that the positive effects of ghrelin deletion may be due to actions on macrophages. Lastly, because of the increased macrophage infiltration within ghrelin knockout tumors, we sought to determine their repose to an immunotherapy targeting macrophages, namely anti-CD47. Notably, ghrelin deleted tumors displayed a positive response to the immunotherapy and further reduction in tumor growth (~80% reduction in tumor volume compared to 67NR tumors). Whereas, 67NR tumors were unresponsive to the immunotherapy. These data add to the literature detailing the complex effects of ghrelin on tumor growth and suggest that ghrelin may be a druggable target to slow tumor development. Citation Format: William H Walker II, Brittany D Elliott, Claire O Kisamore, Randy J Nelson, A. Courtney DeVries. Ghrelin deletion reduces mammary tumor growth and enhances response to immunotherapy [abstract]. In: Proceedings of the AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics; 2023 Oct 11-15; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2023;22(12 Suppl):Abstract nr A072.

Chronic Semaglutide Treatment in Rats Leads to Daily Excessive Concentration-Dependent Sucrose Intake.

The glucagon-like peptide-1 receptor (GLP-1R) agonist semaglutide (SEMA) produces 15% weight loss when chronically administered to humans with obesity. In 2 separate experiments, rats received daily injections of either vehicle (VEH) or SEMA starting at 7 µg/kg body weight (BW) and increasing over 10 days to the maintenance dose (70 µg/kg-BW), emulating clinical dose escalation strategies. During dose escalation and maintenance, SEMA rats reduced chow intake and bodyweight. Experiment 2 meal pattern analysis revealed that meal size, not number, mediated these SEMA-induced changes in chow intake. This suggests SEMA affects neural processes controlling meal termination and not meal initiation. Two-bottle preference tests (vs water) began after 10 to 16 days of maintenance dosing. Rats received either an ascending sucrose concentration series (0.03-1.0 M) and 1 fat solution (Experiment 1) or a 4% and 24% sucrose solution in a crossover design (Experiment 2). At lower sucrose concentrations, SEMA-treated rats in both experiments drank sometimes >2× the volume consumed by VEH controls; at higher sucrose concentrations (and 10% fat), intake was similar between treatment groups. Energy intake of SEMA rats became similar to VEH rats. This was unexpected because GLP-1R agonism is thought to decrease the reward and/or increase the satiating potency of palatable foods. Despite sucrose-driven increases in both groups, a significant bodyweight difference between SEMA- and VEH-treated rats remained. The basis of the SEMA-induced overconsumption of sucrose at lower concentrations relative to VEH controls remains unclear, but the effects of chronic SEMA treatment on energy intake and BW appear to depend on the caloric sources available.

Breastfeeding is associated with a delayed decrease in postprandial maternal glucose concentration.

Breastfeeding has long-term benefits in reducing the risk of diabetes; however, information about the acute influence on maternal glucose profile is scarce. Thus, the aim of the study was to assess maternal glucose fluctuations associated with breastfeeding episodes in women with normal glucose status. We performed an observational study of glucose fluctuations with breastfeeding episodes in 26 women with normal glucose status in fasting and postprandial state. Continuous glucose monitoring was performed using CGMS MiniMed Gold®/iPro2® (Medtronic, Dublin, Ireland) three months after delivery under real-life conditions. We compared fasting and postprandial periods of 150 minutes affected or not by a breastfeeding episode. Mean glucose concentration of postprandial periods affected by breastfeeding was lower than not affected (-6.31 mg/dL [95% CI: -11.17, -1.62] P<0.01). Glucose concentration was significantly lower between 50 and 105 minutes after meal initiation (maximum difference -9.19 mg/dL [95% CI: -16.03, -2.16] at 91-95 min). Mean glucose concentrations of fasting periods affected by breastfeeding were similar to those not affected (-0.18 mg/dL [95% CI: -2.7, 0] P=0.831). In women with normal glucose status, breastfeeding episodes are associated with a lower glucose concentration in the postprandial but not in the fasting state.

D1 and D2 neurons in the nucleus accumbens enable positive and negative control over sugar intake in mice

Although the consumption of carbohydrates is needed for survival, their potent reinforcing properties drive obesity worldwide. In turn, sugar overconsumption reveals a major role for brain reward systems in regulating sugar intake. However, it remains elusive how different cell types within the reward circuitries control the initiation and termination of sugary meals. Here, we identified the distinct nucleus accumbens cell types that mediate the chemosensory versus postprandial properties of sweet sugars. Specifically, D1 neurons enhance sugar intake via specialized connections to taste ganglia, whereas D2 neurons mediate the termination of sugary meals via anatomical connections to circuits involved in appetite suppression. Consistently, D2, but not D1, neurons partially mediate the satiating effects of glucagon-like peptide 1 (GLP-1) agonists. Thus, these nucleus accumbens cell types function as a behavioral switch, enabling positive versus negative control over sugar intake. Our study contributes to unveiling the cellular and circuit substrates of sugar overconsumption.

Novel sensory trigger for gastrocolonic response.

Gastrocolonic response (GCR) is a physiologic increase in motor activity of the colon following meal ingestion. The presence of GCR, in colonic manometry (CM) studies, is used as a marker of normal colonic motor activity. Our aim was to investigate whether GCR could be induced by sensory stimulation (visual or olfactory) prior to food ingestion, and to describe the characteristics of patients with this response. We prospectively marked time of meal presence and initiation on CM tracings of patients with idiopathic constipation. We reviewed electronic medical records and normal CM studies. Presence of sensory GCR was defined as an increase by at least 25% of the baseline motility index (MI) after exposure to meal, prior to food ingestion. Manometry characteristics of patients with a sensory GCR response were compared to those without. Eighty-nine patients, (47% females, median age 9 years) met the inclusion criteria. Forty-seven (52.8%) patients had a positive sensory GCR. This cohort had a higher proportion of postprandial GCR (93.6% vs. 76.2%, p-value=0.02) and lower fasting MI (2.08 mm Hg vs. 3.54 mm Hg, p < 0.01). Thirteen (14.6%) patients who had no postprandial GCR had higher baseline MI (median of 3.69 vs. 2.46 mm Hg, p < 0.05). Visualizing or smelling food resulted in a significant increase in baseline MI in more than 50% of patients. Our findings propose a novel, alternate pathway that can induce GCR. This central sensory pathway may have clinical relevance in the diagnosis and management of patients with colonic dysmotility.

GLUT2 expression by glial fibrillary acidic protein-positive tanycytes is required for promoting feeding-response to fasting

Feeding behavior is a complex process that depends on the ability of the brain to integrate hormonal and nutritional signals, such as glucose. One glucosensing mechanism relies on the glucose transporter 2 (GLUT2) in the hypothalamus, especially in radial glia-like cells called tanycytes. Here, we analyzed whether a GLUT2-dependent glucosensing mechanism is required for the normal regulation of feeding behavior in GFAP-positive tanycytes. Genetic inactivation of Glut2 in GFAP-expressing tanycytes was performed using Cre/Lox technology. The efficiency of GFAP-tanycyte targeting was analyzed in the anteroposterior and dorsoventral axes by evaluating GFP fluorescence. Feeding behavior, hormonal levels, neuronal activity using c-Fos, and neuropeptide expression were also analyzed in the fasting-to-refeeding transition. In basal conditions, Glut2-inactivated mice had normal food intake and meal patterns. Implementation of a preceeding fasting period led to decreased total food intake and a delay in meal initiation during refeeding. Additionally, Glut2 inactivation increased the number of c-Fos-positive cells in the ventromedial nucleus in response to fasting and a deregulation of Pomc expression in the fasting-to-refeeding transition. Thus, a GLUT2-dependent glucose-sensing mechanism in GFAP-tanycytes is required to control food consumption and promote meal initiation after a fasting period.

Effect of weekend hospitalization on the duration of fasting in patients with aspiration pneumonia.

BackgroundDecreased swallowing function is an important risk factor for the development of aspiration pneumonia. A previous study reported that a long duration of fasting decreased swallowing function and increased mortality. The purpose of this study is to clarify the relationship between weekend hospitalization and fasting duration in older patients with aspiration pneumonia.MethodsIn this retrospective cohort study using hospital claims data and electronic medical record data between April 1, 2018, and March 31, 2020, 238 patients hospitalized for aspiration pneumonia were enrolled. Patients admitted from Monday to Friday were defined as the weekday admission group, and patients admitted on Saturday, Sunday, and holidays were defined as the weekend admission group. The primary endpoint was the duration of fasting. Multiple regression analysis was performed with age, gender, place of living, Functional Oral Intake Scale before admission, severity of pneumonia, and weekend admission as the independent variables.ResultsThere were 41 patients in the weekend admission group and 103 patients in the weekday admission group. The baseline characteristics of the two groups were similar. There was a median difference in the fasting duration of 23.3 h; the fasting duration in the weekend admission group was significantly longer than the weekday admission group by 20.03 h (95% confidence interval: 2.81–37.25) in the multiple regression analysis.ConclusionsWeekend hospitalization was significantly associated with a longer fasting duration in patients hospitalized for aspiration pneumonia. There is a need to establish a system to enable early meal initiation for patients admitted on weekends.

Prediction of Personal Glycemic Responses to Food for Individuals With Type 1 Diabetes Through Integration of Clinical and Microbial Data.

Despite technological advances, results from various clinical trials have repeatedly shown that many individuals with type 1 diabetes (T1D) do not achieve their glycemic goals. One of the major challenges in disease management is the administration of an accurate amount of insulin for each meal that will match the expected postprandial glycemic response (PPGR). The objective of this study was to develop a prediction model for PPGR in individuals with T1D. We recruited individuals with T1D who were using continuous glucose monitoring and continuous subcutaneous insulin infusion devices simultaneously to a prospective cohort and profiled them for 2 weeks. Participants were asked to report real-time dietary intake using a designated mobile app. We measured their PPGRs and devised machine learning algorithms for PPGR prediction, which integrate glucose measurements, insulin dosages, dietary habits, blood parameters, anthropometrics, exercise, and gut microbiota. Data of the PPGR of 900 healthy individuals to 41,371 meals were also integrated into the model. The performance of the models was evaluated with 10-fold cross validation. A total of 121 individuals with T1D, 75 adults and 46 children, were included in the study. PPGR to 6,377 meals was measured. Our PPGR prediction model substantially outperforms a baseline model with emulation of standard of care (correlation of R = 0.59 compared with R = 0.40 for predicted and observed PPGR respectively; P < 10-10). The model was robust across different subpopulations. Feature attribution analysis revealed that glucose levels at meal initiation, glucose trend 30 min prior to meal, meal carbohydrate content, and meal's carbohydrate-to-fat ratio were the most influential features for the model. Our model enables a more accurate prediction of PPGR and therefore may allow a better adjustment of the required insulin dosage for meals. It can be further implemented in closed loop systems and may lead to rationally designed nutritional interventions personally tailored for individuals with T1D on the basis of meals with expected low glycemic response.

The physiological control of eating: signals, neurons, and networks.

During the past 30 yr, investigating the physiology of eating behaviors has generated a truly vast literature. This is fueled in part by a dramatic increase in obesity and its comorbidities that has coincided with an ever increasing sophistication of genetically based manipulations. These techniques have produced results with a remarkable degree of cell specificity, particularly at the cell signaling level, and have played a lead role in advancing the field. However, putting these findings into a brain-wide context that connects physiological signals and neurons to behavior and somatic physiology requires a thorough consideration of neuronal connections: a field that has also seen an extraordinary technological revolution. Our goal is to present a comprehensive and balanced assessment of how physiological signals associated with energy homeostasis interact at many brain levels to control eating behaviors. A major theme is that these signals engage sets of interacting neural networks throughout the brain that are defined by specific neural connections. We begin by discussing some fundamental concepts, including ones that still engender vigorous debate, that provide the necessary frameworks for understanding how the brain controls meal initiation and termination. These include key word definitions, ATP availability as the pivotal regulated variable in energy homeostasis, neuropeptide signaling, homeostatic and hedonic eating, and meal structure. Within this context, we discuss network models of how key regions in the endbrain (or telencephalon), hypothalamus, hindbrain, medulla, vagus nerve, and spinal cord work together with the gastrointestinal tract to enable the complex motor events that permit animals to eat in diverse situations.

Inhibiting ventral hippocampal NMDA receptors and Arc increases energy intake in male rats.

Research into the neural mechanisms that underlie higher-order cognitive control of eating behavior suggests that ventral hippocampal (vHC) neurons, which are critical for emotional memory, also inhibit energy intake. We showed previously that optogenetically inhibiting vHC glutamatergic neurons during the early postprandial period, when the memory of the meal would be undergoing consolidation, caused rats to eat their next meal sooner and to eat more during that next meal when the neurons were no longer inhibited. The present research determined whether manipulations known to interfere with synaptic plasticity and memory when given pretraining would increase energy intake when given prior to ingestion. Specifically, we tested the effects of blocking vHC glutamatergic N-methyl-D-aspartate receptors (NMDARs) and activity-regulated cytoskeleton-associated protein (Arc) on sucrose ingestion. The results showed that male rats consumed a larger sucrose meal on days when they were given vHC infusions of the NMDAR antagonist APV or Arc antisense oligodeoxynucleotides than on days when they were given control infusions. The rats did not accommodate for that increase by delaying the onset of their next sucrose meal (i.e., decreased satiety ratio) or by eating less during the next meal. These data suggest that vHC NMDARs and Arc limit meal size and inhibit meal initiation.

A mathematical model of food intake.

The metabolic, hormonal and psychological determinants of the feeding behavior in humans are numerous and complex. A plausible model of the initiation, continuation and cessation of meals taking into account the most relevant such determinants would be very useful in simulating food intake over hours to days, thus providing input into existing models of nutrient absorption and metabolism. In the present work, a meal model is proposed, incorporating stomach distension, glycemic variations, ghrelin dynamics, cultural habits and influences on the initiation and continuation of meals, reflecting a combination of hedonic and appetite components. Given a set of parameter values (portraying a single subject), the timing and size of meals are stochastic. The model parameters are calibrated so as to reflect established medical knowledge on data of food intake from the National Health and Nutrition Examination Survey (NHANES) database during years 2015 and 2016.

Zona incerta neurons projecting to the ventral tegmental area promote action initiation towards feeding.

Key points The zona incerta (ZI) and ventral tegmental area (VTA) are brain areas that are both implicated in feeding behaviour. The ZI projects to the VTA, although it has not yet been investigated whether this projection regulates feeding.We experimentally (in)activated the ZI to VTA projection by using dual viral vector technology, and studied the effects on feeding microstructure, the willingness to work for food, general activity and body temperature.Activity of the ZI to VTA projection promotes feeding by facilitating action initiation towards food, as reflected in meal frequency and the willingness to work for food reward, without affecting general activity or directly modulating body temperature.We show for the first time that activity of the ZI to VTA projection promotes feeding, which improves the understanding of the neurobiology of feeding behaviour and body weight regulation. Both the zona incerta (ZI) and the ventral tegmental area (VTA) have been implicated in feeding behaviour. The ZI provides prominent input to the VTA, although it has not yet been investigated whether this projection regulates feeding. Therefore, we investigated the role of ZI to VTA projection neurons in the regulation of several aspects of feeding behaviour. We determined the effects of (in)activation of ZI to VTA projection neurons on feeding microstructure, food‐motivated behaviour under a progressive ratio schedule of reinforcement, locomotor activity and core body temperature. To activate or inactivate ZI neurons projecting to the VTA, we used a combination of canine adenovirus‐2 in the VTA, as well as Cre‐dependent designer receptors exclusively activated by designer drugs (DREADD) or tetanus toxin (TetTox) light chain in the ZI. TetTox‐mediated inactivation of ZI to VTA projection neurons reduced food‐motivated behaviour and feeding by reducing meal frequency. Conversely, DREADD‐mediated chemogenetic activation of ZI to VTA projection neurons promoted food‐motivated behaviour and feeding. (In)activation of ZI to VTA projection neurons did not affect locomotor activity or directly regulate core body temperature. Taken together, ZI neurons projecting to the VTA exert bidirectional control overfeeding behaviour. More specifically, activity of ZI to VTA projection neurons facilitate action initiation towards feeding, as reflected in both food‐motivated behaviour and meal initiation, without affecting general activity.

Feasibility of totally laparoscopic pylorus-preserving gastrectomy with intracorporeal gastro-gastrostomy for early gastric cancer: a retrospective cohort study

BackgroundPylorus-preserving gastrectomy (PPG) has been accepted as a function-preserving surgery for the treatment of early gastric cancer in East Asian countries. Therefore, this study aimed to evaluate the feasibility and safety of totally laparoscopic PPG (TLPPG) with intracorporeal anastomosis.MethodsA total of 43 patients with early gastric cancer underwent laparoscopy-assisted PPG (LAPPG) with extracorporeal anastomosis between May 2006 and November 2012. The operative outcomes of 22 patients who underwent TLPPG between November 2012 and February 2019 were evaluated, and data were compared with that of the LAPPG group.ResultsNo significant difference in the operative time was observed between the two groups. Blood loss was lower in the TLPPG group (18.5 mL) than in the LAPPG group (30.7 mL, p = 0.008), and the length of abdominal incision was shorter in the TLPPG group (3.8 cm) than in the LAPPG group (4.7 cm, p < 0.001). No significant difference in the complication rate was observed between the two groups (13.6% in the TLPPG vs. 9.3% in the LAPPG group, p = 0.594). No anastomosis-related complications occurred in either group. No significant between-group difference was observed in the delayed gastric emptying (TLPPG, 9.1 vs. LAPPG, 7%, p = 0.762). The initiation of postoperative fluid (TLPPG, 1.0 day vs. LAPPG, 3.0 days, p < 0.001) and meal (TLPPG, 3.0 days vs. LAPPG, 4.0 days, p < 0.001) intake was earlier in the TLPPG group than in the LAPPG group. No significant between-group difference was observed in the postoperative hospital stay.ConclusionsThe findings of this study suggest that TLPPG with intracorporeal reconstruction not only is as feasible and safe as LAPPG for the treatment of patients with early gastric cancer but also provides certain advantages such as reduced blood loss and wound size.

A Novel Automated System Yields Reproducible Temporal Feeding Patterns in Laboratory Rodents

ABSTRACTBackgroundThe impact of temporal feeding patterns remains a major unanswered question in nutritional science. Progress has been hampered by the absence of a reliable method to impose temporal feeding in laboratory rodents, without the confounding influence of food-hoarding behavior.ObjectiveThe aim of this study was to develop and validate a reliable method for supplying crushed diets to laboratory rodents in consistent, relevant feeding patterns for prolonged periods.MethodsWe programmed our experimental feeding station to deliver a standard diet [StD; Atwater Fuel Energy (AFE) 13.9% fat] or high-fat diet (HFD; AFE 45% fat) during nocturnal grazing [providing 1/24th of the total daily food intake (tdF/I) of ad libitum–fed controls every 30 min] and meal-fed (3 × 1-h periods of ad libitum feeding) patterns in male rats (Sprague-Dawley: 4 wk old, 72–119 g) and mice [C57/Bl6J wild-type (WT): 6 mo old, 29–37 g], and ghrelin-null littermates (Ghr−/−; 27–34 g).ResultsGrazing yielded accurate, consistent feeding events in rats, with an approximately linear rise in nocturnal cumulative food intake [tdF/I (StD): 97.4 ± 1.5% accurate compared with manual measurement; R2 = 0.86; tdF/I (HFD): 99.0 ± 1.4% accurate; R2 = 0.86]. Meal-feeding produced 3 nocturnal meals of equal size and duration in StD-fed rats (tdF/I: 97.4 ± 0.9% accurate; R2 = 0.90), whereas the second meal size increased progressively in HFD-fed rats (44% higher on day 35 than on day 14; P < 0.01). Importantly, cumulative food intake in grazing and meal-fed rats was identical. Similar results were obtained in WT mice except that less restricted grazing induced hyperphagia (compared with meal-fed WT mice; P < 0.05 from day 1). This difference was abolished in Ghr−/− mice, with meal initiation delayed and meal duration enhanced. Neither pattern elevated corticosterone secretion in rats, but meal-feeding aligned ultradian pulses.ConclusionsWe have established a consistent, measurable, researcher-defined, stress-free method for imposing temporal feeding patterns in rats and mice. This approach will facilitate progress in understanding the physiologic impact of feeding patterns.

Effects of rate and amount of propionic acid infused into the rumen on feeding behavior of Holstein cows in the postpartum period

The objective of this study was to determine the effects of 2 amounts of propionic acid (PA) infused intraruminally at 2 rates of infusion at the initiation of meals on the feeding behavior of Holstein cows in the postpartum period. We hypothesized that the amount and length of time of infusions would interact to affect feeding behavior: rapid infusion of a higher dose of PA would result in larger meal size with greater time between meals compared with a slower rate, whereas faster infusion of a lower dose of PA would reduce meal size and the time between meals compared with a slower infusion of the same dose. Eight ruminally cannulated, multiparous Holstein cows were used in a 4 × 4 Latin square design experiment. Cows were blocked by parturition date and randomly assigned to treatment sequence within square. Treatments were infusion of 2.5 L of 0.5 M (HI) or 0.2 M (LO) solutions of PA at initiation of meals over 5 min (FST) or 15 min (SLW) for 12 h following feed delivery. Contrary to our hypothesis, no interaction between amount and rate of infusion was detected for any feeding behavior parameter measured. The FST treatments did not affect dry matter intake or metabolizable energy intake compared with SLW. The FST treatments tended to increase meal length compared with SLW (28.1 vs. 22.7) but did not affect meal size. The FST treatments tended to decrease total eating time (108 vs. 122 min/12 h) but did not affect meal frequency compared with SLW. The HI treatments decreased dry matter intake (7.4 vs. 11.5 kg/12 h) and total metabolizable energy intake (22.5 vs. 29.1 Mcal/12 h) compared with LO by decreasing meal frequency (5.8 vs. 7.5 meals/12 h). The HI treatments decreased eating time (103 vs. 127 min/12 h) compared with LO but did not affect meal size. Further research is warranted on the effects of the temporal supply of propionate on propionate metabolism and feeding behavior.

Postmeal Optogenetic Inhibition of Dorsal or Ventral Hippocampal Pyramidal Neurons Increases Future Intake.

Memory of a recently eaten meal can serve as a powerful mechanism for controlling future eating behavior because it provides a record of intake that likely outlasts most physiological signals generated by the meal. In support, impairing the encoding of a meal in humans increases the amount ingested at the next eating episode. However, the brain regions that mediate the inhibitory effects of memory on future intake are unknown. In the present study, we tested the hypothesis that dorsal hippocampal (dHC) and ventral hippocampal (vHC) glutamatergic pyramidal neurons play a critical role in the inhibition of energy intake during the postprandial period by optogenetically inhibiting these neurons at specific times relative to a meal. Male Sprague Dawley rats were given viral vectors containing CaMKIIα-eArchT3.0-eYFP or CaMKIIα-GFP and fiber optic probes into dHC of one hemisphere and vHC of the other. Compared to intake on a day in which illumination was not given, inhibition of dHC or vHC glutamatergic neurons after the end of a chow, sucrose, or saccharin meal accelerated the onset of the next meal and increased the amount consumed during that next meal when the neurons were no longer inhibited. Inhibition given during a meal did not affect the amount consumed during that meal or the next one but did hasten meal initiation. These data show that dHC and vHC glutamatergic neuronal activity during the postprandial period is critical for limiting subsequent ingestion and suggest that these neurons inhibit future intake by consolidating the memory of the preceding meal.

Oleoylethanolamide: A novel pharmaceutical agent in the management of obesity-an updated review.

Obesity as a multifactorial disorder has been shown a dramatically growing trend recently. Besides genetic and environmental factors, dysregulation of the endocannabinoid system tone is involved in the pathogenesis of obesity. This study reviewed the potential efficacy of Oleoylethanolamide (OEA) as an endocannabinoid-like compound in the energy homeostasis and appetite control in people with obesity. OEA as a lipid mediator and bioactive endogenous ethanolamide fatty acid is structurally similar to the endocannabinoid system compounds; nevertheless, it is unable to induce to the cannabinoid receptors. Unlike endocannabinoids, OEA negatively acts on the food intake and suppress appetite via various mechanisms. Indeed, OEA as a ligand of PPAR-α, GPR-119, and TRPV1 receptors participates in the regulation of energy intake and energy expenditure, feeding behavior, and weight gain control. OEA delays meal initiation, reduces meal size, and increases intervals between meals. Considering side effects of some approaches used for the management of obesity such as antiobesity drugs and surgery as well as based on sufficient evidence about the protective effects of OEA in the improvement of common abnormalities in people with obese, its supplementation as a novel efficient and FDA approved pharmaceutical agent can be recommended.

Assessing vulnerability and coping capacities of rural women to drought: A case study of Zvishavane district, Zimbabwe

This study analysed the vulnerabilities and coping capacities of rural women to drought in Zvishavane district in Zimbabwe. The study utilised quantitative research approach in which a structured questionnaire was used to collect data from the sampled households. The result revealed that low and erratic rainfall, lack of alternative livelihood options, lack of land and property ownership amongst others were identified as some of the indicators of vulnerability among rural women in Zvishavane. Despite the vulnerabilities surrounding them, rural women are not passive victims of drought. They have developed and adopted drought coping strategies such as; purchasing food stuffs from neighbouring communities and stocking it for consumption in dry periods, selling or trading their small livestock for grain, cultivation of drought resistant crop varieties, skipping meals and reducing meal portions and initiation of market gardens to supplement their harvests. Various institutions such as Non-Governmental Organisations (NGOs), the government and religious organisations are also providing necessary support to these women. In order to mitigate drought impacts on rural women, interventions such as; boosting of irrigation activities, inclusion of women in programme implementation and drought mitigation planning, diversification of livelihoods, establishment and promotion of drought buffers and social networks are needed. In addition, reforms aimed at correcting the imbalances in land ownership and rectification of gender discrimination and imbalances from past practices and policies are some of the important policy options that should be looked into.

Temporal effects of ruminal propionic acid infusion on feeding behavior of Holstein cows in the postpartum period

The objective of this study was to determine the temporal effects of intraruminal infusion of propionic acid at the initiation of meals on feeding behavior of cows in the postpartum period. Propionic acid derived from ruminal fermentation can reduce energy intake of dairy cows. The suppression of appetite by propionic acid is likely caused by a signal related to the hepatic oxidation of fuels. Greater propionate flux to the liver is expected to result in faster oxidation of acetyl coenzyme A, which can stimulate satiety and reduce feed intake. Therefore, the rate of propionate supply to the liver, within the timeframe of meals, might be an important limitation to feed intake. Our hypothesis was that faster rate of propionate infusion during meals would decrease meal size and feed intake by decreasing the time required to stimulate satiety within a meal. Six ruminally cannulated, multiparous Holstein cows in the postpartum period were used in a duplicated 3 × 3 Latin square design experiment balanced for carryover effects. Treatments included control (no infusion) or 1.25 mol of propionic acid infused over 5 min (FST) or 15 min (SLW) at each meal. Infusions were initiated at the conditioned meal at feeding (1200 h) and were triggered at each spontaneous meal for 22 h. Contrary to our hypothesis, SLW decreased meal size 29% (0.87 vs. 1.23 kg of dry matter) compared with FST, and FST decreased meal frequency 27% (8.5 vs. 11.2 per d) compared with SLW. Dry matter intake was similar between FST and SLW, but propionic acid decreased dry matter intake 46% compared with control. A potential explanation is that FST resulted in greater liver bypass of propionate compared with SLW, extending anaplerosis of the tricarboxylic acid cycle, hepatic oxidation of acetyl coenzyme A, and satiety over a longer time after meals.