Affect Energy Balance Research Articles

Delayed meal timing after exercise is associated with reduced appetite and energy intake in adolescents with obesity.

While the beneficial effects of exercise on appetite might depend on its timing during the day or relative to a meal, this remains poorly explored in youth. To examine the importance of meal timing (+30 vs +90 minutes) after performing exercise on energy intake, appetite and food reward in adolescents with obesity. Eighteen adolescents with obesity randomly completed three conditions: (a) lunch (12:00 pm) set 30 minutes after a rest session (11:00 am); (b) lunch (12:00 pm) set 30 minutes after an exercise session (11:00 am)(MEAL-30); (c) lunch (01:00 pm) set 90 minutes after an exercise session (11:00 am)(MEAL-90). Lunch and dinner ad libitum energy intake was assessed, food reward (LFPQ) assessed before and after lunch, and before dinner, appetite sensations were assessed at regular intervals. Energy intake was lower at MEAL-90 than MEAL-30 and CON at lunch (P < .05 and P < .01, respectively) and lunch + dinner combined (P < .001). A decrease in intake (g) of protein, fat and carbohydrate was observed. Post-exercise hunger was lower on MEAL-90 compared with CON. No condition effects were found at lunch for food reward. Delaying the timing of the meal after exercise might help affect energy balance by decreasing ad libitum energy intake without increasing hunger and by improving satiety in adolescents with obesity.

Does exercising before or after a meal affect energy balance in adolescents with obesity?

Background and aimExercise timing has been suggested to affect appetite and energy intake (EI). The aim of this study was to examine the impact of exercising immediately before or after a meal on EI, appetite sensations and food reward (FR) in adolescents with obesity. Methods and resultsSeventeen adolescents with obesity completed 3 experimental sessions (randomized controlled trial): rest + lunch (CON); exercise + lunch (EX-MEAL); lunch + exercise (MEAL-EX). The exercise consisted of cycling 30 min at 65%V̇O2peak. Outcomes included ad libitum EI (weighed lunch and dinner), FR (Leeds Food Preference Questionnaire at pre- and post-combination of exercise/rest and lunch, and pre-dinner) and appetite sensations (visual analogue scales). EI was not different between conditions. Compared with CON, relative EI at lunch was lower in EX-MEAL and MEAL-EX (p ≤ 0.05) and daily only in MEAL-EX (p < 0.01). Postprandial fullness was higher in EX-MEAL compared to CON. Compared with CON, both EX-MEAL and MEAL-EX attenuated the increase in wanting for sweet food and reduced explicit liking for fat. ConclusionsThese preliminary results suggest that exercising immediately before or after a meal produce few differences in appetite and have small beneficial effects on overall energy balance in adolescents with obesity, as well as on FR. Clinical trialsNCT03967782.

Whey Protein and Its Components Lactalbumin and Lactoferrin Affect Energy Balance and Protect against Stroke Onset and Renal Damage in Salt-Loaded, High-Fat Fed Male Spontaneously Hypertensive Stroke-Prone Rats

Whey protein (WH)-enriched diets are reported to aid in weight loss and to improve cardiovascular health. However, the bioactive components in whey responsible for causing such effects remain unidentified. We determined the effects of whey and its components [α-lactalbumin (LA) and lactoferrin (LF)] on energy balance, glucose tolerance, gut hormones, renal damage, and stroke onset in rats. Male spontaneously hypertensive stroke-prone (SHRSP) rats (age 8 wk) were fed isocaloric high-fat (40%kcal) and high-salt (4%wt/wt) diets (n=8-10/group) and randomized for 8 wk to diets enriched as follows: control (CO): 15%kcal from egg albumin, 45%kcal from carbohydrate; WH: 20%kcal WH isolate+15%kcal egg albumin; LA: 20%kcal LA +15%kcal egg albumin; or LF: 20%kcal lactoferrin+15%kcal egg albumin. Measurements included energy balance (food intake, energy expenditure, and body composition), stroke-related behaviors, brain imaging, glucose tolerance, metabolic hormones, and tissue markers of renal damage. Data were analyzed by linear mixed models with repeated measures or 1-way ANOVA. Diets enriched with WH, LA, or LF increased survival, with 25% of rats fed these diets exhibiting stroke-associated morbidity, whereas 90% of CO rats were morbid by 8 wk (P<0.05). The nephritis scores of rats fed WH-, LA-, or LF-enriched diets were 80%, 92%, and 122% lower than those of COs (P=0.001). The mRNA abundances of renin and osteopontin were 100-600% lower in rats fed WH-, LA-, or LF-enriched diets than in COs (P<0.05). Urine albumin concentrations and albumin-to-creatinine ratios were 200% lower in rats fed LF-enriched diets than in COs (P<0.05). Compared with COs, rats fed LF-enriched diets for 2-3 wk had food intake decreased by 29%, body weight decreased by 13-19%, lean mass decreased by 12-19%, and fat mass decreased by 20% (P<0.001). Relative to COs, rats fed WH and LA had food intake decreased by 10% (P<0.1), but COs had 12-45% lower weight than rats fed LA- and WH-enriched diets by 3 wk (P<0.01). Compared with COs, rats fed WH-enriched diets increased energy expenditure by 7%, whereas, rats fed LA-enriched diets had energy expenditure acutely decreased by 7% during the first 4 d, and rats fed LF-enriched diets had energy expenditure decreased by 7-17% throughout the first week ( P<0.001). Rats fed LA- and LF-enriched diets had blood glucose decreased by 14-19% (P<0.05) and WH by 9% (P=0.1), relative to COs. Compared with COs, rats fed LF had GIP decreased by 90% and PYY by 87% (P<0.05). Together, these findings indicate that whey and its components α-lactalbumin and lactoferrin improved energy balance and glycemic control, and protected against the onset of neurological deficits associated with stroke and renal damage in male SHRSP rats.

Effect of fermented goat milk on body composition, basal metabolism, and food intake control in rats

Introduction: it is known that diet plays a key role in body composition and affects energy balance. However, scarce information is available in the scientific literature about the influence of food and specific nutrients such us dairy products, a basic food group and an important source of nutrients in the diet. Objective: the objective of this work was to evaluate the influence of fermented dairy products (goat or cow milk) on body composition and appetite regulation in adult animals. Material and methods: twenty adult male Wistar albino rats were fed fermented goat or cow milk-based diets for 30 days. The evolution of body composition and plasma concentrations of adipokines (leptine and adiponectine), intermediary metabolism regulating hormones (ghrelin, insulin, thyroid stimulating hormone, triyodotironine, thyroxine), and non-esterified fatty acid (NEFA) were analyzed. Results: body weight and body fat percentage were lower (p < 0.001) in rats fed fermented goat milk versus those fed fermented cow milk, whereas lean mass percentage was higher (p < 0.01). Plasma thyroid hormone and insulin concentrations did not show significant differences between diets. The fermented goat milk-based diet decreased ghrelin and adiponectin levels (p < 0.001), and increased leptine and NEFA concentrations (p < 0.001). Conclusion: fermented goat milk consumption decreases adiposity and body weight in adult rats by increasing energy expenditure, lipolysis, and satiety sensation.

Net Energy Net Energy Net EnergyNet EnerNet Energy of high-protein sunflower meal fed to growing pigs and effect of dietary phosphorus on measured values of NE.

An experiment was carried out to determine energy values of high-protein sunflower meal (HP-SFM) and to compare the energy values of HP-SFM determined using either a phosphorus (P)-deficient basal diet or a P-adequate basal diet. Twenty-four growing barrows were randomly assigned to 1 of 4 dietary treatments with 6 replicates per treatment. Four experimental diets including 2 basal diets containing 2 levels of standardized total tract digestible P (i.e., P-deficient and P-adequate) and the other 2 diets containing 30% HP-SFM with each basal diet (i.e., HP-SFM 1 diet and HP-SFM 2 diet) were formulated to determine the energy values of HP-SFM and to compare energy values of HP-SFM determined by the difference method using 2 basal diets. Pigs were fed diets for 15 d including 10 d for adaptation and 5 d for total collections. Pigs were then moved to indirect calorimetry chambers to determine total heat production (THP) and fasting heat production (FHP). A reduced (P < 0.01) amount of nitrogen was retained in pigs fed the P-deficient basal diet compared with those fed the other diets. The THP of pigs fed the HP-SFM 1 and 2 diets was greater (P < 0.01) than those fed the P-deficient basal diet with the intermediate value for pigs fed the P-adequate basal diet. The retained energy (RE) as protein of pigs fed the P-deficient basal diet was less (P < 0.01) but RE as lipid was greater (P < 0.01) than those fed the P-adequate basal, or HP-SFM 1 and 2 diets. However, there was no difference in FHP of pigs among the dietary treatments. The NE of HP-SFM determined using the P-deficient basal diet was 2,062 kcal/kg, as-fed basis, whereas the value determined using the P-adequate basal diet was 2,151 kcal/kg. Although no differences were observed in energy values, the amount of P in basal diet might affect energy balance by modifying N utilization, thus, a diet containing adequate amount of P is a more suitable basal diet when the difference method is used for calculation of NE in a feed ingredient.

IDOL regulates systemic energy balance through control of neuronal VLDLR expression.

Liver X receptors limit cellular lipid uptake by stimulating the transcription of Inducible Degrader of the LDL Receptor (IDOL), an E3 ubiquitin ligase that targets lipoprotein receptors for degradation. The function of IDOL in systemic metabolism is incompletely understood. Here we show that loss of IDOL in mice protects against the development of diet-induced obesity and metabolic dysfunction by altering food intake and thermogenesis. Unexpectedly, analysis of tissue-specific knockout mice revealed that IDOL affects energy balance, not through its actions in peripheral metabolic tissues (liver, adipose, endothelium, intestine, skeletal muscle), but by controlling lipoprotein receptor abundance in neurons. Single-cell RNA sequencing of the hypothalamus demonstrated that IDOL deletion altered gene expression linked to control of metabolism. Finally, we identify VLDLR rather than LDLR as the primary mediator of IDOL effects on energy balance. These studies identify a role for the neuronal IDOL-VLDLR pathway in metabolic homeostasis and diet-induced obesity.

Evaluation of prolactin and insulin resistance in women with polycystic ovarian syndrome

Background: Polycystic ovarian syndrome has been one of a major public health problem in India that leads to medical consequences. It causes multifactorial in etiology such as menstrual dysfunction, hyperandrogenism, hirsutism, insulin resistance, dyslipidemia and obesity which increased risk of diabetes mellitus and cardiovascular disease. Prolactin has been reported as a potent lipogenic and diabetogenic factor, that affecting energy balance and fuel metabolism. The present study was designed to assess serum prolactin and insulin resistance in PCOS women and to compare them with healthy women as controls. Material and Methods: A comparative study including 50 women diagnosed as PCOS and 50 age and BMI matched healthy women as controls was conducted. The age group for the study was 18-35 years. Body Mass Index was calculated as a physical parameter. Fasting blood samples were drawn to assess serum prolactin, serum insulin, HbA1c and fasting blood sugar. Insulin resistance was calculated by homeostasis model assessment. Results: A significant increase in fasting serum insulin (p<0.001) and HOMA – IR (p<0.001) were found in patients with PCOS in comparison with controls. Mean BMI, prolactin, HbA1c and FBS were found elevated in the PCOS women but they were not statistically significant. No significant correlations were found between BMI, serum prolactin and serum insulin. Conclusions: The current study provides further evidence that significantly higher fasting insulin and HOMA in PCOS group indicates presence of IR. IR in PCOS group may have a potential role in the prediction of dysglycemic disease in women with PCOS. This study could not find any significant correlation between serum prolactin, serum insulin and BMI.

1992-P: Early and Chronic Exposure to Penicillin Increases Obesity and Insulin Resistance in High-Fat Diet-Fed Mice

Increasing prevalence of antibiotic use may have health consequences given their effects on gut microbiome. Male and female C57BL/6J mice were exposed to a low-dose penicillin (7 mg/L) during the first 4 weeks of life via maternal drinking water (PCN; n=6-10) or continuously (PCN-C; n=4-5), and a high-fat diet (HFD) was started at 6 weeks of age. Whole body fat mass began to increase in male PCN and PCN-C groups after 5 weeks of HFD (Figure 1). This was largely due to 20% decrease in physical activity in PCN mice. Insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamp after 20 weeks of HFD, and glucose infusion rate (GIR) and glucose turnover (GT) were significantly reduced in PCN-C group. The PCN group showed increased hepatic insulin resistance compared to Control (n=12; Figure 2). In female mice, PCN effects were more pronounced with increased fat mass after 1 week of HFD (Figure 3). This was due to 30% decrease in physical activity in female PCN mice compared to Control (n=5). After 20 weeks of HFD, female Control mice remained insulin sensitive, but female PCN-C mice developed insulin resistance with 20% decreases in GIR and GT (Figure 4). In conclusion, these results show that early life or chronic exposure to penicillin negatively affects energy balance and glucose metabolism in mice with larger effects in female mice. Our findings indicate an important role of antibiotic exposure in obesity and insulin resistance. Disclosure H. Noh: None. S. Suk: None. R.H. Friedline: None. X. Hu: None. D.A. Tran: None. L.A. Tauer: None. J. Choi: None. M. Ko: None. B. Kim: None. T. Surapaneni: None. M.J. Blaser: None. J.K. Kim: None. Funding National Institutes of Health (5U2C-DK093000)

The Catalytic Subunit β of PKA Affects Energy Balance and Catecholaminergic Activity.

The protein kinase A (PKA) signaling system mediates the effects of numerous hormones, neurotransmitters, and other molecules to regulate metabolism, cardiac function, and more. PKA defects may lead to diverse phenotypes that largely depend on the unique expression profile of the affected subunit. Deletion of the Prkarcb gene, which codes for PKA catalytic subunit β (Cβ), protects against diet-induced obesity (DIO), yet the mechanism for this phenotype remains unclear. We hypothesized that metabolic rate would be increased in Cβ knockout (KO) mice, which could explain DIO resistance. Male, but not female, CβKO mice had increased energy expenditure, and female but not male CβKO mice had increased subcutaneous temperature and increased locomotor activity compared with wild-type (WT) littermates. Urinary norepinephrine (NE) and normetanephrine were elevated in female CβKO mice. CβKO mice had increased heart rate (HR); blocking central NE release normalized HR to that of untreated WT mice. Basal and stimulated PKA enzymatic activities were unchanged in adipose tissue and heart and varied in different brain regions, suggesting that Prkacb deletion may mediate signaling changes in specific brain nuclei and may be less important in the peripheral regulation of PKA expression and activity. This is a demonstration of a distinct effect of the PKA Cβ catalytic subunit on catecholamines and sympathetic nerve signaling. The data provide an unexpected explanation for the metabolic phenotype of CβKO mice. Finally, the sexual dimorphism is consistent with mouse models of other PKA subunits and adds to the importance of these findings regarding the PKA system in human metabolism.

Association between REM sleep and obstructive sleep apnea in obese and overweight adolescents.

Overweight and obese children have demonstrated reduced rapid eye movement (REM) sleep, affecting energy balance regulation and predisposition to weight gain. Obstructive sleep apnea (OSA) is a known cause of decreased REM sleep. The purpose of this study is to examine the association between the percentage of REM sleep, BMI z-score, and OSA severity in overweight and obese adolescents. We performed a cross-sectional study of 92 (43% female) overweight and obese adolescents (13-17years old) who underwent overnight polysomnography (PSG) at Children's Hospital Los Angeles between 2010 and 2017. The average Body Mass Index (BMI) z-score was 2.27 ± 0.47, with 71% having BMI z-score ≥ 2. REM% during PSG was 15.6 ± 6.8, and obstructive apnea-hypopnea index was 17.1 ± 24.3. The distribution across categories of OSA severity was 27% none (≤ 1.5events/h), 24% mild (> 1.5-5events/h), 8% moderate (> 5-10events/h), and 41% severe (> 10events/h). REM% was not associated with BMI z-score, either on univariate or multivariate regression with adjustment for age, gender, and apnea-hypopnea index (AHI). When subdivided into OSA categories, a 1-unit increase in BMI z-score was associated with a 5.96 (p = 0.03) increase in REM% in mild OSA and an 8.86 (p = 0.02) decrease in REM% in severe OSA. There was no association between BMI z-score and REM% in none and moderate OSA. Among overweight and obese adolescents, BMI z-score was associated with decreased REM% in severe OSA and unexpectedly increased REM% in mild OSA, but there was no association in none or moderate OSA.

Parabens and their relation to obesity.

Parabens are a group of chemicals used as preservatives in the food, cosmetic and pharmaceutical industries. They are known to possess estrogenic effects, and therefore have been classified as endocrine disruptors. In addition to the classical endocrine organs, other tissues have endocrine activity, including adipose tissue. Several chemicals are known to cause obesogenic effects, and parabens are currently being studied in this context. The aim of this study was to investigate the possible connections of paraben exposure and obesity. Blood plasma from 27 healthy women was collected during their menstrual cycle. Basal anthropometric measures, levels of parabens (methylparaben, ethylparaben and propylparaben), adipokines (adiponectin, adipsin, leptin, resistin and visfatin) and hormones affecting energy balance and metabolic health (c-peptide, ghreline, GIP, GLP-1, glucagon, insulin, PAI-1) were measured. A Kolmogorov-Smirnov test showed higher methylparaben and propylparaben levels in women with BMI 25-34.9 compared to those with BMI 18.5-24.9. Plasma levels of methylparaben as well as the sum of parabens were positively associated with the plasma adipsin levels. Negative associations for methylparaben were found for glucagon, leptin and PAI-1. In accordance with other experimental studies we observed important associations of methylparaben and hormones affecting energy balance and metabolic health, indicating its obesogenic potential.

Effects of timing of palmitic acid supplementation during early lactation on nutrient digestibility, energy balance, and metabolism of dairy cows

The objective of our study was to evaluate the effects of timing of palmitic acid (C16:0) supplementation during early lactation on nutrient digestibility, energy intake and balance, and metabolic responses of dairy cows. Fifty-two multiparous cows were used in a randomized complete block design experiment. During the fresh (FR) period (1-24 d in milk) cows were assigned to either a control diet containing no supplemental fat (CON) or a C16:0-supplemented diet [PA; 1.5% of diet dry matter (DM)]. During the peak (PK) period (25-67 d in milk) cows were assigned to either a CON diet or a PA diet (1.5% of diet DM) in a 2 × 2 factorial arrangement of treatments considering the diet that they received during the FR period. During the FR period, compared with CON, PA increased DM digestibility by 3.0 percentage units and neutral detergent fiber (NDF) digestibility by 4.4 percentage units, and the increase in these variables was consistent over time. Although PA did not affect 18-carbon fatty acid (FA) digestibility, it decreased 16-carbon FA digestibility by 10.8 percentage units and total FA digestibility by 4.7 percentage units compared with CON. We observed a tendency for an interaction between treatment and time for total FA digestibility and 16-carbon FA digestibility due to the difference in FA digestibility between PA and CON reducing over time. Compared with CON, PA increased digestible energy intake by 3.9 Mcal/d, metabolizable energy intake by 3.5 Mcal/d, and net energy for lactation intake by 2.5 Mcal/d. The PA diet also increased milk energy output, negative energy balance, and plasma nonesterified fatty acid concentration and reduced plasma insulin concentration. We also observed a tendency for an interaction between treatment and time for energy balance due to cows receiving the PA treatment being in a greater negative energy balance over time. During the PK period, PA increased DM digestibility by 2.9 percentage units and NDF digestibility by 3.5 percentage units compared with CON. Although PA decreased 16-carbon FA digestibility by 7.0 percentage units, PA did not affect 18-carbon FA digestibility or total FA digestibility. Feeding PA during the PK period increased energy intake and milk energy output and did not affect energy balance. In conclusion, feeding a C16:0 supplement to early-lactation cows consistently increased DM and NDF digestibilities and energy intake compared with a control diet containing no supplemental fat. Feeding C16:0 markedly increased milk energy output in both the FR and PK periods but increased negative energy balance only in the FR period.

Analysis of Airborne Optical and Thermal Imagery for Detection of Water Stress Symptoms

High-resolution airborne thermal infrared (TIR) together with sun-induced fluorescence (SIF) and hyperspectral optical images (visible, near- and shortwave infrared; VNIR/SWIR) were jointly acquired over an experimental site. The objective of this study was to evaluate the potential of these state-of-the-art remote sensing techniques for detecting symptoms similar to those occurring during water stress (hereinafter referred to as ‘water stress symptoms’) at airborne level. Flights with two camera systems (Telops Hyper-Cam LW, Specim HyPlant) took place during 11th and 12th June 2014 in Latisana, Italy over a commercial grass (Festuca arundinacea and Poa pratense) farm with plots that were treated with an anti-transpirant agent (Vapor Gard®; VG) and a highly reflective powder (kaolin; KA). Both agents affect energy balance of the vegetation by reducing transpiration and thus reducing latent heat dissipation (VG) and by increasing albedo, i.e., decreasing energy absorption (KA). Concurrent in situ meteorological data from an on-site weather station, surface temperature and chamber flux measurements were obtained. Image data were processed to orthorectified maps of TIR indices (surface temperature (Ts), Crop Water Stress Index (CWSI)), SIF indices (F687, F780) and VNIR/SWIR indices (photochemical reflectance index (PRI), normalised difference vegetation index (NDVI), moisture stress index (MSI), etc.). A linear mixed effects model that respects the nested structure of the experimental setup was employed to analyse treatment effects on the remote sensing parameters. Airborne Ts were in good agreement (∆T &lt; 0.35 K) compared to in situ Ts measurements. Maps and boxplots of TIR-based indices show diurnal changes: Ts was lowest in the early morning, increased by 6 K up to late morning as a consequence of increasing net radiation and air temperature (Tair) and remained stable towards noon due to the compensatory cooling effect of increased plant transpiration; this was also confirmed by the chamber measurements. In the early morning, VG treated plots revealed significantly higher Ts compared to control (CR) plots (p = 0.01), while SIF indices showed no significant difference (p = 1.00) at any of the overpasses. A comparative assessment of the spectral domains regarding their capabilities for water stress detection was limited due to: (i) synchronously overpasses of the two airborne sensors were not feasible, and (ii) instead of a real water stress occurrence only water stress symptoms were simulated by the chemical agents. Nevertheless, the results of the study show that the polymer di-1-p-menthene had an anti-transpiring effect on the plant while photosynthetic efficiency of light reactions remained unaffected. VNIR/SWIR indices as well as SIF indices were highly sensitive to KA, because of an overall increase in spectral reflectance and thus a reduced absorbed energy. On the contrary, the TIR domain was highly sensitive to subtle changes in the temperature regime as induced by VG and KA, whereas VNIR/SWIR and SIF domain were less affected by VG treatment. The benefit of a multi-sensor approach is not only to provide useful information about actual plant status but also on the causes of biophysical, physiological and photochemical changes.

Specific subpopulations of hypothalamic leptin receptor-expressing neurons mediate the effects of early developmental leptin receptor deletion on energy balance

ObjectiveTo date, early developmental ablation of leptin receptor (LepRb) expression from circumscribed populations of hypothalamic neurons (e.g., arcuate nucleus (ARC) Pomc- or Agrp-expressing cells) has only minimally affected energy balance. In contrast, removal of LepRb from at least two large populations (expressing vGat or Nos1) spanning multiple hypothalamic regions produced profound obesity and metabolic dysfunction. Thus, we tested the notion that the total number of leptin-responsive hypothalamic neurons (rather than specific subsets of cells with a particular molecular or anatomical signature) subjected to early LepRb deletion might determine energy balance. MethodsWe generated new mouse lines deleted for LepRb in ARC GhrhCre neurons or in Htr2cCre neurons (representing roughly half of all hypothalamic LepRb neurons, distributed across many nuclei). We compared the phenotypes of these mice to previously-reported models lacking LepRb in Pomc, Agrp, vGat or Nos1 cells. ResultsThe early developmental deletion of LepRb from vGat or Nos1 neurons produced dramatic obesity, but deletion of LepRb from Pomc, Agrp, Ghrh, or Htr2c neurons minimally altered energy balance. ConclusionsAlthough early developmental deletion of LepRb from known populations of ARC neurons fails to substantially alter body weight, the minimal phenotype of mice lacking LepRb in Htr2c cells suggests that the phenotype that results from early developmental LepRb deficiency depends not simply upon the total number of leptin-responsive hypothalamic LepRb cells. Rather, specific populations of LepRb neurons must play particularly important roles in body energy homeostasis; these as yet unidentified LepRb cells likely reside in the DMH.

The hindbrain is a site of energy balance action for prolactin-releasing peptide: feeding and thermic effects from GPR10 stimulation of the nucleus tractus solitarius/area postrema.

Prolactin-releasing peptide (PrRP) is a neuropeptide that suppresses food intake and increases body temperature when delivered to the forebrain ventricularly or parenchymally. However, PrRP's receptor GPR10 is widely distributed throughout the brain with particularly high levels found in the dorsomedial hindbrain. Thus, we hypothesized that hindbrain-directed PrRP administration would affect energy balance and motivated feeding behavior. To address this hypothesis, a range of behavioral and physiologic variables were measured in Sprague-Dawley rats that received PrRP delivered to the fourth ventricle (4V) or the nucleus of the solitary tract (NTS) at the level of the area postrema (AP). 4V PrRP delivery decreased chow intake and body weight, in part, through decreasing meal size in ad libitum maintained rats tested at dark onset. PrRP inhibited feeding when delivered to the nucleus tractus solitarius (NTS), but not to more ventral hindbrain structures. In addition, 4V as well as direct NTS administration of PrRP increased core temperature. By contrast, 4V PrRP did not reduce ad libitum intake of highly palatable food or the motivation to work for or seek palatable foods. The dorsomedial hindbrain and NTS/AP, in particular, are sites of action in PrRP/GPR10-mediated control of chow intake, core temperature, and body weight.

High orange juice consumption with or in-between three meals a day differently affects energy balance in healthy subjects

Sugar-containing beverages like orange juice can be a risk factor for obesity and type 2 diabetes although the underlying mechanisms are less clear. We aimed to investigate if intake of orange juice with or in-between meals differently affects energy balance or metabolic risk. Twenty-six healthy adults (24.7 ± 3.2 y; BMI 23.2 ± 3.2 kg/m2) participated in a 4-week cross-over intervention and consumed orange juice (20% of energy requirement) either together with 3 meals/d (WM) or in-between 3 meals/d (BM) at ad libitum energy intake. Basal and postprandial insulin sensitivity (primary outcome), daylong glycaemia, glucose variability and insulin secretion were assessed. Body fat mass was measured by air-displacement plethysmography. After BM-intervention, fat mass increased (+1.0 ± 1.8 kg; p < 0.05) and postprandial insulin sensitivity tended to decrease (ΔMatsudaISI: −0.89 ± 2.3; p = 0.06). By contrast, after WM-intervention fat mass and gamma-glutamyl transferase (GGT) decreased (−0.30 ± 0.65 kg; −2.50 ± 3.94; both p < 0.05), whereas glucose variability was higher (ΔMAGE: +0.45 ± 0.59, p < 0.05). Daylong glycaemia, insulin secretion, changes in basal insulin sensitivity, and triglycerides did not differ between WM- and BM-interventions (all p > 0.05). In young healthy adults, a conventional 3-meal structure with orange juice consumed together with meals had a favorable impact on energy balance, whereas juice consumption in-between meals may contribute to a gain in body fat and adverse metabolic effects.

The development of probiotics therapy to obesity: a therapy that has gained considerable momentum.

Obesity is a growing epidemic worldwide. The most frequent cause leading to the development of obesity is an imbalance between energy intake and energy expenditure. The gut microbiota is an environmental factor involved in obesity and metabolic disorders which reveals that obese animal and human subjects present alterations in the composition of the gut microbiota compared to their lean counterparts. Furthermore, evidence has so far demonstrated that the gut microbiota, which influences whole-body metabolism, by affecting energy balance, but also inflammation and gut barrier function, integrates peripheral and central food intake regulatory signals, thereby altering body weight. At the same time, these data suggest that species of intestinal commensal bacteria may play either a pathogenic or a protective role in the development of obesity. Though still a relatively nascent field of research, evidence to date suggests that manipulating the gut microbiome may represent effective treatment for the prevention or management of obesity. Various studies have described the beneficial effects of specific bacteria on the characteristics of obesity. However, the available data in this field remain limited and the relevant scientific work has only recently begun. This review aims to summarize the notable advances and contributions in the field that may prove useful for identifying probiotics that target obesity and its related disorders.

Novel role of GLP-1 receptor signaling in energy expenditure during chronic high fat diet feeding in rats

ObjectiveGlucagon-like peptide-1 (GLP-1) secreted from intestinal L-cells plays a major role in meal termination and glucose-dependent insulin secretion. Several lines of evidence indicate, however, that the acute satiating and incretin effects of GLP-1 are attenuated with high fat diet (HFD) exposure. Here we tested the hypothesis that endogenous GLP-1 differentially affects energy balance and glucose homeostasis dependent on whether rats are fed chow or HFD (60% energy from fat). MethodsWe blocked GLP-1 receptor (GLP-1R) signaling by daily intraperitoneal (IP) injection of the GLP-1R antagonist exendin (9–39) (Ex9, 10 μg/kg) or vehicle for 5 weeks in male Sprague-Dawley rats fed either chow or HFD, recorded body weight (BW) and food intake throughout, and assessed energy expenditure (3rd week) and glucose tolerance (4th week). ResultsFive week daily Ex9 injections reduced BW gain in HFD-fed rats, but did not affect BW in chow-fed rats. On the other hand, chronic Ex9 treatment did not affect daily food intake in either chow or HFD-fed rats during the entire study. The reduced BW gain in HFD-fed rats was associated with an increase in energy expenditure. Interestingly, chronic Ex9 treatment induced glucose intolerance in chow-fed rats, but not in HFD-fed rats, suggesting a differential role of GLP-1R signaling in glucose metabolism during chow and HFD feeding. ConclusionsOur findings reveal a novel role of GLP-1R signaling, modulating energy expenditure rather than eating behavior during HFD feeding. Furthermore, these results suggest a previously unrecognized contribution of GLP-1R signaling to the pathophysiology of obesity.

The antidepressant fluoxetine acts on energy balance and leptin sensitivity via BDNF

Leptin and Brain Derived Neurotrophic Factor (BDNF) pathways are critical players in body weight homeostasis. Noninvasive treatments like environmental stimulation are able to increase response to leptin and induce BDNF expression in the brain. Emerging evidences point to the antidepressant selective serotonin reuptake inhibitor Fluoxetine (FLX) as a drug with effects similar to environmental stimulation. FLX is known to impact on body weight, with mechanisms yet to be elucidated. We herein asked whether FLX affects energy balance, the leptin system and BDNF function. Adult lean male mice chronically treated with FLX showed reduced weight gain, higher energy expenditure, increased sensitivity to acute leptin, increased hypothalamic BDNF expression, associated to changes in white adipose tissue expression typical of “brownization”. In the Ntrk2tm1Ddg/J model, carrying a mutation in the BDNF receptor Tyrosine kinase B (TrkB), these effects are partially or totally reversed. Wild type obese mice treated with FLX showed reduced weight gain, increased energy output, and differently from untreated obese mice, a preserved acute response to leptin in terms of activation of the intracellular leptin transducer STAT3. In conclusion, FLX impacts on energy balance and induces leptin sensitivity and an intact TrkB function is required for these effects to take place.

Home alone: a systematic review and meta-analysis on the effects of individual housing on body weight, food intake and visceral fat mass in rodents.

Rats and mice are widely used to study environmental effects on psychological and metabolic health. Study designs differ widely and are often characterized by varying (social) housing conditions. In itself, housing has a profound influence on physiology and behaviour of rodents, affecting energy balance and sustainable metabolic health. However, evidence for potential long-term consequences of individual versus social housing on body weight and metabolic phenotype is inconsistent. We conducted a systematic literature review and meta-analyses assessing effects of individual versus social housing of rats and mice, living under well-accepted laboratory conditions, on measures of metabolic health, including body weight, food intake and visceral adipose tissue mass. Seventy-one studies were included in this review; 59 were included in the meta-analysis. Whilst housing did not affect body weight, both food intake and visceral adipose tissue mass were significantly higher in individually compared with socially housed animals. A combination of emotional stress and lack of social thermoregulation likely contributed to these effects. Increased awareness of consequences and improved specifications of housing conditions are necessary to accurately evaluate efficacy of drugs, diets or other interventions on metabolic and other health outcomes because housing conditions are rarely considered as possible moderators of reported outcomes.