Influence Energy Balance Research Articles

Does genetic risk of obesity modify associations between the neighbourhood environment and body-mass index? A cross-sectional analysis of the UK Biobank dataset

BackgroundIn studies of gene–environment interactions and obesity, the term environment usually refers to individual behavioural factors that influence energy balance. However, evidence suggests that the built environments in which individuals live, work, and play are associated with obesity and may therefore be environmental triggers of genetic risk. No studies have explored whether individual response to such environmental determinants of obesity varies with genetic risk. We aimed to examine whether genetic risk of obesity modifies associations between various neighbourhood characteristics and body-mass index (BMI). MethodsOur sample included 245 532 adults aged 40–69 years from UK Biobank with cross-sectional data on neighbourhood exposures, BMI, potential confounders, and BMI-linked single nucleotide polymorphisms (SNPs). We derived a composite measure of residential neighbourhood environment based on proximity of fast-food stores, availability of physical activity facilities, and neighbourhood green-ness. We also examined each component separately. We constructed a genetic risk score (GRS) as the weighted average of 70 SNPs, where weights were published estimates of genetic effect sizes, scaled to account for the number of available SNPs. In adjusted mixed-effects regression models of neighbourhood environment–BMI associations we examined possible effect modification by genetic risk by testing GRS-by-neighbourhood measure interaction terms and estimating GRS-stratified associations. FindingsSome evidence of an interaction with genetic risk was observed for the composite measure (pinteraction=0·040); the magnitude of the main association with BMI was somewhat larger among people in the highest genetic risk quintile (0·12 lower BMI for each unit increase in composite score [95% CI −0·15 to −0·08]) compared with those in the lowest GRS quintile (β=–0·07; 95% CI −0·11 to −0·03). Less evidence of interaction was observed for the component neighbourhood exposures (fast-food proximity, availability of PA facilities, and neighbourhood greenness), but some results were sensitive (particularly fast-food proximity findings) to alternative model specification and GRS definitions. InterpretationThis preliminary analysis suggests that any gene–environment interaction is fairly weak. People at some levels of genetic risk of obesity might be more sensitive to some neighbourhood characteristics in combination. It is possible that obesogenic environments are so pervasive that low genetic risk affords limited protection. Results were sensitive to analytical decisions, and further examination of this possible gene–environment interaction is necessary. Measurement error in the neighbourhood exposures and UK Biobank's low response fraction remain potential sources of bias. FundingCommonwealth Scholarship Commission.

Leptin and insulin do not exert redundant control of metabolic or emotive function via dopamine neurons

Leptin and insulin's hunger-suppressing and activity-promoting actions on hypothalamic neurons are well characterized, yet the mechanisms by which they modulate the midbrain dopamine system to influence energy balance remain less clear. A subset of midbrain dopamine neurons express receptors for leptin (Lepr) and insulin (Insr). Leptin-dopamine signaling reduces running reward and homecage activity. However, dopamine-specific deletion of Lepr does not affect body weight or food intake in mice. We hypothesized insulin-dopamine signaling might compensate for disrupted leptin-dopamine signaling. To investigate the degree to which insulin and leptin exert overlapping (i.e. redundant) versus discrete control over dopamine neurons, we generated transgenic male and female mice exhibiting dopamine-specific deletion of either Lepr (Lepr KO), Insr (Insr KO) or both Lepr and Insr (Dbl KO) and assessed their feeding behavior, voluntary activity, and energy expenditure compared to control mice. No differences in body weight, daily food intake, energy expenditure or hyperphagic feeding of palatable chow were observed between Lepr, Insr or Dbl KO mice and control mice. However, consistent with previous findings, Lepr KO (but not Insr or Dbl KO) male mice exhibited significantly increased running wheel activity compared to controls. These data demonstrate that insulin and leptin do not exert redundant control of dopamine neuron-mediated modulation of energy balance. Furthermore, our results indicate neither leptin nor insulin plays a critical role in the modulation of dopamine neurons regarding hedonic feeding behavior or anxiety-related behavior.

Activation of mTORC1 Signaling in Gastric X/A-Like Cells Induces Spontaneous Pancreatic Fibrosis and Derangement of Glucose Metabolism

Background: Pancreatic fibrosis is a pathophysiological process associated with excessive deposition of extracellular matrix in pancreas, leading to reduced insulin secretion and derangement of glucose metabolism. X/A-like cells, a group of unique endocrine cells in gastric oxyntic mucosa, produce and secret ghrelin to influence energy balance. Whether gastric X/A-like cells affect pancreatic fibrosis and subsequent glucose homeostasis remains unclear. Methods: We established a Ghrl-cre transgene in which the cre enzyme is expressed in X/A-like cells under the control of ghrelin-promoter. TSC1flox/flox mice were bred with Ghrl-cre mice to generate Ghrl-TSC1-/- (TG) mice, within which mTORC1 signaling was activated in X/A-like cells. Pancreatic fibrosis and insulin secretion were analyzed in the TG mice. Findings: Activation of mTORC1 signaling by deletion of TSC1 gene in gastric X/A-like cells induced spontaneous pancreatic fibrosis. This alteration was associated with reduced insulin expression and secretion, as well as impaired glucose metabolism. Activation of mTORC1 signaling in gastric X/A-like cells reduced gastric and circulating ghrelin levels. Exogenous ghrelin reversed pancreatic fibrosis and glucose intolerance induced by activation of mTORC1 signaling in these cells. Rapamycin, an inhibitor of mTOR, reversed the decrease of ghrelin levels and pancreatic fibrosis. Interpretation: Activation of mTORC1 signaling in gastric X/A-like cells induces spontaneous pancreatic fibrosis and subsequently impairs glucose homeostasis via suppression of ghrelin. Funding Statement: This research was supported by grants from the National Key R&D Program of China (2017YFC0908900), and the National Natural Science Foundation of China (81730020, 81330010, 81390354). Declaration of Interests: All authors declare no conflict of interests. Ethics Approval Statement: All experimental protocols were approved by the Animal Care and Use Committee of Peking University (Permit Number: LA2012-60).

Microbial enterotypes in personalized nutrition and obesity management

Human gut microbiota has been suggested to play an important role in nutrition and obesity. However, formulating meaningful and clinically relevant dietary advice based on knowledge about gut microbiota remains a key challenge. A number of recent studies have found evidence that stratification of individuals according to 2 microbial enterotypes (dominance of either Prevotella or Bacteroides) may be useful in predicting responses to diets and drugs. Here, we review enterotypes in a nutritional context and discuss how enterotype stratification may be used in personalized nutrition in obesity management. Enterotypes are characterized by distinct digestive functions with preference for specific dietary substrate, resulting in short-chain fatty acids that may influence energy balance in the host. Consequently, the enterotype potentially affects the individual's ability to lose weight when following a specific diet. In short, a high-fiber diet seems to optimize weight loss among Prevotella-enterotype subjects but not among Bacteroides-enterotype subjects. In contrast, increasing bifidobacteria in the gut among Bacteroides-enterotype subjects improves metabolic parameters, suggesting that this approach can be used as an alternative weight loss strategy. Thus, enterotypes, as a pretreatment gut microbiota biomarker, have the potential to become an important tool in personalized nutrition and obesity management, although further interventions assessing their applicability are warranted.

Activation of mTORC1 signaling in gastric X/A-like cells induces spontaneous pancreatic fibrosis and derangement of glucose metabolism by reducing ghrelin production.

BackgroundPancreatic fibrosis is a pathophysiological process associated with excessive deposition of extracellular matrix in pancreas, leading to reduced insulin secretion and derangement of glucose metabolism. X/A-like cells, a group of unique endocrine cells in gastric oxyntic mucosa, produce and secret ghrelin to influence energy balance. Whether gastric X/A-like cells affect pancreatic fibrosis and subsequent glucose homeostasis remains unclear.MethodsWe established a Ghrl-cre transgene in which the cre enzyme is expressed in X/A-like cells under the control of ghrelin-promoter. TSC1flox/flox mice were bred with Ghrl-cre mice to generate Ghrl-TSC1−/− (TG) mice, within which mTORC1 signaling was activated in X/A-like cells. Pancreatic fibrosis and insulin secretion were analyzed in the TG mice.FindingsActivation of mTORC1 signaling by deletion of TSC1 gene in gastric X/A-like cells induced spontaneous pancreatic fibrosis. This alteration was associated with reduced insulin expression and secretion, as well as impaired glucose metabolism. Activation of mTORC1 signaling in gastric X/A-like cells reduced gastric and circulating ghrelin levels. Exogenous ghrelin reversed pancreatic fibrosis and glucose intolerance induced by activation of mTORC1 signaling in these cells. Rapamycin, an inhibitor of mTOR, reversed the decrease of ghrelin levels and pancreatic fibrosis.InterpretationActivation of mTORC1 signaling in gastric X/A-like cells induces spontaneous pancreatic fibrosis and subsequently impairs glucose homeostasis via suppression of ghrelin.

3-Iodothyronamine Activates a Set of Membrane Proteins in Murine Hypothalamic Cell Lines.

3-Iodothyronamine (3-T1AM) is an endogenous thyroid hormone metabolite. The profound pharmacological effects of 3-T1AM on energy metabolism and thermal homeostasis have raised interest to elucidate its signaling properties in tissues that pertain to metabolic regulation and thermogenesis. Previous studies identified G protein-coupled receptors (GPCRs) and transient receptor potential channels (TRPs) as targets of 3-T1AM in different cell types. These two superfamilies of membrane proteins are largely expressed in tissue which influences energy balance and metabolism. As the first indication that 3-T1AM virtually modulates the function of the neurons in hypothalamus, we observed that intraperitoneal administration of 50 mg/kg bodyweight of 3-T1AM significantly increased the c-FOS activation in the paraventricular nucleus (PVN) of C57BL/6 mice. To elucidate the underlying mechanism behind this 3-T1AM-induced signalosome, we used three different murine hypothalamic cell lines, which are all known to express PVN markers, GT1-7, mHypoE-N39 (N39) and mHypoE-N41 (N41). Various aminergic GPCRs, which are the known targets of 3-T1AM, as well as numerous members of TRP channel superfamily, are expressed in these cell lines. Effects of 3-T1AM on activation of GPCRs were tested for the two major signaling pathways, the action of Gαs/adenylyl cyclase and Gi/o. Here, we demonstrated that this thyroid hormone metabolite has no significant effect on Gi/o signaling and only a minor effect on the Gαs/adenylyl cyclase pathway, despite the expression of known GPCR targets of 3-T1AM. Next, to test for other potential mechanisms involved in 3-T1AM-induced c-FOS activation in PVN, we evaluated the effect of 3-T1AM on the intracellular Ca2+ concentration and whole-cell currents. The fluorescence-optic measurements showed a significant increase of intracellular Ca2+ concentration in the three cell lines in the presence of 10 μM 3-T1AM. Furthermore, this thyroid hormone metabolite led to an increase of whole-cell currents in N41 cells. Interestingly, the TRPM8 selective inhibitor (10 μM AMTB) reduced the 3-T1AM stimulatory effects on cytosolic Ca2+ and whole-cell currents. Our results suggest that the profound pharmacological effects of 3-T1AM on selected brain nuclei of murine hypothalamus, which are known to be involved in energy metabolism and thermoregulation, might be partially attributable to TRP channel activation in hypothalamic cells.

Determination of Energy Expenditure

Nutrition interventions are often designed to influence energy balance, ultimately optimizing the health of individuals or groups. Goals include weight loss in obese and overweight individuals or weight gain in growing children, pregnant women, and the underweight. In some cases, weight maintenance is the intention for healthy weight adults or children who have the opportunity to grow into their current weight. Determining the energy requirements for each person can help explain the presence or absence of weight changes and direct subsequent nutrition goals and interventions. Quantifying energy requirements also helps to avoid over- and under- feeding. This is particularly relevant in people suffering from acute or chronic disease or illness. In the acute care setting overfeeding can worsen metabolic disturbances including, but not limited to, hyperglycemia and hypercarbia while underfeeding can negatively impact immunity, organ function, and activities of daily living. This review contains 3 Figures, 5 Tables and 66 references Key words: nutrition, energy expenditure, body composition, calorimetry, bioelectrical impedance analysis (BIA), doubly-labeled water (DLW), reverse Fick equation, Harris-Benedict equation, Millfin-St. Jeor Equation, Owen Equation, Ireton-Jones Equations, Penn State Equations, hypocaloric feeding

Acute and Chronic Effects of Exercise on Appetite, Energy Intake, and Appetite-Related Hormones: The Modulating Effect of Adiposity, Sex, and Habitual Physical Activity.

Exercise facilitates weight control, partly through effects on appetite regulation. Single bouts of exercise induce a short-term energy deficit without stimulating compensatory effects on appetite, whilst limited evidence suggests that exercise training may modify subjective and homeostatic mediators of appetite in directions associated with enhanced meal-induced satiety. However, a large variability in responses exists between individuals. This article reviews the evidence relating to how adiposity, sex, and habitual physical activity modulate exercise-induced appetite, energy intake, and appetite-related hormone responses. The balance of evidence suggests that adiposity and sex do not modify appetite or energy intake responses to acute or chronic exercise interventions, but individuals with higher habitual physical activity levels may better adjust energy intake in response to energy balance perturbations. The effect of these individual characteristics and behaviours on appetite-related hormone responses to exercise remains equivocal. These findings support the continued promotion of exercise as a strategy for inducing short-term energy deficits irrespective of adiposity and sex, as well as the ability of exercise to positively influence energy balance over the longer term. Future well-controlled studies are required to further ascertain the potential mediators of appetite responses to exercise.

Model Simulation of Soybean (Glycine Max (L.) Merrill) Growth by Energy Balance Approach

<p>Intercepted solar radiation by leaf will influence energy balance in plant. The energy balance in leaf is a complex process, which results in biomass growth. Here, we modeled leaf energy balance to estimate dry matter growth in soybean. In the field, we measured intercepted radiation in canopy (1 meter above surface) with two treatments: soybean with 50% shading (N50%M0) and no-shading (N0%M0) twice a week. Then we sampled a biomass with destructive technique every week in each treatment. Our results showed that the intercepted radiation in no-shading treatment was higher (400 J/m<sup>2</sup>) than those in shading one (250 J/m<sup>2</sup>). The results were consistence with the high biomass growth at 12 weeks after planting, which observed in no-shading treatment. Then we validated our model by 1:1 plot test. Our finding revealed that no-shading treatment showed a good agreement with the observed biomass (closed to 1:1 plot), whereas the shading treatment tended to predict under estimate of biomass.</p>

The effect of mastication on food intake, satiety and body weight

As mastication is the major component of the oral processing of solid foods a better understanding of its influence on ingestion, digestion and metabolism may lead to new approaches to improve health. A growing number of studies provide evidence that mastication may influence energy balance through several routes: activation of histaminergic neurons, reducing eating rate, altered digestion kinetics, and changes in macronutrient availability. Indeed, accumulating evidence indicates that increasing the number of masticatory cycles before swallowing reduces food intake and increases satiety. However, while slowing eating rate has been shown to limit weight gain in children and adolescents it is not clear that slowing eating rate by increasing the number of masticatory cycles or slowing mastication rate is a viable method to aid weight management ([10], [15]). Further research is required to determine the influence of mastication on energy balance and how it could be manipulated to aid weight management. This narrative review will provide a brief overview of the effect of mastication on food intake, satiety and body weight.

Association between systemic leptin and neurotensin concentration in adult individuals with and without type 2 diabetes mellitus

Leptin is an adipokine which regulates appetite and energy balance through a mechanism partially mediated by neurotensin (NT) in central nervous system. Besides acting as a neurotransmitter, NT is expressed in human intestine where it promotes fat absorption and its circulating levels associate with obesity, type 2 diabetes mellitus (T2DM) and cardiovascular disease. Whether a relation exists between circulating leptin and NT levels has not been investigated yet. The aim of this study was to test the hypothesis of an association between plasma leptin and NT concentration in adults with or without T2DM. We recruited a population of 72 subjects (M/F: 39/33; age: 49.5±10.6years; BMI: 26.5±4.7kg/m2) including individuals with T2DM (n=32) referring to our Diabetes Outpatient Clinics, Sapienza University of Rome, and healthy controls. Study participants underwent metabolic characterization; plasma leptin was measured by MILLIPLEX, Luminex, and proneurotensin (proNT), a stable precursor of NT, by chemiluminometric sandwich immunoassay. Circulating median (25°-75°) leptin levels were 2.75 (1.27-4.93)ng/mL and did not differ between T2DM and non-diabetic subjects. Leptin concentration directly correlated with proNT (r=0.41; p=0.015); higher leptin levels were also associated with age, male gender, obesity, higher HOMA-IR, systolic blood pressure and C-reactive protein. Belonging to the highest pro-NT quartile correlated with greater leptin levels independent of age, gender and other confounders (r2=0.82, p=0.02). Circulating leptin is associated with higher proNT levels independent of diabetes, obesity and metabolic syndrome components; besides its effects on central leptin signaling, NT may influence energy balance by modulating circulating leptin concentration likely through a mechanism involving gut fat absorption.

Longitudinal designs to study neighbourhood effects on the development of obesity: a scoping review protocol

IntroductionThe prevalence of obesity has increased significantly in the last three decades and became an important public health concern. Evidence of weight status variability at the neighbourhood level has led...

Homeostatic and non-homeostatic appetite control along the spectrum of physical activity levels: An updated perspective.

The current obesogenic environment promotes physical inactivity and food consumption in excess of energy requirements, two important modifiable risk factors influencing energy balance. Habitual physical activity has been shown to impact not only energy expenditure, but also energy intake through mechanisms of appetite control. This review summarizes recent theory and evidence underpinning the role of physical activity in the homeostatic and non-homeostatic mechanisms controlling appetite. Energy intake along the spectrum of physical activity levels (inactive to highly active) appears to be J-shaped, with low levels of physical activity leading to dysregulated appetite and a mismatch between energy intake and expenditure. At higher levels, habitual physical activity influences homeostatic appetite control in a dual-process action by increasing the drive to eat through greater energy expenditure, but also by enhancing post-meal satiety, allowing energy intake to better match energy expenditure in response to hunger and satiety signals. There is clear presumptive evidence that physical activity energy expenditure can act as a drive (determinant) of energy intake. The influence of physical activity level on non-homeostatic appetite control is less clear, but low levels of physical activity may amplify hedonic states and behavioural traits favouring overconsumption indirectly through increased body fat. More evidence is required to understand the interaction between physical activity, appetite control and diet composition on passive overconsumption and energy balance. Furthermore, potential moderators of appetite control along the spectrum of physical activity, such as body composition, sex, and type, intensity and timing of physical activity, remain to be fully understood.

No metabolic effects of mustard allyl-isothiocyanate compared with placebo in men

Background: Induction of nonshivering thermogenesis can be used to influence energy balance to prevent or even treat obesity. The pungent component of mustard, allyl-isothiocyanate (AITC), activates the extreme cold receptor transient receptor potential channel, subfamily A, member 1 and may thus induce energy expenditure and metabolic changes.Objective: The objective of our study was to evaluate the potential of mustard AITC to induce thermogenesis (primary outcome) and alter body temperature, cold and hunger sensations, plasma metabolic parameters, and energy intake (secondary outcomes).Design: Energy expenditure in mice was measured after subcutaneous injection with vehicle, 1 mg norepinephrine/kg, or 5 mg AITC/kg. In our human crossover study, 11 healthy subjects were studied under temperature-controlled conditions after an overnight fast. After ingestion of 10 g of capsulated mustard or uncapsulated mustard or a capsulated placebo mixture, measurements of energy expenditure, substrate oxidation, core temperature, cold and hunger scores, and plasma parameters were repeated every 30 min during a 150-min period. Subjects were randomly selected for the placebo and capsulated mustard intervention; 9 of 11 subjects received the uncapsulated mustard as the final intervention because this could not be blinded. After the experiments, energy intake was measured with the universal eating monitor in a test meal.Results: In mice, AITC administration induced a 32% increase in energy expenditure compared with vehicle (17.5 ± 4.9 J · min−1 · mouse−1 compared with 12.5 ± 1.2 J · min−1 · mouse−1, P = 0.03). Of the 11 randomly selected participants, 1 was excluded because of intercurrent illness after the first visit and 1 withdrew after the second visit. Energy expenditure did not increase after ingestion of capsulated or uncapsulated mustard compared with placebo. No differences in substrate oxidation, core temperature, cold and hunger scores, or plasma parameters were found, nor was the energy intake at the end of the experiment different between the 3 conditions.Conclusion: The highest tolerable dose of mustard we were able to use did not elicit a relevant thermogenic response in humans. This trial was registered at www.controlled-trials.com as ISRCTN19147515.

A pre‐breeding immune challenge delays reproduction in the female dark‐eyed junco Junco hyemalis

Precise timing of life‐history transitions in predictably changing environments is hypothesized to aid in individual survival and reproductive success, by appropriately matching an animal's physiology and behavior with prevailing environmental conditions. Therefore, it is imperative for individuals to time energetically costly life‐history stages (i.e. reproduction) so they overlap with seasonal peaks in food abundance and quality. Female lifetime reproductive fitness is affected by several factors that influence energy balance, including arrival date, timing of egg production, and energetic condition. Therefore, any extra energetic costs during reproduction may negatively affect timing of egg production, and ultimately a female's fitness. For example, mounting an immunological response elicits a high energetic cost, and this transfer of resources towards cell and immune system maintenance could have direct negative effects on reproductive timing. In order to determine whether an immune challenge delays onset of breeding (i.e. egg production), we administered either a humoral immune challenge (keyhole limpet hemocyanin (KLH)) (treatment) or physiological saline (control) to free‐living female dark‐eyed juncos Junco hyemalis in the period immediately prior to egg‐laying (∼4 weeks). We found that KLH‐injected females artificially delayed clutch initiation when compared to control females. These data help to refine our understanding of how free‐living birds allocate resources between reproduction and self‐maintenance processes during the critical pre‐laying period of the annual cycle.

Lack of Lrp5 Signaling in Osteoblasts Sensitizes Male Mice to Diet-Induced Disturbances in Glucose Metabolism

Wnt signaling through the low-density lipoprotein-related receptor 5 (Lrp5) coreceptor regulates osteoblast maturation, matrix mineralization, and intermediary metabolism. In the mature osteoblast, signals downstream of Lrp5 are required for normal long-chain fatty acid β-oxidation. Mice rendered deficient for this coreceptor in osteoblasts and osteocytes accumulate body fat with elevated serum lipid levels but retain normal insulin sensitivity. In the present study, we challenged Lrp5-mutant mice with a high-fat diet (HFD) to determine whether they were more susceptible to diet-induced disturbances in glucose homeostasis. The HFD-fed Lrp5 mutant mice maintained a low bone mass phenotype with an increase in adipose tissue mass and hypertriglyceridemia and hypercholesterolemia. Examination of glucose metabolism revealed that Lrp5 deficiency in the osteoblast also resulted in hyperglycemia and hyperinsulinemia, with reductions in glucose tolerance, insulin sensitivity, and serum undercarboxylated osteocalcin. The results from in vivo genetic epistasis and in vitro studies suggest that this phenotype proceeds via the accumulation of diacylglycerol species and impaired insulin signaling in Lrp5-deficient osteoblasts. In turn, glucose uptake and osteocalcin production are diminished in mutant osteoblasts. Taken together, these data identify a link between Wnt-Lrp5 signaling and insulin signaling in the osteoblast that has the potential to influence energy balance and compound the detrimental effects of a HFD on whole-body metabolism.

Substituting whole grains for refined grains in a 6-wk randomized trial favorably affects energy-balance metrics in healthy men and postmenopausal women1–3

Background: The effect of whole grains on the regulation of energy balance remains controversial.Objective: We aimed to determine the effects of substituting whole grains for refined grains, independent of body weight changes, on energy-metabolism metrics and glycemic control.Design: The study was a randomized, controlled, parallel-arm controlled-feeding trial that was conducted in 81 men and postmenopausal women [49 men and 32 women; age range: 40–65 y; body mass index (in kg/m2): <35.0]. After a 2-wk run-in period, participants were randomly assigned to consume 1 of 2 weight-maintenance diets for 6 wk. Diets differed in whole-grain and fiber contents [mean ± SDs: whole grain–rich diet: 207 ± 39 g whole grains plus 40 ± 5 g dietary fiber/d; refined grain–based diet: 0 g whole grains plus 21 ± 3 g dietary fiber/d] but were otherwise similar. Energy metabolism and body-composition metrics, appetite, markers of glycemic control, and gut microbiota were measured at 2 and 8 wk.Results: By design, body weight was maintained in both groups. Plasma alkylresorcinols, which are biomarkers of whole-grain intake, increased in the whole grain–rich diet group (WG) but not in the refined grain–based diet group (RG) (P-diet-by-time interaction < 0.0001). Beta ± SE changes (ΔWG compared with ΔRG) in the resting metabolic rate (RMR) (43 ± 25 kcal/d; P = 0.04), stool weight (76 ± 12 g/d; P < 0.0001), and stool energy content (57 ± 17 kcal/d; P = 0.003), but not in stool energy density, were higher in the WG. When combined, the favorable energetic effects in the WG translated into a 92-kcal/d (95% CI: 28, 156-kcal/d) higher net daily energy loss compared with that of the RG (P = 0.005). Prospective consumption (P = 0.07) and glycemia after an oral-glucose-tolerance test (P = 0.10) trended toward being lower in the WG than in the RG. When nonadherent participants were excluded, between-group differences in stool energy content and glucose tolerance increased, and between-group differences in the RMR and prospective consumption were not statistically significant.Conclusion: These findings suggest positive effects of whole grains on the RMR and stool energy excretion that favorably influence energy balance and may help explain epidemiologic associations between whole-grain consumption and reduced body weight and adiposity. This trial was registered at clinicaltrials.gov as NCT01902394.

Feather corticosterone during non-breeding correlates with multiple measures of physiology during subsequent breeding in a migratory seabird

Carry-over effects in migratory birds are likely mediated by physiological processes that are activated in response to environmental variation. Such processes affect body condition and/or reproductive success, and can include corticosterone (CORT) because this hormone responds to environmental stressors and influences energy balance. Few studies have considered how CORT levels during non-breeding relate to a broader physiological profile during subsequent breeding, and fewer still have considered measures other than body condition. To explore CORT's potential role in carry-over effects, we investigated the relationship between CORT and foraging ecology of northern gannets (Morus bassanus) during the non-breeding period, and tested for associations between these factors and variation in a suite of physiological and biochemical metrics during subsequent breeding. Northern gannets are the largest seabird top predator in the North Atlantic and were among the hardest hit by the Deepwater Horizon oil blowout in the Gulf of Mexico in 2010. We used light-level geolocators to confirm winter origins of individuals in our study. No interrelationships were found among levels of CORT from feathers grown during non-breeding (CORTf) and variation in foraging ecology, measured by stable isotopes of carbon (δ13C) and nitrogen (δ15N) from the same feathers. CORTf was correlated negatively with hematocrit and positively with triglyceride measured during subsequent incubation, and explained more variation in these variables than did body mass during incubation. These findings provide support for the hypothesis that energy management, measured using CORTf, during non-breeding carries over to influence physiological measures other than body condition. Gannets that previously wintered within the Gulf of Mexico in the years following the Deepwater Horizon oil blowout had higher levels of CORTf compared to birds that wintered along the Atlantic coast, suggesting an increased energetic cost associated with visiting the Gulf of Mexico. Our results indicate that CORT during non-breeding is associated with a broader physiological profile during subsequent breeding than previously reported in birds.

Estradiol Regulation of Brown Adipose Tissue Thermogenesis.

Physiologically, estrogens carry out a myriad of functions, the most essential being the regulation of the reproductive axis. Currently, it is also dogmatic that estrogens play an important role modulating energy balance and metabolism. In this sense, it is well known that low estrogens levels, occurring due to ovarian insufficiency, in conditions such as menopause or ovariectomy (OVX), are associated with increased food intake and decreased energy expenditure, leading to weight gain and obesity at long term. Concerning energy expenditure, the main effect of estradiol (E2) is on brown adipose tissue (BAT) thermogenesis. Thus, acting through a peripheral or a central action, E2 activates brown fat activity and increases body temperature, which is negatively associated with body weight. Centrally, the hypothalamic AMP-activated protein kinase (AMPK) mediates the E2 action on BAT thermogenesis. In this chapter, we will summarize E2 regulation of BAT thermogenesis and how this can influence energy balance and metabolism in general.

12 Month Behavioral Weight Loss Intervention With Varying Doses Of Physical Activity

Secondary data analysis from intervention studies has suggested that ≥250 min/wk of moderate-to-vigorous physical activity (MVPA) is associated with improved long-term weight loss within the context of a behavioral weight loss intervention; however, randomized clinical trials are needed to support these findings and to determine the feasibility of adults who are overweight or obese to achieve this recommended level of MVPA. PURPOSE: This study examined the ability of a behavioral intervention to achieve MVPA levels recommended for public health (150 min/wk) or weight control (250 min/wk). This study also examine whether weight loss, within the context of a comprehensive weight management program, varied by these prescribed levels of MVPA in adults who were overweight or obese across 12 months. METHODS: Data were examined from sedentary adults (N=230; BMI: 32.1±3.8 kg/m2; age=46.2±7.7 years) enrolled in a behavioral program and randomized to a reduced calorie diet (DIET, N=71), diet plus a moderate dose of MVPA (MOD-EX, N=82), or diet plus a high dose of MVPA (HIGH-EX, N=77). All groups received weekly intervention sessions in months 1–6 followed by 2 group and 2 telephone contacts per month in months 7–12, and were prescribed a diet to reduce energy intake (1200–1800 kcal/day). MOD-EX was prescribed unsupervised MVPA that progressed to 150 min/wk, whereas HIGH-EX was progressed to 250 min/wk. MVPA and weight were assessed at 0, 6, and 12 months. RESULTS: MVPA at 0, 6, and 12 months was 52.3±60.5, 82.3±93.4, and 85.7±110.6 min/wk in DIET; 53.8±78.7, 173.1±112.1, and 185.8±134.5 min/wk in MOD-EX, and 73.2±92.2, 254.1±127.8, and 236.0±154.9 min/wk in HIGH-EX (Group X Time p-value <0.001). Weight significantly decrease in all groups at 6 months (DIET: −9.2±5.8 kg, MOD-EX: −10.2±6.4 kg, HIGH-EX: −9.5±5.4 kg; p<0.001) and 12 months (DIET: −9.7±7.5 kg, MOD-EX: −11.0±8.2 kg, HIGH-EX: −9.7±7.1 kg; p<0.001), with no significant difference between groups. CONCLUSIONS: The MOD-EX and HIGH-EX interventions were successful at achieving the prescribed dose of MVPA in adults with obesity. The lack of additional weight loss with participation in higher amounts of MVPA may suggest that there is a compensatory response in factors influencing energy balance that warrant further investigation. Supported by: NIH (R01 HL103646)