Reviewing the effects of food provisioning on wildlife immunity

While urban expansion increasingly encroaches on natural habitats, many wildlife species capitalize on anthropogenic food resources, which have the potential to both positively and negatively influence their responses to infection. Here we examine how food availability and key nutrients have been reported to shape innate and adaptive immunity in wildlife by drawing from field-based studies, as well as captive and food restriction studies with wildlife species. Examples of food provisioning and key nutrients enhancing immune function were seen across the three study type distinctions, as were cases of trace metals and pharmaceuticals impairing the immunity of wildlife species. More generally, food provisioning in field studies tended to increase innate and adaptive responses to certain immune challenges, whereas patterns were less clear in captive studies. Mild food restriction often enhanced, whereas severe food restriction frequently impaired immunity. However, to enable stronger conclusions we stress a need for further research, especially field studies, and highlight the importance of integrating nutritional manipulation, immune challenge, and functional outcomes. Despite current gaps in research on this topic, modern high throughput molecular approaches are increasingly feasible for wildlife studies and offer great opportunities to better understand human influences on wildlife health.This article is part of the theme issue 'Anthropogenic resource subsidies and host-parasite dynamics in wildlife'

A central role for C1q/TNF-related protein 13 (CTRP13) in modulating food intake and body weight.

C1q/TNF-related protein 13 (CTRP13), a hormone secreted by adipose tissue (adipokines), helps regulate glucose metabolism in peripheral tissues. We previously reported that CTRP13 expression is increased in obese and hyperphagic leptin-deficient mice, suggesting that it may modulate food intake and body weight. CTRP13 is also expressed in the brain, although its role in modulating whole-body energy balance remains unknown. Here, we show that CTRP13 is a novel anorexigenic factor in the mouse brain. Quantitative PCR demonstrated that food restriction downregulates Ctrp13 expression in mouse hypothalamus, while high-fat feeding upregulates expression. Central administration of recombinant CTRP13 suppressed food intake and reduced body weight in mice. Further, CTRP13 and the orexigenic neuropeptide agouti-related protein (AgRP) reciprocally regulate each other's expression in the hypothalamus: central delivery of CTRP13 suppressed Agrp expression, while delivery of AgRP increased Ctrp13 expression. Food restriction alone reduced Ctrp13 and increased orexigenic neuropeptide gene (Npy and Agrp) expression in the hypothalamus; in contrast, when food restriction was coupled to enhanced physical activity in an activity-based anorexia (ABA) mouse model, hypothalamic expression of both Ctrp13 and Agrp were upregulated. Taken together, these results suggest that CTRP13 and AgRP form a hypothalamic feedback loop to modulate food intake and that this neural circuit may be disrupted in an anorexic-like condition

Food Restriction and Atherosclerotic Plaque Stabilization

Food restriction is a promising therapy for many age-associated pathologies as it stimulates the health-supportive mechanism autophagy. Because atherosclerosis is an inflammatory, age-related disease, dietary modification can be an important strategy in preventing atherosclerotic plaque development. A cholesterol-supplemented diet, used to induce plaque formation in rabbits, induces a pronounced hypercholesterolemia, which can be reversed after 4 weeks of normal diet. However, food restriction induces a further increase in circulating LDL cholesterol. These elevated cholesterol levels are associated with the induction of autophagy. Although neither a short-term normal diet nor food restriction alters plaque size, rabbits fed a normal diet show signs of increased plaque stability such as elevated collagen content and decreased expression of vascular cell adhesion molecule (VCAM)-1. Surprisingly, these favorable effects are not present after 4 weeks of food restriction. On the contrary, atherosclerotic plaques of food-restricted rabbits displayed enhanced apoptosis, a process known to further undermine plaque stability. In conclusion, severe short-term food restriction in rabbits prevents stabilization of atherosclerotic plaques as observed after regular cholesterol withdrawal via a normal diet

Insula Activation and What it May Tell Us About Food Motivation in Anorexia Nervosa: A Systematic Literature Review

• Anorexia nervosa (AN) is a severe psychiatric disorder characterized by recurrent refusal of caloric intake, resulting in emaciation. • Identifying whether neural networks that process food-related stimuli are affected in AN is important for understanding the biological basis of this illness, particularly severe food restriction. • The insular cortex is a key area that has been implicated; this brain region is associated with interoceptive awareness and gustation

Recent advances in understanding anorexia nervosa.

Anorexia nervosa is a complex psychiatric illness associated with food restriction and high mortality. Recent brain research in adolescents and adults with anorexia nervosa has used larger sample sizes compared with earlier studies and tasks that test specific brain circuits. Those studies have produced more robust results and advanced our knowledge of underlying biological mechanisms that may contribute to the development and maintenance of anorexia nervosa. It is now recognized that malnutrition and dehydration lead to dynamic changes in brain structure across the brain, which normalize with weight restoration. Some structural alterations could be trait factors but require replication. Functional brain imaging and behavioral studies have implicated learning-related brain circuits that may contribute to food restriction in anorexia nervosa. Most notably, those circuits involve striatal, insular, and frontal cortical regions that drive learning from reward and punishment, as well as habit learning. Disturbances in those circuits may lead to a vicious cycle that hampers recovery. Other studies have started to explore the neurobiology of interoception or social interaction and whether the connectivity between brain regions is altered in anorexia nervosa. All together, these studies build upon earlier research that indicated neurotransmitter abnormalities in anorexia nervosa and help us develop models of a distinct neurobiology that underlies anorexia nervosa

Differential acylated ghrelin, peptide YY3-36, appetite, and food intake responses to equivalent energy deficits created by exercise and food restriction

Context: Acute energy deficits imposed by food restriction increase appetite and energy intake; however, these outcomes remain unchanged when energy deficits are imposed by exercise.Objective: Our objective was to determine the potential role of acylated ghrelin and peptide YY3-36 (PYY3-36) in mediating appetite and energy intake responses to identical energy deficits imposed by food restriction and exercise.Design: Twelve healthy males completed three 9-h trials (exercise deficit, food deficit, and control) in a randomized counterbalanced design. Participants ran for 90 min (70% of VO2 max) at the beginning of the exercise deficit trial and then rested for 7.5 h. Participants remained sedentary throughout the food deficit and control trials. Test meals were consumed by participants at 2 and 4.75 h in all trials. The amount provided in the food deficit trial was restricted so that an energy deficit (equivalent to that imposed by exercise) was induced relative to control. Participants were permitted access to a buffet meal at 8 h.Results: The energy deficits imposed by food restriction (4820 +/- 151 kJ) and exercise (4715 +/- 113 kJ) were similar. Appetite and ad libitum energy intake responded in a compensatory fashion to food restriction yet were not influenced by exercise. Plasma acylated ghrelin concentrations increased, whereas PYY3-36 decreased, in response to food restriction (two-way ANOVA, trial x time interaction, P < 0.001 for each). Exercise did not induce such compensatory responses.Conclusions: These findings suggest a mediating role of acylated ghrelin and PYY3-36 in determining divergent feeding responses to energy deficits imposed by food restriction and exercise. (J Clin Endocrinol Metab 96: 1114-1121, 2011

Colon tumor promotion, is it a selection process? Effects of cholate, phytate, and food restriction in rats on proliferation and apoptosis in normal and aberrant crypts

Promotion would suppose the selection of initiated cells. We tested the selection of aberrant crypt cells by cholic acid, a colon cancer promoter, and the effect of protectors, phytate and food restriction. After an azoxymethane injection, rats were allocated to a control diet, or to supplements of cholic acid, sodium phytate, or to a 50% food restriction. The proliferation and apoptosis of 1200 crypts were assessed, after immuno-staining for BrdU. Cholic acid increased the proliferation of aberrant crypts but not of normal crypts. Phytate and food restriction decreased the proliferation of normal crypts, but not of aberrant crypts. Apoptosis was not affected by diets. Results support the hypothesis that cholic acid can select initiated cells in the colon

Rhinoceros auklet developmental responses to moderate food restriction

Thesis (M.S.) University of Alaska Fairbanks, 2007Seabird nestlings are vulnerable to food restriction because their parents may not buffer them from prey shortages. I conducted a captive study to explore how rhinoceros auklet chicks (Cerorhinca monocerata) may cope with food restriction and avoid long-term fitness consequences. I predicted auklet nestlings would be adapted to moderate levels of food-stress, and investigated how morphological allocation, glucocorticoid stress response, and fledging behavior change under conditions of a 50% calorie restriction. I also investigated effects of growth and food restriction on carbon and nitrogen stable isotope ratios ([delta]¹³C and [delta]¹⁵N) in auklet tissues. I found that food-restricted auklets allocated resources heavily toward skeletal growth, most notably toward wingchord growth. Restricted auklets exhibited a muted adrenocortical response, increasing glucocorticoid levels only slightly in response to food restriction. Fledging decision was not affected by restriction, with restricted and well-fed chicks fledging at approximately the same age. Both growth and food restriction caused decreases in [delta]¹⁵N of auklet red blood cells (RBCs), but caused no change in [delta]¹³C. Sampling of free-living auklets revealed that natural levels of variability were low for RBC isotope ratios, indicating that the effects of growth and restriction detected in the captive study are of biological significance.1. Rhinoceros auklet development responses to food limitation : potential coping mechanisms and post-fledging consequences -- 2. Disentagling effects of age and nutritional status on seabird stable isotope ratios -- General conclusion

Editorial: Why should we read Dalit literature?

<p>(A) BDNF and (B) NCAM1 expression in the VTA of mice exposed to ABA conditions. Insets indicate mean BDNF and NCAM1 expression during restriction for the independent measure depicted. Results expressed as mean log2(RQ) ± S.E.M. p<0.05. STV, starved mice exposed to food restriction and house without a wheel; RUN, mice exposed to wheel running; ABA, mice exposed to ABA conditions; W, wheel; FR, food restriction.</p

Food restriction enhances visual cortex plasticity in adulthood

Neural circuits display a heightened sensitivity to external stimuli during well-established windows in early postnatal life. After the end of these critical periods, brain plasticity dramatically wanes. The visual system is one of the paradigmatic models for studying experience-dependent plasticity. Here we show that food restriction can be used as a strategy to restore plasticity in the adult visual cortex of rats. A short period of food restriction in adulthood is able both to reinstate ocular dominance plasticity and promote recovery from amblyopia. These effects are accompanied by a reduction of intracortical inhibition without modulation of brain-derived neurotrophic factor expression or extracellular matrix structure. Our results suggest that food restriction could be investigated as a potential way of modulating plasticity