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While there is an increasing prevalence of dieting in the overall population, weight loss (WL) practices could be a risk factor for weight gain (WG) in normal-weight (NW) individuals. The aim of the present work was to systematically review all the studies implicating diet restriction and body weight (BW) evolution in NW people. The literature search was registered in PROSPERO (CRD42021281442) and was performed in three databases from April 2021 to June 2022 for articles involving healthy NW adults. From a total of 1487 records initially identified, eighteen were selected in the systematic review. Of the eight dieting interventional studies, only one found a higher BW after weight recovery, but 75 % of them highlighted metabolic adaptations in response to WL favouring weight regain and persisting during/after BW recovery. Eight of the ten observational studies showed a relationship between dieting and major later WG, while the meta-analysis of observational studies results indicated that ‘dieters’ have a higher BW than ‘non-dieters’. However, considering the high methodological heterogeneity and the publication bias of the studies, this result should be taken with caution. Moreover, the term ‘diet’ was poorly described, and we observed a large heterogeneity of the methods used to assess dieting status. Present results suggest that dieting could be a major risk factor for WG in the long term in NW individuals. There is, however, a real need for prospective randomised controlled studies, specifically assessing the relationship between WL induced by diet and subsequent weight in this population.

Anorexia nervosa is an eating disorder characterized by intense fear of gaining weight and a distorted body image which usually leads to low caloric intake and hyperactivity. The underlying mechanism and pathogenesis of anorexia nervosa is still poorly understood. In order to learn more about the underlying pathophysiology of anorexia nervosa and to find further possible treatment options, several animal models mimicking anorexia nervosa have been developed. The aim of this review is to systematically search different databases and provide an overview of existing animal models and to discuss the current knowledge gained from animal models of anorexia nervosa. For the systematic data search, the Pubmed—Medline database, Embase database, and Web of Science database were searched. After removal of duplicates and the systematic process of selection, 108 original research papers were included in this systematic review. One hundred and six studies were performed with rodents and 2 on monkeys. Eighteen different animal models for anorexia nervosa were used in these studies. Parameters assessed in many studies were body weight, food intake, physical activity, cessation of the estrous cycle in female animals, behavioral changes, metabolic and hormonal alterations. The most commonly used animal model (75 of the studies) is the activity-based anorexia model in which typically young rodents are exposed to time-reduced access to food (a certain number of hours a day) with unrestricted access to a running wheel. Of the genetic animal models, one that is of particular interest is the anx/anx mice model. Animal models have so far contributed many findings to the understanding of mechanisms of hunger and satiety, physical activity and cognition in an underweight state and other mechanisms relevant for anorexia nervosa in humans.

RationalCaloric restriction increases the risk of relapse in abstinent drug users. Hormones involved in the regulation of energy balance and food intake, such as leptin and ghrelin, are implicated in drug-related behaviors.ObjectivesWe investigated the role of leptin and ghrelin in the augmentation of heroin seeking induced by chronic food restriction.MethodsRats self-administered heroin (0.1 mg/kg/infusion) for 10 days followed by 14 days of drug withdrawal. During withdrawal, rats were food restricted to 90% of their original body weight or were given free access to food. In experiment 1, we measured the plasma concentrations of leptin and ghrelin following heroin self-administration and withdrawal. In experiment 2, leptin was administered centrally (2.0 or 4.0 μg; i.c.v.) prior to a heroin-seeking test under extinction conditions. High density of both leptin and ghrelin receptors was previously identified in the ventral tegmental area (VTA), suggesting a direct effect on reward and motivation. Hence, we administered leptin (experiment 3; 0.125 or 0.250 μg/side), or ghrelin receptor antagonist JMV 2959 (experiment 4; 2.0 or 10.0 μg/side) directly into the VTA prior to the heroin-seeking test.ResultsChronic food restriction significantly decreased plasma levels of leptin and elevated plasma levels of ghrelin. Central administration of leptin had no statistically significant effect on heroin seeking. Intra-VTA administration of either leptin or JMV 2959 dose-dependently and selectively decreased heroin seeking in the food-restricted rats.ConclusionsLeptin and ghrelin transmission in the VTA can modulate the augmentation of heroin seeking induced by chronic food restriction.

Mammals have evolved sex-specific adaptations to reduce energy usage in times of food scarcity. These adaptations are well described for peripheral tissue, though much less is known about how the energy-expensive brain adapts to food restriction, and how such adaptations differ across the sexes. Here, we examined how food restriction impacts energy usage and function in the primary visual cortex (V1) of adult male and female mice. Molecular analysis and RNA sequencing in V1 revealed that in males, but not in females, food restriction significantly modulated canonical, energy-regulating pathways, including pathways associated waith AMP-activated protein kinase, peroxisome proliferator-activated receptor alpha, mammalian target of rapamycin, and oxidative phosphorylation. Moreover, we found that in contrast to males, food restriction in females did not significantly affect V1 ATP usage or visual coding precision (assessed by orientation selectivity). Decreased serum leptin is known to be necessary for triggering energy-saving changes in V1 during food restriction. Consistent with this, we found significantly decreased serum leptin in food-restricted males but no significant change in food-restricted females. Collectively, our findings demonstrate that cortical function and energy usage in female mice are more resilient to food restriction than in males. The neocortex, therefore, contributes to sex-specific, energy-saving adaptations in response to food restriction.

Further examination of the molecular regulators of long-term calorie restriction (CR), reported to have an anxiolytic effect, may highlight novel therapeutic targets for anxiety disorders. Here, adult male Hooded Wistar rats were exposed to a 25% CR whilst anxiety-like behaviour was assessed at 6-, 12-, and 18-months of age via the elevated plus maze, open field, and acoustic startle tests. Next-generation sequencing was then used to measure transcriptome-wide gene expression in the hypothalamus, amygdala, pituitary, and adrenal glands. Results showed an anxiolytic behavioural profile across early, middle, and late adulthood by CR, with the strongest effects noted at 6-months. Transcriptomic analysis by seven attribute weighting algorithms, including Info Gain Ratio, Rule, Chi Squared, Gini Index, Uncertainty, Relief, and Info Gain, led to the development of a signature of long-term CR, independent of region. Complement C1q A chain (C1qa), an extracellular protein, expression was significantly decreased by CR in most regions examined. Furthermore, text mining highlighted the positive involvement of C1qa in anxiety, depression, neurodegeneration, stress, and ageing, collectively identifying a suitable biomarker candidate for CR. Overall, the current study identified anxiety-related phenotypic changes and a novel transcriptome signature of long-term CR, indicating potential therapeutic targets for anxiety, depression, and neurodegeneration.

Objective: This study aims to compare food neophobia (FN) in groups of neurodivergent and neurotypical children with and without food restrictions. Methods: This cross-sectional study used a convenience sample of participants from all Brazilian Federative Units through the snowball method. Participants were separated into four groups for comparison: neurodivergent children without dietary restrictions; neurodivergent children with dietary restrictions; neurotypical children with dietary restrictions; and neurotypical children without dietary restrictions. The Brazilian Children’s Food Neophobia Questionnaire (BCFNeo) was selected and administered to caregivers of Brazilian children between four and eleven years old. The categorization of FN scores followed a previously validated protocol. Results: The sample was composed of the caregivers of 2387 children. Considering the sample as a whole (neurodiversity), the prevalence of high FN was 44.2%. Boys are significantly more neophobic (p < 0.001) than girls. FN does not decrease with age. Older children (eight to eleven years) are equally neophobic as younger children (four to seven years). The prevalence of high FN was greater in neurodivergent children (without dietary restrictions—62.8% and with dietary restrictions—62.4%) than in neurotypical children (with dietary restrictions—29.4% and without dietary restrictions—33.4%). Conclusions: FN is more prevalent in boys and neurodivergent children, regardless of food restrictions and age. More longitudinal and experimental studies are necessary to evaluate the factors influencing FN in these groups and to develop intervention strategies.

Female Fischer 344 rats were divided into control (access to food ad libitum) and weight cycling (60% diet restriction followed by ad libitum refeeding) groups. The weight cycles consisted of two weeks dietary restriction and three weeks refeeding for three cycles. Fecal microbiome samples were collected following the initial dietary restriction, the initial refeeding, and the final refeeding periods (and corresponding times in control rats). We observed significant differences in alpha diversity between fecal microbiomes following the initial dietary restriction and the final refeeding period. We additionally observed a significant recovery of alpha diversity following the first refeeding period that we did not observe following the third refeeding in the weight cycling group. Differences in relative abundances of taxa included a higher relative abundance of Bacillota (synonym Firmicutes) in the weight cycling group. Species richness of the weight cycling fecal microbiomes significantly decreased across the study period. Inguinal fat tissue was significantly lower in the weight cycling than ad libitum group, yet heart weight and postprandial HOMA‐IR were significantly higher. Together, these results suggest that repeated weight cycling from repeated periods of dietary restriction has adverse effects on host condition and microbial diversity, potentially leading to long‐term negative health outcomes.

Growth hormone (GH) is secreted by somatotropic cells of the anterior pituitary gland. The classical effects of GH comprise the stimulation of cell proliferation, tissue and body growth, lipolysis, and insulin resistance. The GH receptor (GHR) is expressed in numerous brain regions. Notably, a growing body of evidence indicates that GH-induced GHR signaling in specific neuronal populations regulates multiple physiological functions, including energy balance, glucose homeostasis, stress response, behavior, and several neurological/cognitive aspects. The importance of central GHR signaling is particularly evident when the organism is under metabolic stress, such as pregnancy, chronic food deprivation, hypoglycemia, and prolonged exercise. These particular situations are associated with elevated GH secretion. Thus, central GH action represents an internal signal that coordinates metabolic, neurological, neuroendocrine, and behavioral adaptations that are evolutionarily advantageous to increase the chances of survival. This review summarizes and discusses recent findings indicating that the brain is an important target of GH, and GHR signaling in different neuronal populations regulates essential physiological functions.

RationaleDepressed individuals demonstrate debilitating symptoms, including depressed mood, anhedonia, and effort-related deficits. Effort-related decision-making can be measured through providing subjects with a choice between high effort/reward and low effort/reward options, which is a dopamine (DA)–dependent behavior. While previous research has shown sex differences in depression rates, this has not been examined within operant-based effort-related decision-making tasks nor has DA been shown to underlie this behavior in female rats.ObjectivesThe current study investigated sex differences in an effort-related decision-making task prior to and following administration of the DA D2 receptor antagonist haloperidol (HAL).MethodsAdult rats were food restricted or fed freely and trained in an effort-related progressive ratio choice task. After stable responding, HAL was administered acutely (0.05–0.2 mg/kg) prior to testing.ResultsResults indicate a significant effect of sex on training variables, with males having a greater number of lever presses, higher ratios, and longer active lever times. Pretreatment with HAL significantly reduced the same measures in both sexes for the high-valued reward, while increasing chow consumption in the food restricted males. Food restricted rats showed a greater number of total lever presses and achieved higher ratios; however, the effect in male food restricted rats was greatest.ConclusionsThese data suggest that, although there are sex differences in training, HAL decreases behavior across sexes, demonstrating that the D2 mechanism is similar in both sexes. These findings provide a better understanding of motivational dysfunction in both sexes and potential treatment targets for depression.

The appropriate allocation of nutrients between the mother and the fetus during mammalian pregnancy primarily depends on a healthy placenta. Fetal growth restriction (FGR) is frequently associated with inadequate maternal nutrition supply and impaired placental function. The precise mechanisms linking maternal nutrient deficiency to compromised fetal and placental development remain largely elusive. In this study, we conducted an in‐depth analysis by integrating single‐cell/single‐nucleus RNA sequencing data from human and mouse placentas along with transcriptomic data from FGR placenta, identifying the GAB1 (GRB2‐associated binding protein 1) gene as a potential mediator of dysregulated maternal–fetal exchange, thereby affecting fetal growth. Using a mouse model, we demonstrated that food restriction significantly impeded fetal growth and disrupted placental labyrinth development. Through an in vitro trophoblast differentiation model, we revealed that nutritional restriction impaired GAB1 stability via LC3‐interacting region (LIR) motif‐mediated selective autophagic degradation, thereby hindering GAB1‐MAPK signalling‐enhanced trophoblast syncytialisation. These findings elucidate the mechanisms by which placental GAB1 links maternal nutrition status with fetal growth and suggest potential therapeutic strategies for managing pregnancy complications such as FGR. Maternal nutrient restriction disrupts placental homeostasis via GAB1 dysregulation—involving both transcriptional downregulation and autophagy‐dependent protein degradation. These molecular alterations inhibit MAPK signalling‐mediated trophoblast fusion, leading to structural and functional deficits in the maternal–fetal exchange interface.