Tremendous progress has been made in the field of ferroptosis since this regulated cell death process was first named in 2012. Ferroptosis is initiated upon redox imbalance and driven by excessive phospholipid peroxidation. Levels of multiple intracellular nutrients (iron, selenium, vitamin E and coenzyme Q10) are intimately related to the cellular antioxidant system and participate in the regulation of ferroptosis. Dietary intake of monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA) regulates ferroptosis by directly modifying the fatty acid composition in cell membranes. In addition, amino acids and glucose (energy stress) manipulate the ferroptosis pathway through the nutrient-sensitive kinases mechanistic target of rapamycin complex 1 (mTORC1) and AMP-activated protein kinase (AMPK). Understanding the molecular interaction between nutrient signals and ferroptosis sensors might help in the identification of the roles of ferroptosis in normal physiology and in the development of novel pharmacological targets for the treatment of ferroptosis-related diseases.

The development and maintenance of body composition and functions require an adequate protein intake with a continuous supply of amino acids (AA) to tissues. Body pool and AA cellular concentrations are tightly controlled and maintained through AA supply (dietary intake, recycled from proteolysis and de novo synthesis), AA disposal (protein synthesis and other AA-derived molecules) and AA losses (deamination and oxidation). Different molecular regulatory pathways are involved in the control of AA sufficiency including the mechanistic target of rapamycin complex 1, the general control non-derepressible 2/activating transcription factor 4 system or the fibroblast growth factor 21. There is a tight control of protein intake, and human subjects and animals appear capable of detecting and adapting food and protein intake and metabolism in face of foods or diets with different protein contents. A severely protein deficient diet induces lean body mass losses and ingestion of sufficient dietary energy and protein is a prerequisite for body protein synthesis and maintenance of muscle, bone and other lean tissues and functions. Maintaining adequate protein intake with age may help preserve muscle mass and strength but there is an ongoing debate as to the optimal protein intake in older adults. The protein synthesis response to protein intake can also be enhanced by prior completion of resistance exercise but this effect could be somewhat reduced in older compared to young individuals and gain in muscle mass and function due to exercise require regular training over an extended period.

Sensing of nutrients by chemosensory cells in the gastrointestinal tract plays a key role in transmitting food-related signals, linking information about the composition of ingested foods to digestive processes. In recent years, a number of G protein-coupled receptors (GPCR) responsive to a range of nutrients have been identified. Many are localised to intestinal enteroendocrine (chemosensory) cells, promoting hormonal and neuronal signalling locally, centrally and to the periphery. The field of gut sensory systems is relatively new and still evolving. Despite huge interest in these nutrient-sensing GPCR, both as sensors for nutritional status and targets for preventing the development of metabolic diseases, major challenges remain to be resolved. However, the gut expressed sweet taste receptor, resident in L-enteroendocrine cells and responsive to dietary sweetener additives, has already been successfully explored and utilised as a therapeutic target, treating weaning-related disorders in young animals. In addition to sensing nutrients, many GPCR are targets for drugs used in clinical practice. As such these receptors, in particular those expressed in L-cells, are currently being assessed as potential new pathways for treating diabetes and obesity. Furthermore, growing recognition of gut chemosensing of microbial-produced SCFA acids has led further attention to the association between nutrition and development of chronic disorders focusing on the relationship between nutrients, gut microbiota and health. The central importance of gut nutrient sensing in the control of gastrointestinal physiology, health promotion and gut–brain communication offers promise that further therapeutic successes and nutritional recommendations will arise from research in this area.

The anatomical structure and function of beaks, bills and tongue together with the mechanics of deglutition in birds have contributed to the development of a taste system denuded of macrostructures visible to the human naked eye. Studies in chickens and other birds have revealed that the avian taste system consists of taste buds not clustered in papillae and located mainly (60 %) in the upper palate hidden in the crevasses of the salivary ducts. That explains the long delay in the understanding of the avian taste system. However, recent studies reported 767 taste buds in the oral cavity of the chicken. Chickens appear to have an acute sense of taste allowing for the discrimination of dietary amino acids, fatty acids, sugars, quinine, Ca and salt among others. However, chickens and other birds have small repertoires of bitter taste receptors (T2R) and are missing the T1R2 (related to sweet taste in mammals). Thus, T1R2-independent mechanisms of glucose sensing might be particularly relevant in chickens. The chicken umami receptor (T1R1/T1R3) responds to amino acids such as alanine and serine (known to stimulate the umami receptor in rodents and fish). Recently, the avian nutrient chemosensory system has been found in the gastrointestinal tract and hypothalamus related to the enteroendocrine system which mediates the gut–brain dialogue relevant to the control of feed intake. Overall, the understanding of the avian taste system provides novel and robust tools to improve avian nutrition.

Mounting evidence showed that bitter-tasting compounds modulate eating behaviour through bitter taste receptors in the gastrointestinal tract. This study aimed at evaluating the influence of microencapsulated bitter compounds on human appetite and energy intakes. A microencapsulated bitter ingredient (EBI) with a core of bitter Gentiana lutea root extract and a coating of ethylcellulose–stearate was developed and included in a vanilla microencapsulated bitter ingredient-enriched pudding (EBIP). The coating masked bitterness in the mouth, allowing the release of bitter secoiridoids in the gastrointestinal tract. A cross-over randomised study was performed: twenty healthy subjects consumed at breakfast EBIP (providing 100 mg of secoiridoids) or the control pudding (CP) on two different occasions. Blood samples, glycaemia and appetite ratings were collected at baseline and 30, 60, 120 and 180 min after breakfast. Gastrointestinal peptides, endocannabinoids (EC) and N-acylethanolamines (NAE) were measured in plasma samples. Energy intakes were measured at an ad libitum lunch 3 h after breakfast and over the rest of the day (post lunch) through food diaries. No significant difference in postprandial plasma responses of gastrointestinal hormones, glucose, EC and NAE and of appetite between EBIP and CP was found. However, a trend for a higher response of glucagon-like peptide-1 after EBIP than after CP was observed. EBIP determined a significant 30 % lower energy intake over the post-lunch period compared with CP. These findings were consistent with the tailored release of bitter-tasting compounds from EBIP along the gastrointestinal tract. This study demonstrated that microencapsulated bitter secoiridoids were effective in reducing daily energy intake in humans.

In this study, we chose a carnivorous fish, turbot (Scophthalmus maximus L.), to examine its nutrient-sensing and metabolic responses after ingestion of diets with fishmeal (FM), or 45 % of FM replaced by soyabean meal (34·6 % dry diet) balanced with or without essential amino acids (EAA) to match the amino acid profile of FM diet for 30 d. After a 1-month feeding trial, fish growth, feed efficiency and nutrient retention were markedly reduced by soyabean meal-incorporated (SMI) diets. Compared with the FM diet, SMI led to a reduction of postprandial influx of free amino acids, hypoactivated target of rapamycin signalling and a hyperactivated amino acid response pathway after refeeding, a status associated with reduced protein synthesis, impaired postprandial glycolysis and lipogenesis. These differential effects were not ameliorated by matching an EAA profile of soyabean meal to that of the FM diet through dietary amino acid supplementation. Therefore, this study demonstrated that the FM diet and SMI diets led to distinct nutrient-sensing responses, which in turn modulated metabolism and determined the utilisation efficiency of diets. Our results provide a new molecular explanation for the role of nutrient sensing in the inferior performance of aquafeeds in which FM is replaced by soyabean meal.

The mammalian target of rapamycin complex 1 (mTORC1) pathway is known to couple different environmental cues to the regulation of several energy-demanding functions within the cell, spanning from protein translation to mitochondrial activity. As a result, at the organism level, mTORC1 activity affects energy balance and general metabolic homoeostasis by modulating both the activity of neuronal populations that play key roles in the control of food intake and body weight, as well as by determining storage and use of fuel substrates in peripheral tissues. This review focuses on recent advances made in understanding the role of the mTORC1 pathway in the regulation of energy balance. More particularly, it aims at providing an overview of the status of knowledge regarding the mechanisms underlying the ability of certain amino acids, glucose and fatty acids, to affect mTORC1 activity and in turn illustrates how the mTORC1 pathway couples nutrient sensing to the hypothalamic regulation of the organisms’ energy homoeostasis and to the control of intracellular metabolic processes, such as glucose uptake, protein and lipid biosynthesis. The evidence reviewed pinpoints the mTORC1 pathway as an integrator of the actions of nutrients on metabolic health and provides insight into the relevance of this intracellular pathway as a potential target for the therapy of metabolic diseases such as obesity and type-2 diabetes.

There is considerable disagreement regarding what constitutes a healthy diet. Ever since the influential work of Cannon and Richter, it was debated whether the ‘wisdom of the body’ will automatically direct us to the foods we need for healthy lives or whether we must carefully learn to eat the right foods, particularly in an environment of plenty. Although it is clear that strong mechanisms have evolved to prevent consumption of foods that have previously made us sick, it is less clear whether reciprocal mechanisms exist that reinforce the consumption of healthy diets. Here, we review recent progress in providing behavioural evidence for the regulation of intake and selection of proteins, carbohydrates and fats. We examine new developments in sensory physiology enabling recognition of macronutrients both pre- and post-ingestively. Finally, we propose a general model for central neural processing of nutrient-specific appetites. We suggest that the same basic neural circuitry responsible for the homoeostatic regulation of total energy intake is also used to control consumption of specific macro- and micronutrients. Similar to salt appetite, specific appetites for other micro- and macronutrients may be encoded by unique molecular changes in the hypothalamus. Gratification of such specific appetites is then accomplished by engaging the brain motivational system to assign the highest reward prediction to exteroceptive cues previously associated with consuming the missing ingredient. A better understanding of these nutrient-specific neural processes could help design drugs and behavioural strategies that promote healthier eating.

Recent advances highlight that nutrient receptors (such as T1R1/T1R3 heterodimer, Ca sensing receptor and GPR93 for amino acids and protein, GPR40, GPR41, GPR43 and GPR120 for fatty acids, T1R2/T1R3 heterodimer for monosaccharides) are expressed in the apical face of the gut and sense nutrients in the lumen. They transduce signals for the regulation of nutrient transporter expressions in the apical face. Interestingly, they are also localised in enteroendocrine cells (EEC) and mainly exert a direct control on the secretion in the lamina propria of gastro-intestinal peptides such as cholecystokinin, glucagon-like peptide-1 and peptide YY in response to energy nutrient transit and absorption in the gut. This informs central nuclei involved in the control of feeding such as the hypothalamus and nucleus of the solitary tract of the availability of these nutrients and thus triggers adaptive responses to maintain energy homoeostasis. These nutrient receptors then have a prominent position since they manage nutrient absorption and are principally the generator of the first signal of satiation mechanisms mainly transmitted to the brain by vagal afferents. Moreover, tastants are also able to elicit gut peptides secretion via chemosensory receptors expressed in EEC. Targeting these nutrient and tastant receptors in EEC may thus be helpful to promote satiation and so to fight overfeeding and its consequences.