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Simple Summary: There is limited information regarding dietary nutrient sensors in chickens. This study explored the expression of amino acid (AA) and fatty acid (FA) sensors in the gastrointestinal tract (GIT) of broilers. This research focused on quantifying gene expression of AA and FA sensors in ten tissues, including the upper, middle, and lower GIT sections of 7 and 26-day-old birds. Early in life (7 days), chicks develop a high sensing capability in the oral cavity for AA and the cecum and colon for short-chain fatty acids, presumably related to bacterial fermentation. In turn, at 26 days of age, a strong emergence of the role of the jejunum sensing AA and FA occurs, indicating the major role of the middle GIT section in nutrient digestion, absorption, and the gut-brain axis. This work aimed to evaluate the gene expression of amino acids (AA) and fatty acids (FA) sensors in the gastrointestinal tract (GIT) of chickens at two different ages (7 and 26 days post-hatch). Sixteen broilers (Ross 308) were selected, and ten sections of the GIT, including upper (tongue base, upper palate, crop, proventriculus), middle (gizzard, duodenum, jejunum, ileum), and lower GIT section (cecum, colon) were collected for analysis. Relative gene expression of AA (T1R1, T1R3, mGluR1, mGluR4, CaSR, GPR139, GPRC6A, GPR92) and FA (FFAR2, FFAR3, FFAR4) sensors were assessed using qPCR. The statistical model included age, GIT section, and gene. In addition, the correlations between gene expressions were calculated. At day 7, a significantly (p = 0.004) higher expression of AA sensors in the oral cavity and FA sensors in the lower GIT section (i.e., cecum and colon) compared to the middle section was recorded. A higher expression of AA compared to FA sensors was detected at the upper GIT section in 7 (p < 0.001) and 26-day-old chickens (p = 0.026). Thus, at day 7, AA sensors were predominantly (p < 0.05) expressed in the upper GIT section (mainly oral cavity), while FA sensors were mainly expressed in the lower GIT section, at cecum (FFR2 and 4) or colon (FFAR3). These results may indicate that in early life, both ends of the GIT are fundamental for feed intake (oral cavity) and development of the microbiota (cecum and colon). In contrast, at 26 days of age, the results showed the emergence of both AA and FA sensors in the jejunum, presumably indicating the essential role of the jejunum in the digestion absorption of nutrients and the signaling to the brain (gut-brain axis) through the enteroendocrine system. Significant positive correlations were observed between T1R1 and T1R3 (r = 0.85, p < 0.001), CaSR and T1R1 (r = 0.78, p < 0.001), CaSR and T1R3 (r = 0.45, p < 0.050), and mGluR1 and FFAR3 (r = 0.46, p < 0.050). It is concluded that the gene expression is greater in the oral cavity for AA sensors and the lower gut for FA sensors. On day 26, the role of jejunum regarding nutrient sensing is highlighted. [ABSTRACT FROM AUTHOR]

For decades bitter taste receptors (TAS2R) were thought to be located only in the mouth and to serve as sensors for nutrients and harmful substances. However, in recent years Tas2r have also been reported in extraoral tissues such as the skin, the lungs, and the intestine, where their function is still uncertain. To better understand the physiological role of these receptors, in this paper we focused on the intestine, an organ in which their activation may be similar to the receptors found in the mouth. We compare the relative presence of these receptors along the gastrointestinal tract in three main species of biomedical research (mice, rats and humans) using sequence homology. Current data from studies of rodents are scarce and while more data are available in humans, they are still deficient. Our results indicate, unexpectedly, that the reported expression profiles do not always coincide between species even if the receptors are orthologs. This may be due not only to evolutionary divergence of the species but also to their adaptation to different dietary patterns. Further studies are needed in order to develop an integrated vision of these receptors and their physiological functionality along the gastrointestinal tract.

Animals increase their locomotion activity and reduce sleep duration under starved conditions. This suggests that sleep and metabolic status are closely interconnected. The nutrient and hunger sensors in the Drosophila brain, including diuretic hormone 44 (DH44)–, CN–, and cupcake-expressing neurons, detect circulating glucose levels in the internal milieu, regulate the insulin and glucagon secretion and promote food consumption. Food deprivation is known to reduce sleep duration, but a potential role mediated by the nutrient and hunger sensors in regulating sleep and locomotion activity remains unclear. Here, we show that DH44 neurons are involved in regulating starvation-induced sleep suppression, but CN neurons or cupcake neurons may not be involved in regulating starvation-induced sleep suppression or baseline sleep patterns. Inactivation of DH44 neurons resulted in normal daily sleep durations and patterns under fed conditions, whereas it ablated sleep reduction under starved conditions. Inactivation of CN neurons or cupcake neurons, which were proposed to be nutrient and hunger sensors in the fly brain, did not affect sleep patterns under both fed and starved conditions. We propose that the glucose-sensing DH44 neurons play an important role in mediating starvation-induced sleep reduction. [ABSTRACT FROM AUTHOR]

The ease of accepting or donating electrons is the raison d'être for the pivotal role iron (Fe) plays in a multitude of vital processes. In the presence of oxygen, however, this very property promotes the formation of immobile Fe(III) oxyhydroxides in the soil, which limits the concentration of Fe that is available for uptake by plant roots to levels well below the plant's demand. To adequately respond to a shortage (or, in the absence of oxygen, a possible surplus) in Fe supply, plants have to perceive and decode information on both external Fe levels and the internal Fe status. As a further challenge, such cues have to be translated into appropriate responses to satisfy (but not overload) the demand of sink (i.e., non-root) tissues. While this seems to be a straightforward task for evolution, the multitude of possible inputs into the Fe signaling circuitry suggests diversified sensing mechanisms that concertedly contribute to govern whole plant and cellular Fe homeostasis. Here, we review recent progress in elucidating early events in Fe sensing and signaling that steer downstream adaptive responses. The emerging picture suggests that Fe sensing is not a central event but occurs in distinct locations linked to distinct biotic and abiotic signaling networks that together tune Fe levels, Fe uptake, root growth, and immunity in an interwoven manner to orchestrate and prioritize multiple physiological readouts. [ABSTRACT FROM AUTHOR]

The ease of accepting or donating electrons is the raison d’être for the pivotal role iron (Fe) plays in a multitude of vital processes. In the presence of oxygen, however, this very property promotes the formation of immobile Fe(III) oxyhydroxides in the soil, which limits the concentration of Fe that is available for uptake by plant roots to levels well below the plant’s demand. To adequately respond to a shortage (or, in the absence of oxygen, a possible surplus) in Fe supply, plants have to perceive and decode information on both external Fe levels and the internal Fe status. As a further challenge, such cues have to be translated into appropriate responses to satisfy (but not overload) the demand of sink (i.e., non-root) tissues. While this seems to be a straightforward task for evolution, the multitude of possible inputs into the Fe signaling circuitry suggests diversified sensing mechanisms that concertedly contribute to govern whole plant and cellular Fe homeostasis. Here, we review recent progress in elucidating early events in Fe sensing and signaling that steer downstream adaptive responses. The emerging picture suggests that Fe sensing is not a central event but occurs in distinct locations linked to distinct biotic and abiotic signaling networks that together tune Fe levels, Fe uptake, root growth, and immunity in an interwoven manner to orchestrate and prioritize multiple physiological readouts.

The enteroendocrine system of the gut regulates energy homeostasis through the release of hormones. Of the gut-derived hormones, GLP-1 is particularly interesting, as analogs of the hormone have proven to be highly effective for the treatment of type 2 diabetes mellitus and obesity. Observations on increased levels of GLP-1 following gastric bypass surgery have enhanced the interest in endogenous hormone secretion and highlighted the potential of endogenous secretion in therapy. The macronutrients and their digestive products stimulate the secretion of GLP-1 through various mechanisms that we have only begun to understand. From findings obtained from different experimental models, we now have strong indications for a role for both Sodium-Glucose Transporter 1 (SGLT1) and the K+ATP channel in carbohydrate-induced GLP-1 secretion. For fat, the free fatty acid receptor FFA1 and the G-protein-coupled receptor GPR119 have been linked to GLP-1 secretion. For proteins, Peptide Transporter 1 (Pept1) and the Calcium-Sensing Receptor (CaSR) are thought to mediate the secretion. However, attempts at clinical application of these mechanisms have been unsuccessful, and more work is needed before we fully understand the mechanisms of nutrient-induced GLP-1 secretion. [ABSTRACT FROM AUTHOR]

Dietary oils─rich in omega-3, -6, and -9 fatty acids─exhibit critical impacts on health parameters such as cardiovascular function, bodily inflammation, and neurological development. There has emerged a need for low-cost, accessible method to assess dietary oil consumption and its health implications. Existing methods typically require specialized, complex equipment and extensive sample preparation steps, rendering them unsuitable for home use. Addressing this gap, herein, we study passive wireless, biocompatible biosensors that can be used to monitor dietary oils directly from foods either prepared or cooked in oil. This design uses broad-coupled split ring resonators interceded with porous silk fibroin biopolymer (requiring only food-safe materials, such as aluminum foil and biopolymer). These porous biopolymer films absorb oils at rates proportional to their viscosity/fatty acid composition and whose response can be measured wirelessly without any microelectronic components touching food. The engineering and mechanism of such sensors are explored, alongside their ability to measure the oil presence and fatty acid content directly from foods. Its simplicity, portability, and inexpensiveness are ideal for emerging needs in precision nutrition─such sensors may empower individuals to make informed dietary decisions based on direct-from-food measurements.

Increasing clarity of Delta waters, the emergence of harmful algal blooms, the proliferation of aquatic water weeds, and the altered food web of the Delta have brought nutrient dynamics to the forefront. This paper focuses on the sources of nutrients, the transformation and uptake of nutrients, and the links of nutrients to primary producers. The largest loads of nutrients to the Delta come from the Sacramento River with the San Joaquin River seasonally important, especially in the summer. Nutrient concentrations reflect riverine inputs in winter and internal biological processes during periods of lower flow with internal nitrogen losses within the Delta estimated at approximately 30% annually. Light regime, grazing pressure, and nutrient availability influence rates of primary production at different times and locations within the Delta. The roles of the chemical form of dissolved inorganic nitrogen in growth rates of primary producers in the Delta and the structure of the open-water algal community are currently topics of much interest and considerable debate. Harmful algal blooms have been noted since the late 1990s, and the extent of invasive aquatic macrophytes (both submerged and free-floating forms) has increased especially during years of drought. Elevated nutrient loads must be considered in terms of their ability to support this excess biomass. Modern sensor technology and networks are now deployed that make high-frequency measurements of nitrate, ammonium, and phosphate. Data from such instruments allow a much more detailed assessment of the spatial and temporal dynamics of nutrients. Four fruitful directions for future research include utilizing continuous sensor data to estimate rates of primary production and ecosystem respiration, linking hydrodynamic models of the Delta with the transport and fate of dissolved nutrients, studying nutrient dynamics in various habitat types, and exploring the use of stable isotopes to trace the movement and fate of effluent-derived nutrients.

The knowledge regarding hypothalamic integration of metabolic and endocrine signaling resulting in regulation of food intake is scarce in fish. Available studies pointed to a network in which the activation of the nutrient-sensing (glucose, fatty acid, and amino acid) systems would result in AMP-activated protein kinase (AMPK) inhibition and activation of protein kinase B (Akt) and mechanistic target of rapamycin (mTOR). Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART). The present mini-review summarizes information on the topic and identifies gaps for future research.

The enteroendocrine system of the gut regulates energy homeostasis through the release of hormones. Of the gut-derived hormones, GLP-1 is particularly interesting, as analogs of the hormone have proven to be highly effective for the treatment of type 2 diabetes mellitus and obesity. Observations on increased levels of GLP-1 following gastric bypass surgery have enhanced the interest in endogenous hormone secretion and highlighted the potential of endogenous secretion in therapy. The macronutrients and their digestive products stimulate the secretion of GLP-1 through various mechanisms that we have only begun to understand. From findings obtained from different experimental models, we now have strong indications for a role for both Sodium-Glucose Transporter 1 (SGLT1) and the K+ATP channel in carbohydrate-induced GLP-1 secretion. For fat, the free fatty acid receptor FFA1 and the G-protein-coupled receptor GPR119 have been linked to GLP-1 secretion. For proteins, Peptide Transporter 1 (Pept1) and the Calcium-Sensing Receptor (CaSR) are thought to mediate the secretion. However, attempts at clinical application of these mechanisms have been unsuccessful, and more work is needed before we fully understand the mechanisms of nutrient-induced GLP-1 secretion.

The knowledge regarding hypothalamic integration of metabolic and endocrine signaling resulting in regulation of food intake is scarce in fish. Available studies pointed to a network in which the activation of the nutrient-sensing (glucose, fatty acid, and amino acid) systems would result in AMP-activated protein kinase (AMPK) inhibition and activation of protein kinase B (Akt) and mechanistic target of rapamycin (mTOR). Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART). The present mini-review summarizes information on the topic and identifies gaps for future research. [ABSTRACT FROM AUTHOR]

AMP-activated protein kinase (AMPK) is considered as the master cellular metabolism regulator that activates various proteins, including O-GlcNAc transferase (OGT). Physiological roles of AMPK and OGT, including the relationship between their mRNA expression and food intake, are poorly understood in channel catfish. This study examined the tissue distribution of AMPK and OGT mRNA and changes in their expression in response to changes in food intake in channel catfish. Expression of all AMPK subunit and OGT mRNA was detectable in the whole brain, liver, heart, spleen, white muscle, and kidney of channel catfish. The OGT mRNA was highly localized in the brain compared to other tissues. 28-day fasting increased hepatic expression of AMPK α1, β1, and OGT mRNA while refeeding fish for 14 days after the 14-day fast decreased their expression to the level similar to that of fish that were fed daily. No changes were noted in the expression of muscle and brain AMPK mRNA or OGT mRNA by fasting and refeeding. Hepatic AMPK α1, α2 and β1 mRNA decreased in response to increased feeding frequency, whereas no changes in the expression of AMPK or OGT mRNA were noted in the brain or the muscle. Results of the current study indicated that the hepatic expression of AMPK and OGT mRNA appeared to be more sensitive to changes in food intake in channel catfish. However, further studies are needed to clearly demonstrate if food intake influences the expression of AMPK and OGT mRNA in various tissues, including the hypothalamus. Unlabelled Image • The distribution of AMPK and OGT mRNA in channel catfish was similar to mammalian counterpart • The AMPK and OGT mRNA expression in the liver increased after fasting but decreased when fish received food after fasting. • Brain and muscle OGT mRNA and AMPK mRNA expression was unaffected by fasting. • Increased feeding frequency decreased the expression of AMPK mRNA in the liver but not the OGT mRNA expression. • Expression of AMPK and OGT mRNA in the muscle was unaffected by the food intake. [ABSTRACT FROM AUTHOR]

Fetal growth restriction is one of the most common obstetrical complications resulting in significant perinatal morbidity and mortality. The most frequent etiology of human singleton fetal growth restriction is placental insufficiency, which occurs secondary to reduced utero-placental perfusion, abnormal placentation, impaired trophoblast invasion and spiral artery remodeling, resulting in altered nutrient and oxygen transport. Two nutrient-sensing proteins involved in placental development and glucose and amino acid transport are mechanistic target of rapamycin (mTOR) and O-linked N-acetylglucosamine transferase (OGT), which are both regulated by availability of oxygen. Impairment in either of these pathways is associated with fetal growth restriction and accompanied by cellular stress in the forms of hypoxia, oxidative and endoplasmic reticulum (ER) stress, metabolic dysfunction and nutrient starvation in the placenta. Recent evidence has emerged regarding the potential impact of nutrient sensors on fetal stress response, which occurs in a sexual dysmorphic manner, indicating a potential element of genetic gender susceptibility to fetal growth restriction. In this mini review, we focus on the known role of mTOR and OGT in placental development, nutrient regulation and response to cellular stress in human fetal growth restriction with supporting evidence from rodent models. [ABSTRACT FROM AUTHOR]

Evidence obtained in recent years in a few species, especially rainbow trout, supports the presence in fish of nutrient sensing mechanisms. Glucosensing capacity is present in central (hypothalamus and hindbrain) and peripheral [liver, Brockmann bodies (BB, main accumulation of pancreatic endocrine cells in several fish species), and intestine] locations whereas fatty acid sensors seem to be present in hypothalamus, liver and BB. Glucose and fatty acid sensing capacities relate to food intake regulation and metabolism in fish. Hypothalamus is as a signaling integratory center in a way that detection of increased levels of nutrients result in food intake inhibition through changes in the expression of anorexigenic and orexigenic neuropeptides. Moreover, central nutrient sensing modulates functions in the periphery since they elicit changes in hepatic metabolism as well as in hormone secretion to counter-regulate changes in nutrient levels detected in the CNS. At peripheral level, the direct nutrient detection in liver has a crucial role in homeostatic control of glucose and fatty acid whereas in BB and intestine nutrient sensing is probably involved in regulation of hormone secretion from endocrine cells. [ABSTRACT FROM AUTHOR]

Solid epidemiological evidence indicates that part of the risk of obesity in adulthood could be programmed during prenatal development by the quality of maternal nutrition. Nevertheless, the molecular mechanisms involved are mostly unknown, which hinders our capacity to develop effective intervention policies. Here, we discuss the hypothesis that mechanisms underlying prenatal programming of adult risk are epigenetic and sensitive to environmental cues such as nutrition. While the information encoded in DNA is essentially stable, regulatory epigenetic mechanisms include reversible, covalent modifications of DNA and chromatin, such as methylation, acetylation etc. It is known that dietary availability of methyl donors has an impact on the patterns of gene expression by affecting DNA methylation at regulatory regions, a likely basis for reprogramming developmental plasticity. The Agouti and Axin-fused genes, as well as the embryonic growth factor IGF2/H19 locus are examples of diet-induced modulation of phenotypic traits by affecting methylation of gene-regulatory regions. Recent work has evidenced an unsuspected role for chromatin as metabolic sensor. Chromatin is susceptible to a number of post-translational modifications that modulate gene expression, among them the GlcNAcylation of histone proteins and other epigenetic regulators. Intracellular levels of the precursor molecule UDP-GlcNAc, and hence the degree of global chromatin GlcNAcylation, depend on the energetic state of the cell, making GlcNAcylation a functional link between nutrition and regulation of gene expression. Dietary interference with these regulatory mechanisms could effectively counteract the early-life programming of adult risk. [ABSTRACT FROM AUTHOR]

The suprachiasmatic nucleus (SCN) in the mammalian hypothalamus functions as an endogenous pacemaker that generates and maintains circadian rhythms throughout the body. Next to this central clock, peripheral oscillators exist in almost all mammalian tissues. Whereas the SCN is mainly entrained to the environment by light, peripheral clocks are entrained by various factors, of which feeding/fasting is the most important. Desynchronization between the central and peripheral clocks by, for instance, altered timing of food intake can lead to uncoupling of peripheral clocks from the central pacemaker and is, in humans, related to the development of metabolic disorders, including obesity and Type 2 diabetes. Diets high in fat or sugar have been shown to alter circadian clock function. This review discusses the recent findings concerning the influence of nutrients, in particular fatty acids and glucose, on behavioral and molecular circadian rhythms and will summarize critical studies describing putative mechanisms by which these nutrients are able to alter normal circadian rhythmicity, in the SCN, in non-SCN brain areas, as well as in peripheral organs. As the effects of fat and sugar on the clock could be through alterations in energy status, the role of specific nutrient sensors will be outlined, as well as the molecular studies linking these components to metabolism. Understanding the impact of specific macronutrients on the circadian clock will allow for guidance toward the composition and timing of meals optimal for physiological health, as well as putative therapeutic targets to regulate the molecular clock. [ABSTRACT FROM AUTHOR]

Background and Aims: The rising prevalence of obesity is a major international concern and is associated with a substantial burden of disease. Disrupted circadian behaviours, including late and extended eating patterns, are identified as risk factors for obesity. The circadian rhythm synchronises metabolic functions between and within tissues, optimising physiology to integrate with environmental and behavioural cycles. Cellular circadian rhythms also separate poorly compatible processes and enable adaptive integration of energy metabolism with autophagy. The timing of nutritional input is a key and easily controllable variable that influences circadian function. Misalignment of nutritional input with the centrally generated circadian rhythm may dampen and disrupt circadian metabolic function. This review seeks to provide a mechanistic overview of nutritional circadian entrainment and its downstream metabolic effects. The aims are: to characterise the key cellular and physiological mechanisms involved in the nutritional entrainment of circadian rhythms; and to explore the perturbation of these pathways by misaligned nutritional inputs, with relevance to obesity-associated dysmetabolism., Methods: A systematic two-tranche search strategy was employed. Searches were conducted within PubMed between March and December 2020. Included studies were formally evaluated for quality. Evidence was extracted and coded into key themes., Results: 142 records were screened and 50 accepted. The evidence analysed was moderate-to-high quality and enabled the detailed characterisation of cellular pathways involved in nutritional circadian entrainment. Results indicated that diverse nutritional input pathways converge upon key nutrient/redox sensors and nutritionally sensitive core clock genes, which integrate with circadian metabolic pathways, allowing bidirectional communication between circadian clock function and metabolism. Versus alignment, nutritional misalignment was causally associated with dampening and alteration of core clock rhythms, between-tissue rhythmic decoupling, dysmetabolism, and obesity. Signalling through key circadian nodes, such as NAD + /SIRT, was indicated to have importance in these metabolic changes. Misaligned nutritional inputs were associated with altered core circadian temporal dynamics of metabolism and autophagy, and different time division between insulin-sensitive and insulin-resistant metabolic states. Time-restricted feeding protocols aligned with the natural circadian rhythm (light-dark cycle) relatively strengthened circadian oscillatory patterns and protected against diet-induced obesity., Conclusions: This review suggests potential value in further investigating circadian-normalising nutritional interventions for obesity, such as circadian-aligned time-restricted feeding., Competing Interests: Declaration of competing interest The authors declare no competing interests., (Copyright © 2022 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights reserved.)