Interaction of nanoclay-reinforced packaging nanocomposites with food simulants and compost environments.

The production of engineered nanomaterials (ENMs) has increased exponentially over the last few decades. ENMs, made from use of engineered nanoparticles (ENPs), have been applied to the food, agriculture, pharmaceutical, and automobile industries. Of particular interest are their applications in packaging nanocomposites for consumer and non-consumer goods. ENPs in nanocomposites are of interest as a packaging material because they reduce the amount of polymer needed, while improving the physical properties. However, the transformation of ENPs in nanocomposite production, their fate, and their toxicity remain unknown while in contact with the package content or after the end of life. The objectives of this chapter are (a) to provide an overview of the main nanoclays used in packaging; (b) to categorize the main polymeric packaging nanocomposites; (c) to provide an overview of the fate and mass transport of ENPs, especially nanoclays; (d) to describe the mass transfer of nanoclays in food simulants and in compost environments; and (e) to identify current and future research needs.

Acid sphingomyelinase controls dopamine activity and responses to appetitive stimuli in mice.

Alcohol use disorder and depression show a high comorbidity at clinical level with no treatment available selectively for this condition. A hyperfunction of acid sphingomyelinase (ASM) and resulting ceramide overload were recently identified as one pathway into this comorbidity. Here we analyzed the involvement of ASM, one of the main enzymes involved in ceramide synthesis, in the molecular control of monoaminergic systems in their basal activity and in response to pharmacological and natural reinforcers. The effects of alcohol and a palatable food on the extracellular levels of dopamine (DA), serotonin (5-HT), and noradrenaline (NE) were measured by in-vivo microdialysis in ASM overexpressing mice (tgASM). We found reduced basal extracellular DA levels in the nucleus accumbens (Nac) and dorsal hippocampus (DH) of tgASM mice with little effect on 5-HT and NE levels. In contrast, ASM overexpression potentiated the DA response to alcohol (2 g/kg, i.p.) in the DH and Nac, but reduced NE responses. DA and NE responses to a food stimulus were not altered in tgASM mice, but the Nac 5-HT response was enhanced. An immunohistochemical analysis of the DH showed a preserved dopaminergic and serotonergic innervation in tgASM mice and in mice that consumed alcohol for one month. These findings suggest a direct modulation of monoaminergic basal activity and/or responses to reinforcing stimuli by the sphingolipid regulatory enzyme ASM in mice.

The umami taste: from discovery to clinical use.

In the diversity of the flavor world only five basic tastes have been described. The newest one, umami, has been identified about one hundred years ago by Kikunae Ikeda but widely accepted just in the second half of the twentieth century by international scientific world. There are three umami substances: monosodium glutamate (MSG), inosine-5'-monophosphate (IMP), guanylo-5'-monophosphate (GMP). A real breakthrough in umami history concerned the finding about independent receptors for umami: T1R1 and T1R3 (taste receptors type 1 member 1 and member 3). The palatable, delicious taste of umami and its mechanism determined a lot of research studies on this highlight. Umami substances elicit salivary secretion, enhance appetite and increase food palatability. They are desirable to improve the quality of diet. Moreover, the association between umami substances and the suppression of obesity has been found. Studies suggest that umami is engaged in metabolism but also increases satiety and reduces the post-ingestive recovery of hunger.

Umami flavor enhances appetite but also increases satiety.

BACKGROUND: Monosodium glutamate (MSG) has been shown to increase satiety when combined with protein. Inosine 5'-monophosphate acts synergistically with MSG when tasted, is present in high-protein sources, and may potentially further enhance satiety. OBJECTIVE: We assessed effects of a combination of monosodium glutamate and inosine 5'-monophosphate (MSG/IMP) provided either alone or in a high-energy, high-carbohydrate and -protein soup on appetite during ingestion and postingestive satiety. DESIGN: Fixed portions (450 g) of a low-energy control and high-energy, high-carbohydrate and -protein soup preload with added monosodium glutamate and inosine 5'-monophosphate (MSG/IMP+) or without added monosodium glutamate and inosine 5'-monophosphate (MSG/IMP-) were consumed on 4 nonconsecutive days, and changes in appetite during soup intake and at a subsequent ad libitum lunch were assessed in 26 low-restraint volunteers by using a within-participant design. RESULTS: MSG/IMP+ conditions significantly reduced subsequent intake more than the MSG/IMP- condition did irrespective of energy. The high-carbohydrate and -protein condition also reduced intake independently of MSG/IMP. Energy compensation was greater in the MSG/IMP+ carbohydrate and protein conditions than MSG/IMP- condition. The addition of the MSG/IMP+ also increased the soup pleasantness and caused an immediate increase in appetite when the soup was first tasted. CONCLUSION: The addition of MSG/IMP to a low-energy preload had a biphasic effect on appetite by stimulating appetite during ingestion and enhancing postingestive satiety.

Inconsistencies in the assessment of food intake.

Many peptides and other compounds that influence metabolism also influence food intake, and numerous hypotheses explaining the observed effects in terms of energy homeostasis have been suggested over the years. For example, cholecystokinin (CCK), a duodenal peptide secreted during meals that aids in digestion, also reduces ongoing food intake, thereby contributing to satiation; and insulin and leptin, hormones secreted in direct proportion to body fat, act in the brain to help control adiposity by reducing energy intake. These behavioral actions are often considered to be hard-wired, such that negative experiments, in which an administered compound fails to have its purported effect, are generally disregarded. In point of fact, failures to replicate the effects of compounds on food intake are commonplace, and this occurs both between and within laboratories. Failures to replicate have historically fueled heated debate about the efficacy and/or normal function of one or another compound, leading to confusion and ambiguity in the literature. We review these phenomena and their implications and argue that, rather than eliciting hard-wired behavioral responses in the maintenance of homeostasis, compounds that alter food intake are subjected to numerous influences that can render them completely ineffective at times and that a major reason for this variance is that food intake is not under stringent homeostatic control.

Ghrelin in the control of energy, lipid, and glucose metabolism.

The discovery of ghrelin as the endogenous ligand for the growth hormone secretagogue receptor (GHS-R) led to subsequent studies characterizing the endogenous action of this gastrointestinal hormone. Accordingly, exogenous administration of ghrelin was found to increase food intake and adiposity in a variety of species, including rodents, nonhuman primates, and humans. Later work supported these findings and confirmed that ghrelin acts through hypothalamic neurons to mediate its effects on energy metabolism. Ghrelin acts specifically through GHS-R to promote a positive energy balance as demonstrated by loss of ghrelin action after pharmacological blockade or genetic deletion of GHS-R. More recently, ghrelin was found to be a mediator of glucose metabolism and acts to inhibit insulin secretion from pancreatic ß-cells. Together, the literature highlights a predominant role of ghrelin in regulating energy and glucose metabolism.

Intracerebroventricular O-n-octanoylated ghrelin and its splice variant-induced feeding is blocked by insulin, independent of obestatin or CRF receptor, in satiated rats.

OBJECTIVE: The purpose of this study was to investigate the impact of intracerebroventricular (ICV) injection of the two endogenous forms of acyl ghrelin, O-n-octanoylated ghrelin and des-Gln¹4-ghrelin, on feeding behavior, as well as their interactions with insulin, obestatin, and corticotropin-releasing factor receptor (CRF-R) antagonist in the forebrain to influence food intake. METHODS: We examined the food intake in conscious, freely fed rats, which were chronically implanted with ICV catheters. RESULTS: O-n-octanoylated ghrelin and des-Gln¹4-ghrelin (0.1 nmol/rat) were equally potent in stimulating food intake in freely fed rats, up to 8 h after ICV injection (P < 0.05). In contrast, ICV administration of insulin (8 mU/rat), obestatin (2 nmol/rat), and astressin (2 nmol/rat), a specific CRF-R antagonist, did not modify feeding in freely fed rats. Furthermore, pretreatment with ICV insulin (P < 0.01), but not obestatin or astressin, at the abovementioned dose, blocked central acyl-ghrelin-induced hyperphagic effects. CONCLUSION: ICV O-n-octanoylated ghrelin and its splice variant, des-Gln¹4-ghrelin, are equally potent to elicit food intake in freely fed rats, while these feeding-stimulating effects are opposed by insulin, but independent of obestatin and endogenous CRF-R in the forebrain.

Neurochemistry of drug action: insights from proton magnetic resonance spectroscopic imaging and their relevance to addiction.

Proton magnetic resonance spectroscopy ((1)H MRS) is a noninvasive imaging technique that permits measurement of particular compounds or metabolites within the tissue of interest. In the brain, (1)H MRS provides a snapshot of the neurochemical environment within a defined volume of interest. A search of the literature demonstrates the widespread utility of this technique for characterizing tumors, tracking the progress of neurodegenerative disease, and for understanding the neurobiological basis of psychiatric disorders. As of relatively recently, (1)H MRS has found its way into substance abuse research, and it is beginning to become recognized as a valuable complement in the brain imaging toolbox that also contains positron emission tomography, single-photon-emission computed tomography, and functional magnetic resonance imaging. Drug abuse studies using (1)H MRS have identified several biochemical changes in the brain. The most consistent alterations across drug class were reductions in N-acetylaspartate and elevations in myo-inositol, whereas changes in choline, creatine, and amino acid transmitters also were abundant. Together, the studies discussed herein provide evidence that drugs of abuse may have a profound effect on neuronal health, energy metabolism and maintenance, inflammatory processes, cell membrane turnover, and neurotransmission, and these biochemical changes may underlie the neuropathology within brain tissue that subsequently gives rise to the cognitive and behavioral impairments associated with drug addiction.

The influence of ethanol on feeding in the frugivorous yellow-vented bulbul (Pycnonotus xanthopygos).

The sugars in fleshy fruits provide a rich source of energy to frugivorous animals. However, these carbohydrates also serve as a substrate for alcoholic fermentation by yeasts, ethanol being the main by-product of this process. Ethanol ingestion via frugivory thus occurs in a diverse assemblage of invertebrate and vertebrate taxa, including numerous species of birds. We tested the roles of ethanol as an odor cue for resource location by adult yellow-vented bulbuls (Pycnonotus xanthopygos) and as a possible appetite stimulant in feeding trials with artificial food. We hypothesized (1) that the odor of ethanol does not serve as a food-locating cue in diurnal frugivorous passerine birds, and predicted that the choice of food source and the mass of food eaten by such birds will not be influenced by the odor of ethanol. We further hypothesized (2) that food intake in passerine birds is affected by ingestion of ethanol according to its concentration [EtOH], and predicted that food intake will follow a bell-shaped curve in relation to [EtOH]. In accord with hypothesis (1) and its prediction, we found that the odor of ethanol did not affect food preferences, in either ethanol-naïve or ethanol-experienced yellow-vented bulbuls, when presented at concentrations found in naturally ripe fruit (0.0-1.0%); this suggests that the odor of ethanol is not a food-locating cue for the bulbuls. Hypothesis (2) was partially supported, namely at low [EtOH] (0-3%), food intake was constant and at high [EtOH] (3%) food intake decreased, following only the right half of the predicted bell-shaped response. Ethanol-naïve birds showed no preference towards any [EtOH] presented in two-way choice trials. However, daily food intake in ethanol-experienced bulbuls in single option trials decreased by an average of 36% when the artificial food contained the highest tested concentration of ethanol (3.0%). We suggest that decreasing food intake when food ethanol concentration is relatively high may be a means of avoiding intoxication and is related to the ethanol-metabolizing ability of the bird.

Endocannabinoid system--a novel target for cardiometabolic risk.

The endocannabinoid system (EC) plays a significant role in appetite drive and associated behaviours. Therefore attenuation of the activity of the EC system would have therapeutic benefit in treating disorders that might have a component of excess appetite drive or over-activity of the endocannabinoid system, such as obesity, ethanol and other drug abuse, and a variety of central nervous system and other disorders. Antagonists of cannabinoid receptors have been designed through rational drug discovery essential to exploit these novel targets for potential in obesity, metabolism, addiction, pain and neurologic disorders. Rimonabant is the only compound in this group which along this pathway is now approved as a selective CB (1) (cannabinoid receptor subtype 1) antagonist, or inverse agonist, in the European Union and India and under regulatory review in the United States for the treatment of obesity and associated cardiometabolic risk.

Nutrición basada en la evidencia en el cáncer como enfermedad caquectizante / Evidence-based nutrition in cancer as a cachexia-inducing disease

La caquexia es un síndrome caracterizado por una progresiva e involuntaria pérdida de peso. Se habla del cáncer como enfermedad caquectizante por la prevalencia y la importancia de la caquexia en esta enfermedad. Es sabido que la malnutrición contribuye a menudo a la muerte del paciente con cáncer, pero antes de recomendar una terapia nutricional de forma sistemática debemos conocer los beneficios terapéuticos que realmente proporciona. El objetivo de este trabajo es una actualización del papel del soporte nutricional en el paciente oncológico, especialmente ante la caquexia, basándose en la mayor evidencia científica existente. Para ello, se ha realizado una búsqueda bibliográfica exhaustiva utilizando las bases de datos informáticas MEDLINE y EBM Reviews Multifile PubMed. Pocos son los trabajos que evalúan la nutrición como elemento terapéutico en la caquexia por cáncer. La mayoría no diferencian entre el paciente con o sin malnutrición, e incluso utilizan la malnutrición grave como criterio de exclusión. El soporte nutricional tiene un efecto terapéutico beneficioso en enfermos con cáncer, pero está limitado a un pequeño grupo con malnutrición moderadagrave. Los datos disponibles sugieren que el aumento del aporte calórico-proteico a través de la nutrición artificial convencional no mejora el estado nutricional de los pacientes con enfermedad caquectizante y no altera la progresión de la caquexia. Recientes investigaciones están centradas en el efecto anticaquexia del aceite de pescado, pero las evidencias actuales todavía no son definitivas (AU)

Cachexia is characterized by progressive and involuntary weight loss. Cancer is considered to be a cachexia-inducing disease because of the prevalence and importance of cachexia in malignant neoplastic disease. It is well known that malnutrition frequently contributes to the death of cancer patients. However, before routinely recommending nutritional therapy, the real therapeutic benefits it confers should be identified. The present article aims to provide an update on the role of nutritional support in oncological patients, especially in those with cachexia, based on the best scientific evidence available. An exhaustive literature search was performed in Medline and EBM databases (Reviews Multifile PubMed). Few studies have evaluated nutrition as a therapeutic modality in cancer-induced cachexia. Most studies do not differentiate between patients with or without malnutrition, and even use severe malnutrition as an exclusion criterion. Nutritional support has a beneficial effect in cancer patients but is limited to a small group with moderate to severe malnutrition. The available data suggest that the increase in caloric-protein intake through conventional artificial nutrition does not improve the nutritional status of patients with cachexiainducing disease and does not alter the progression of cachexia. Recent investigations center on the anti-cachexia effect of fish oil but current evidence is still not definitive (AU)

[The role of orexines in appetite regulation]. / Rola oreksyn w regulacji laknienia.

Anorexia nervosa (AN) belongs to the group of eating disorders. Many different factors are taken into consideration as far as the origin of this disorder is concerned, among them: individual factors (genetic, biological), personality factors, sociocultural factors, family factors. Among the biological factors, the role of neuropeptides is considered. Last few years (1998) have resulted in the discovery of two neuropeptides--orexines OXA and OXB which--apart from being regarded as appetite stimulants--are also supposed to be responsible for the energy metabolism of an organism. Orexines, a.k.a. hypocretins, arise from the disintegration of their common precursor--the polypeptide: preorexine. Their name derives from the Greek word for appetite: orexis. The orexine A (OXA) is a 33 amino acid peptide consisting of 2 chains connected by the Cys 6--Cys 12 and Cys 7--Cys 14 bridges. It is a potential food intake and gastric juice secretion stimulant. The connecting bridges in OXA play a crucial role in the receptor OXA-1 activation. The orexine B (OXB) is a 28 amino acid peptide with no connecting bridges between the chains. It mainly plays a role in the energy metabolism of an organism and does not influence the secretion of gastric juice. The OXR-1 receptor is a selective receptor for OXA, while the OXR-2 receptor is not privileged for any of the two orexines--both of them can connect to it. Orexines are produced by a small number of hypothalamus neurons, mainly in the lateral hypothalamus (LHA), but also the posterior hypothalamus--the so-called "eating center". Orexines control: the wakefulness-sleep state, food intake (OXA over 100 times stronger than OXB) and the neuroendocrine system. Their discovery may help in understanding the mechanism of anorexia nervosa.

Synthesis and binding affinity of neuropeptide Y at opiate receptors.

Neuropeptide Y and several metabolic fragments were synthesized and evaluated for binding affinity at non-selective opiate receptors. Neuropeptide Y and several C-terminal fragments were shown to bind to non-selective opiate receptors with an affinity similar to that of Leu-enkephalin.

Design, pharmacology, and NMR structure of a minimized cystine knot with agouti-related protein activity.

The agouti-related protein (AGRP) is an endogenous antagonist of the melanocortin receptors MC3R and MC4R found in the hypothalamus and exhibits potent orexigenic activity. The cysteine-rich C-terminal domain of this protein, corresponding to AGRP(87-132), exhibits receptor binding affinity and antagonism equivalent to that of the full-length protein. The NMR structure of this active domain was recently determined and suggested that melanocortin receptor contacts were made primarily by two loops presented by a well-structured cystine knot domain within AGRP(87-132) [McNulty et al. (2001) Biochemistry 40, 15520-15527]. This hypothesis is tested here with NMR structure and activity studies of a 34-residue AGRP analogue designed to contain only the cystine knot domain. The designed miniprotein folds to a homogeneous product, retains the desired cystine knot architecture, functions as an antagonist, and maintains the melanocortin receptor pharmacological profile of AGRP(87-132). The AGRP-like activity of this molecule supports the hypothesis that indeed the cystine knot region possesses the melanocortin receptor contact points. Moreover, this potent AGRP analogue is synthetically accessible, may serve in the development of therapeutics for the treatment of diseases related to energy balance. and may also find use as a new reagent for probing melanocortin receptor structure and function.

Estimulantes del apetito / No disponible

No disponible

Long term orexigenic effect of a novel melanocortin 4 receptor selective antagonist.

1. We designed and synthesized several novel cyclic MSH analogues and tested their affinities for cells expressing the MC1, MC3, MC4 and MC5 receptors. 2. One of the substances HS028 (cyclic [AcCys11, dichloro-D-phenylalanine14, Cys18, Asp-NH2(22)]-beta-MSH11-22) showed high affinity (Ki of 0.95nM) and high (80 fold) MC4 receptor selectivity over the MC3 receptor. HS028 thus shows both higher affinity and higher selectivity for the MC4 receptor compared to the earlier first described MC4 receptor selective substance HS014. 3. HS028 antagonised a alpha-MSH induced increase in cyclic AMP production in transfected cells expressing the MC3 and MC4 receptors, whereas it seemed to be a partial agonist for the MC1 and MC5 receptors. 4. Chronic intracerebroventricularly (i.c.v.) administration of HS028 by osmotic minipumps significantly increased both food intake and body weight in a dose dependent manner without tachyphylaxis for a period of 7 days. 5. This is the first report demonstrating that an MC4 receptor antagonist can increase food intake and body weight during chronic administration providing further evidence that the MC4 receptor is an important mediator of long term weight homeostasis.

[Orexins--new hypothalamic peptides that stimulate appetite]. / Orexiner--nya hypotalamiska peptider som stimulerar aptit.

A family of novel hypothalamus-specific peptides called orexins have recently been discovered and characterized. The orexins stimulate appetite (the greek word orexis means appetite) when given intraventricularly to rats. Their genes are expressed bilaterally in the lateral hypothalamus, a region previously known to regulate food intake. The two peptides, orexin A (33 amino-acids) and orexin B (28 amino acids), are derived from a common prepro-orexin precursor. The peptides bind to specific G-protein-coupled orexin receptors termed OX-1R and OX-2R. The identification of the orexins will increase our understanding on how the brain regulates food intake.

Gravity and body mass regulation.

NASA: The effects of altered gravity on body mass, food intake, energy expenditure, and body composition are examined. Metabolic adjustments are reviewed in maintenance of energy balance, neural regulation, and humoral regulation are discussed. Experiments with rats indicate that genetically obese rats respond differently to hypergravity than lean rats.^ieng

Increased feeding in fatty Zucker rats by the thiazolidinedione BRL 49653 (rosiglitazone) and the possible involvement of leptin and hypothalamic neuropeptide Y.

1. The thiazolidinedione BRL 49653 (rosiglitazone) induces hyperphagia and weight gain in obese, insulin-resistant fatty Zucker rats but not in lean insulin-sensitive rats. We investigated whether these responses might involve neuropeptide Y (NPY), leptin and insulin. 2. BRL 49653 (1 mg kg(-1) day(-1), orally) was given for 7 or 20 days to fatty and lean Zucker and Wistar rats. 3. In lean rats of either strain, BRL 49653 had no effect on food intake, body weight, plasma insulin and corticosterone, NPY or NPY mRNA levels. 4. Fatty rats given BRL 49653 showed a 30% increase in food intake and accelerated body weight gain (both P<0.01) after 7 and 20 days, but without significant changes in regional hypothalamic NPY or NPY mRNA levels. 5. Plasma leptin levels were twice as high in untreated fatty Zucker rats as in lean rats (P<0.01), but were unaffected by BRL 49653 given for 20 days. However, BRL 49653 reduced insulin levels by 42% and increased corticosterone levels by 124% in fatty rats (both P<0.01). 6. Hyperphagia induced in fatty Zucker rats by BRL 49653 does not appear to be mediated by either a fall in circulating leptin levels or increased activity of hypothalamic NPYergic neurones. The fall in plasma insulin and/or rise in corticosterone levels during BRL 49653 treatment may be involved, consistent with the postulated role of these hormones in the control of food intake.