Effects of the increase in neuronal fatty acids availability on food intake and satiety in mice (original) (raw)
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Brain Regulation of Appetite and Satiety
Endocrinology and Metabolism Clinics of North America, 2008
Interest in the control feeding and has increased as a result of the obesity epidemic and rising incidence of metabolic diseases. The brain detects alterations in energy stores and triggers metabolic and behavioral responses designed to maintain energy balance. Energy homeostasis is controlled mainly by neuronal circuits in the hypothalamus and brainstem, whereas reward and motivation aspects of eating behavior are controlled by neurons in limbic regions and cerebral cortex. This article provides an integrated perspective on how metabolic signals emanating from the gastrointestinal tract, adipose tissue and other peripheral organs target the brain to regulate feeding, energy expenditure and hormones. Knowledge of these complex pathways is crucial to the pathogenesis and treatment of obesity and abnormalities of glucose and lipid metabolism.
Neuropharmacology, 2012
This article reviews the regulation of appetite from a biopsychological perspective. It considers psychological experiences and peripheral nutritional systems (both episodic and tonic) and addresses their relationship with the CNS networks that process and integrate their input. Whilst such regulatory aspects of obesity focus on homeostatic control mechanisms, in the modern environment hedonic aspects of appetite are also critical. Enhanced knowledge of the complexity of appetite regulation and the mechanisms that sustain obesity indicate the challenge presented by management of the obesity epidemic. Nonetheless, effective control of appetite expression remains a critical therapeutic target for weight management. Currently, strategies which utilise a combination of agents to target both homeostatic and hedonic control mechanisms represent the most promising approaches.
Neurotransmitter alterations associated with feeding and satiety
Brain Research, 1987
Chronically malnourished rats were sacrificed in a food-deprived state, following eating a small amount of food, or following feeding to satiation. Regional analysis of brain neurotransmitter, neurotransmitter precursor and metabolite concentrations revealed significantly elevated levels of dopamine metabofites in the corpus striatum and nucleus accumbens of the satiated rats. Food-deprived and both refed groups exhibited elevated concentrations of the serotonin metabolite, 5-hydroxyindoleacetic acid, in most brain areas examined. These results suggest increased metabolism of dopamine to be associated with satiety rather than with the act of feeding alone. Increased serotonin metabolism appears to reflect overall nutritional status rather than the onset of satiety,
Physiology & Behavior, 2019
Food intake patterns are regulated by signals from the gustatory neural circuit, a complex neural network that begins at the tongue and continues to homeostatic and hedonic brain regions involved in eating behavior. The goal of the current study was to investigate the short-term effects of continuous access to a high fat diet (HFD) versus limited access to dietary fat on the gustatory neural circuit. Male Sprague-Dawley rats were fed a chow diet, a HFD (55% kcal from fat), or provided limited, daily (2h/day) or limited, intermittent (2h/day, 3 times/week) access to vegetable shortening for 2 weeks. Real time PCR was used to determine mRNA expression of markers of fat sensing/signaling (e.g. CD36) on the circumvallate papillae, markers of homeostatic eating in the mediobasal hypothalamus (MBH) and markers of hedonic eating in the nucleus accumbens (NAc). Continuous HFD increased mRNA levels of lingual CD36 and serotonin signaling, altered markers of homeostatic and hedonic eating. Limited, intermittent access to dietary fat selectively altered the expression of genes associated with the regulation of dopamine signaling. Overall, these data suggest that short-term, continuous access to HFD leads to altered fat taste and decreased expression of markers of homeostatic and hedonic eating. Limited, intermittent access, or bingelike, consumption of dietary fat led to an overall increase in markers of hedonic eating, without altering expression of lingual fat sensors or homeostatic eating. These data suggest that there are differential effects of meal patterns on gustatory neurocircuitry which may regulate the overconsumption of fat and lead to obesity.
Physiology & Behavior, 2014
Satiety signals arising from the gastrointestinal (GI) tract and related digestive organs during food ingestion and digestion are conveyed by vagal sensory afferents to the hindbrain nucleus of the solitary tract (NST). Two intermingled but chemically distinct NST neuronal populations have been implicated in meal size control: noradrenergic (NA) neurons that comprise the A2 cell group, and glucagon-like peptide-1 (GLP-1)-positive neurons. Previous results indicate that A2 neurons are activated in a meal size-dependent manner in rats that have been acclimated/entrained to a feeding schedule in order to increase meal size, whereas feeding under the same conditions does not activate GLP-1 neurons. The present study was designed to test the hypothesis that both A2 and GLP-1 neuronal populations are recruited in non-entrained rats after voluntarily first-time intake of an unrestricted, satiating volume of liquid Ensure. DBH-positive neurons within the caudal visceral NST were progressively recruited to express cFos in rats that consumed progressively larger volumes of Ensure. Among these DBH-positive neurons, the prolactinreleasing peptide (PrRP)-positive subset was more sensitive to feeding-induced activation than the PrRP-negative subset. Notably, significant activation of GLP-1-positive neurons occurred only in rats that consumed the largest volumes of Ensure, corresponding to nearly 5% of their BW. We interpret these results as evidence that progressive recruitment of NA neurons within the caudal NST, especially the most caudally-situated PrRP-positive subset, effectively "tracks" the magnitude of GI satiety signals and other meal-related sensory feedback. Conversely, GLP-1 neurons may only be recruited in response to the homeostatic challenge of consuming a very large, unanticipated meal.
Proteins activate satiety-related neuronal pathways in the brainstem and hypothalamus of rats
The Journal of nutrition, 2008
Our objective was to study the relationship between the satiety induced by high-protein meals and the activation of brain areas involved in the onset of satiety. In rats, we used immunohistochemistry to monitor brain centers activated by a meal by receiving information from the gastrointestinal tract or via humoral pathways. In the nucleus of the solitary tract (NTS), the acute or chronic intake of high-protein meals led to increased activation of the noradrenergic/adrenergic neurons involved in cholecystokinin-induced satiety. In the arcuate nucleus of the hypothalamus, the melanocortin pathway was also more strongly activated after the acute or chronic intake of high-protein meals. Moreover, the glucagon-like peptide 1 pathway arising from the NTS, which is triggered, among other behaviors, during nonphysiological anorexia, was not activated by high-protein meals, supporting the lack of aversive behavior associated with this diet. Taken together, these results show that the abilit...
The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism
Nature Communications, 2014
Increased intake of dietary carbohydrate that is fermented in the colon by the microbiota has been reported to decrease body weight, although the mechanism remains unclear. Here we use in vivo 11 C-acetate and PET-CT scanning to show that colonic acetate crosses the blood-brain barrier and is taken up by the brain. Intraperitoneal acetate results in appetite suppression and hypothalamic neuronal activation patterning. We also show that acetate administration is associated with activation of acetyl-CoA carboxylase and changes in the expression profiles of regulatory neuropeptides that favour appetite suppression. Furthermore, we demonstrate through 13 C high-resolution magic-angle-spinning that 13 C acetate from fermentation of 13 C-labelled carbohydrate in the colon increases hypothalamic 13 C acetate above baseline levels. Hypothalamic 13 C acetate regionally increases the 13 C labelling of the glutamate-glutamine and GABA neuroglial cycles, with hypothalamic 13 C lactate reaching higher levels than the 'remaining brain'. These observations suggest that acetate has a direct role in central appetite regulation.
Neural Control of Homeostatic Feeding and Food Selection
New Insights Into Metabolic Syndrome [Working Title], 2020
Neural regulation of feeding is key to the control of body energy balance. Recent studies have identified multiple neural circuits that contribute to the control of homeostatic or hedonic feeding, with these circuits acting cooperatively to regulate feeding overall. Neuropeptide Y (NPY)-agouti-related peptide (AgRP) neurons and pro-opiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus appear to be primary and reciprocal regulators of homeostatic food intake. However, the central mechanisms underlying the regulation of nutrient intake remain largely unknown. 5′-Adenosine monophosphate-activated protein kinase (AMPK) is an important molecule in the regulation of energy metabolism. We recently showed that AMPK-regulated corticotrophin-releasing hormone (CRH) neurons in the paraventricular nucleus of the hypothalamus regulate the selection of carbohydrate over a more palatable diet. Here, I address key recent findings that have shed light on the homeostatic regulati...
Peripheral tissue–brain interactions in the regulation of food intake
Proceedings of The Nutrition Society, 2007
More than 70 years ago the glucostatic, lipostatic and aminostatic hypotheses proposed that the central nervous system sensed circulating levels of different metabolites, changing feeding behaviour in response to the levels of those molecules. In the last 20 years the rapid increase in obesity and associated pathologies in developed countries has involved a substantial increase in the knowledge of the physiological and molecular mechanisms regulating body mass. This effort has resulted in the recent discovery of new peripheral signals, such as leptin and ghrelin, as well as new neuropeptides, such as orexins, involved in body-weight homeostasis. The present review summarises research into energy balance, starting from the original classical hypotheses proposing metabolite sensing, through peripheral tissue-brain interactions and coming full circle to the recently-discovered role of hypothalamic fatty acid synthase in feeding regulation. Understanding these molecular mechanisms will provide new pharmacological targets for the treatment of obesity and appetite disorders. Food intake regulation: Gastrointestinal signals: Adipose and pancreatic hormones: Neural control Abbreviations: AgRP, agouti-related peptide; ARC, arcuate nucleus of the hypothalamus; BBB, blood-brain barrier; CART, cocaine-and amphetamineregulated transcript; CCK, cholecystokinin; CB, cannabinoids; CNS, central nervous system; DMH, dorsomedial nucleus of the hypothalamus; EC, endocannabinoids; FAS, fatty acid synthase; GHS-R, growth hormone secretagogue receptor; GLP, glucagon-like peptide; NPY, neuropeptide Y; LHA, lateral hypothalamic area; MCH, melanin-concentrating hormone; MCnR, melanocortin receptor (n 1-5); NTS, nucleus of the solitary tract; OB-Ra-f, isoforms of leptin receptor; OX, orexin; OXM, oxyntomodulin; POMC, pro-opiomelanocortin; PP, pancreatic polypeptide; PVH, paraventricular nucleus of the hypothalamus; PYY, peptide YY; VMH, ventromedial nucleus of the hypothalamus.
Effects of three neurochemical stimuli on delayed feeding and energy metabolism
Brain Research, 2000
Infusions of norepinephrine (NE), the gamma-aminobutyric acid agonist, muscimol (MUS), or neuropeptide Y (NPY) into the paraventricular nucleus (PVN) of the hypothalamus all increase food intake. Such feeding may be due to direct activation of behavioral processes driving ingestion and / or to alterations in nutrient metabolism that feeding serves to normalize. To examine these possibilities, male Sprague-Dawley rats received PVN infusions of vehicle, 20 nmol NE, 1 nmol MUS or 100 pmol NPY at dark onset, then food intake was measured under three feeding conditions: (1) 1 and 2 h immediately after injections, (2) 1 h after a 1 h delay between injections and access to food, and (3) 1 h after a 1 h feeding delay, but with injections occurring just before presenting food. Measures of energy expenditure (EE) and respiratory quotients (RQs) in the absence of food were made over 2 h in parallel experiments. Results confirmed that NE, MUS and NPY all increased dark-onset feeding, but only NPY increased intake above control levels after a 1 h feeding delay. No neurochemically-induced changes in EE were observed, nor were there changes in RQs after NE or MUS. However, NPY reliably enhanced RQs from 30 to 120 min of testing. Our findings imply that NE and MUS initiate relatively immediate, short-term feeding that is not associated with changes in nutrient metabolism and does not summate with cues stimulated by delayed access to food. NPY initiates more protracted feeding temporally linked to enhanced carbohydrate metabolism. This may indicate that part of NPY's feeding stimulatory effects are secondary to physiological processes driving ingestion.