Food consumption and activity levels increase in rats following intranasal Hypocretin-1

Dhuria, Shyeilla V.; Fine, Jared M.; Bingham, Deborah; Svitak, Aleta L.; Burns, Rachel B.; Baillargeon, Amanda M.; Panter, S. Scott; Kazi, Abdul N.; Frey, William H.; Hanson, Leah R.

doi:10.1016/j.neulet.2016.05.053

Cited by 18 publications

(13 citation statements)

References 31 publications

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“…injections of orexin-A at 1 μmol/kg, the most efficient concentration to reduce tumor growth in mice [20], despite the fact that it modulated the expression of few brain neuropeptide receptors in the hypothalamus, did not induce major effects on the various components of energy expenditure and on long-term body weight evolution. However, we report that orexin-A-treated mice ingested their food more quickly than control ones this results is in accordance with a recent study showing that intranasal administration of orexin-A to rats was able to increase food intake during the first 4 hours just after the administration but as we shown, the total amount of food consumption over 24 hours was not increase [31]. A small but significant decrease in visceral fat masses was observed at the end of the 6 weeks treatment.…”

Section: Discussionsupporting

confidence: 92%

Impact of Orexin-A Treatment on Food Intake, Energy Metabolism and Body Weight in Mice

et al. 2017

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Orexin-A and -B are hypothalamic neuropeptides of 33 and 28-amino acids, which regulate many homeostatic systems including sleep/wakefulness states, energy balance, energy homeostasis, reward seeking and drug addiction. Orexin-A treatment was also shown to reduce tumor development in xenografted nude mice and is thus a potential treatment for carcinogenesis. The aim of this work was to explore in healthy mice the consequences on energy expenditure components of an orexin-A treatment at a dose previously shown to be efficient to reduce tumor development. Physiological approaches were used to evaluate the effect of orexin-A on food intake pattern, energy metabolism body weight and body adiposity. Modulation of the expression of brain neuropeptides and receptors including NPY, POMC, AgRP, cocaine- and amphetamine related transcript (CART), corticotropin-releasing hormone (CRH) and prepro-orexin (HCRT), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored. Our results show that orexin-A treatment does not significantly affect the components of energy expenditure, and glucose metabolism but reduces intraperitoneal fat deposit, adiposity and the expression of several brain neuropeptide receptors suggesting that peripheral orexin-A was able to reach the central nervous system. These findings establish that orexin-A treatment which is known for its activity as an inducer of tumor cell death, do have minor parallel consequence on energy homeostasis control.

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Section: Discussionsupporting

confidence: 92%

Impact of Orexin-A Treatment on Food Intake, Energy Metabolism and Body Weight in Mice

et al. 2017

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“…The current studies further demonstrate that age-related alterations in feeding behavior and neurotransmission have an orexinergic basis, and suggest that orexin-based therapies may have utility in treating conditions which have both homeostatic and cognitive components. While virus-mediated upregulation of orexin expression is unlikely to find clinical application in the near future, additional means of enhancing central orexin transmission in aging may be feasible, including intranasal orexin delivery (Deadwyler et al, 2007, Baier et al, 2011, Dhuria et al, 2016) or development of systemically-deliverable small molecule orexin agonists (Scammell and Winrow, 2011). …”

Section: Discussionmentioning

confidence: 99%

Upregulation of orexin/hypocretin expression in aged rats: Effects on feeding latency and neurotransmission in the insular cortex

et al. 2017

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Aging is associated with changes in numerous homeostatic functions, such as food intake, that are thought to be mediated by the hypothalamus. Orexin/hypocretin neurons of the hypothalamus regulate several physiological functions, including feeding, sleep and wakefulness. Evidence from both clinical and animal studies supports the notion that aging is associated with loss or dysregulation of the orexin system. Here, we used virus-mediated gene transfer to manipulate expression of orexin peptides in young and aged rats and examined behavioral and neurochemical correlates of food intake in these animals. Aged rats showed slower feeding latencies when presented with palatable food compared to young control rats, and these deficits were ameliorated by upregulation of orexin expression. Similarly, young animals treated with a virus designed to decrease preproorexin expression showed longer feeding latencies reminiscent of aged control rats. Feeding was also associated with increased acetylcholine, glutamate and GABA efflux in insular cortex of young control animals. Orexin upregulation did not restore deficits in feeding-elicited release of these neurotransmitters in aged rats, but did enhance basal neurotransmitter levels which may have contributed to the behavioral correlates of these genetic manipulations. These studies demonstrate that age-related deficits in behavioral and neurochemical measures of feeding are likely to be mediated, in part, by the orexin system. Because these same neurotransmitter systems have been shown to underlie orexin effects on cognition, treatments which increase orexin function may have potential for improving both physiological and cognitive manifestations of certain age-related disorders.

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“…Hypocoretin-1 (HC, Orexin A) is a neuropeptide that is involved in the regulation of many physiological functions, such as sleep, appetite, and arousal. Recently, a study on rats has shown an increase in the food consumption aft er intranasal administration of HC (Dhuria et al 2016). In addition to orexin expressing cells, LHA contains MCH expressing cells that extend in a wider area.…”

Section: Th E Hypothalamus Role In the Food Intake Controlmentioning

confidence: 99%

Central and peripheral control of food intake

Abdalla

2017

Endocrine Regulations

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Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive. Th e body weight depends on the balance between the energy intake and energy expenditure. Increased food intake over the energy expenditure of prolonged time period results in an obesity. Th e obesity has become an important worldwide health problem, even at low levels. Th e obesity has an evil eff ect on the health and is associated with a shorter life expectancy. A complex of central and peripheral physiological signals is involved in the control of the food intake. Centrally, the food intake is controlled by the hypothalamus, the brainstem, and endocannabinoids and peripherally by the satiety and adiposity signals. Comprehension of the signals that control food intake and energy balance may open a new therapeutic approaches directed against the obesity and its associated complications, as is the insulin resistance and others. In conclusion, the present review summarizes the current knowledge about the complex system of the peripheral and central regulatory mechanisms of food intake and their potential therapeutic implications in the treatment of obesity. Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive (Jequier and Tappy 1999). As a compensatory mechanism, hunger increases and energy expenditure decreases the weight loss. However, opposite responses are triggered when body weight increases. Body weight can change only when energy intake is not equal to energy expenditure over a given period of time (Bray et al. 2012). A complex physiological control system is involved in the maintenance of the energy balance. Th is system includes aff erent signals from the periphery about the state of the energy stores and eff erent signals that affect the energy intake and expenditure (Sandoval et al. 2008). Th is regulatory system is formed by multiple interactions between the gastrointestinal tract (GIT), adipose tissue, and the central nervous system (CNS). It is infl uenced by behavioral, sensorial, autonomic, nutritional, and endocrine mechanisms (Boguszewski et al. 2010). Satiety and adiposity signalsTh e food intake control includes a short-term regulation, which determines the beginning and the end of a meal (hunger and satiation) and the interval between the meals (satiety) and a long-term regulation with factors (signals of adiposity), which help to regulate the body energy depots (Cummings and Overduin 2007).Th e satiation means a suppression of the hunger and termination of the food intake aft er ingestion of Unauthenticated Download Date | 5/11/18 9:54 AM

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Food consumption and activity levels increase in rats following intranasal Hypocretin-1

Cited by 18 publications

References 31 publications

Impact of Orexin-A Treatment on Food Intake, Energy Metabolism and Body Weight in Mice

Impact of Orexin-A Treatment on Food Intake, Energy Metabolism and Body Weight in Mice

Upregulation of orexin/hypocretin expression in aged rats: Effects on feeding latency and neurotransmission in the insular cortex

Central and peripheral control of food intake

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