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Results for “Appetite Regulation”

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At least 631 records · Page 35Linked to original sources
PubMed2005

Astrocytes in the arcuate nucleus and median eminence that take up a fluorescent dye from the circulation express leptin receptors and neuropeptide Y Y1 receptors.

Following systemic injection, several different dyes and markers are found to accumulate rapidly in cells in the arcuate nucleus and median eminence, and the capillaries in this region appear specialised for exchange of molecules. The present study used hydroxystilbamidine (FluoroGold equivalent) to identify cells that take up molecules from the circulation in these regions; 2-6 h following injection, uptake was seen in the external and intermediate zones of the median eminence and the adjacent ventral part of the arcuate nucleus, but not in other regions of the hypothalamus. The labelled cells were small; double-labelling experiments revealed that they expressed glial fibrillary acid protein (GFAP), but not NeuN, Agouti-related protein (AgRP) or beta-endorphin. They had the morphology of astrocytes and were readily distinguished from tanycytes by staining for vimentin. Many of these labelled astrocytes also expressed leptin receptors and neuropeptide Y Y1 receptors. The surrounding neurons that expressed these receptors did not take up this dye. This demonstrates that astrocytes take up molecules from the circulation in the median eminence and adjacent arcuate nucleus, and may have a significant signalling role in regulation of food intake.

Animals↗
PubMed2005

Heredity influences the dietary energy density of free-living humans.

Dietary energy density has been shown to have large effects on short-term food intake. Little is known, however, about its origins. We investigated the influence of heredity, shared (familial) environment, and individual environment on dietary energy density and its relationship to food intake with 110 identical and 102 fraternal same-sex and 53 fraternal mixed gender adult twin pairs who were paid to maintain 7-day food intake diaries. From the diary reports, the total and meal intakes of food energy, the amounts of the macronutrients ingested, and dietary energy density were estimated. Linear structural modeling was applied to investigate the nature and degree of genetic and environmental influences. The analysis revealed significant genetic and individual environmental, but not shared (familial) environmental, influences on the dietary densities of the reported diets. But, there was no genetic or familial influences on the responsiveness of the individual to dietary density. Dietary energy density appears to be another component in a package of genetically determined physiological, sociocultural, and psychological processes that influence the regulation of energy balance.

Adult↗
PubMed2004

Food intake and ageing--the role of the gut.

Healthy ageing is associated with decreased appetite and energy intake and this is generally associated with weight loss after about 70 years of age. The mechanisms responsible for this 'physiological' anorexia are not well understood, but it may predispose to the development of protein-energy malnutrition in older people, which is associated with increased morbidity and mortality. Many sensory and social factors, including olfactory changes and economic status, contribute to under-nutrition in older people; however, normal ageing is associated with a number of significant changes in gastrointestinal function. The control of appetite is complex but it is clear that gastrointestinal signals are important in the regulation of appetite and food intake. This review examines the role of small intestinal hormones and gastrointestinal motor function in the observed changes to appetite and food intake in older people.

Aging↗
PubMed1996

Dexamethasone induces an acute and sustained rise in circulating leptin levels in normal human subjects.

Leptin, the protein product of the ob gene, is thought to have a role in signalling satiety through hypothalamic pathways. Glucocorticoids are potent stimulators of both ob gene expression and circulating leptin levels in the rat, yet are powerful appetite stimulants in humans. We have investigated circulating leptin responses to intermediate term and acute administration of dexamethasone. Dexamethasone 2 mg twice daily resulted in a rapid and sustained rise in 08.00 h leptin levels from basal values of 1.36 +/- 0.25 to 3.58 +/- 1.72 microg/l after 24 hours of treatment. Following placebo administration 24 h profiles confirmed a nocturnal rise in leptin levels with an increase of 73 +/- 37% at midnight compared with 0.9.00 h. After dexamethasone mean leptin levels increased by 123 +/- 51% (p = 0.0016), with an accentuation in the diurnal variation and associated hyperinsulinemia. The study confirms a nocturnal rise in leptin in humans, and demonstrates increases in leptin in response to glucocorticoid administration as previously demonstrated in the rodent. The divergence between appetite stimulating effects of glucocorticoids despite induction of a proposed satiety factor suggests that regulation of leptin levels and regulation of appetite is multifactorial, and other neurotransmitter pathways are presumably involved.

Adult↗
PubMed2005

Early origins of obesity: programming the appetite regulatory system.

There is evidence that changes in perinatal nutrition programme the development of relative fat mass and the regulation of appetite in adult life. These studies have been primarily in the rodent utilizing maternal overnutrition or undernutrition imposed at different stages of pregnancy and beyond, mapping of neuropeptide localization and activity and appropriate null mutant models. Whilst the rodent offers significant advantages in terms of a short gestation and the availability of useful transgenic and null mutant models, there are also advantages to using an animal model more akin to the human, in which all components of the 'fat-brain axis' are present before birth, such as the sheep. This review summarizes recent work on the expression and localization of the 'appetite regulatory' peptides in the fetal rodent and sheep hypothalamus and their potential role in the early programming of postnatal appetite and obesity.

Animals↗
PubMedDate not supplied

[Possibility of affecting the regulation of salt and water uptake in the critical periods of development in rats].

Peculiarities in water and salt (NaCl) appetite were studied in rats under various experimental influences during critical periods of development. When sexual maturation is going on, females consume more salt than males. These sex depending differences may be altered by experimental influences but only during critical periods of development, for instance by injection of androgens into neonatal females or by gonadectomy of males, by premature cessation of rearing, etc. The effects of those early interventions manifest themselves after the termination of sexual maturation.

Age Factors↗
PubMed2006

Automatic and controlled processes and the development of addictive behaviors in adolescents: a review and a model.

This paper presents a review and a model of the development of addictive behaviors in (human) adolescents, with a focus on alcohol. The model proposes that addictive behaviors develop as the result of an imbalance between two systems: an appetitive, approach-oriented system that becomes sensitized with repeated alcohol use and a regulatory executive system that is not fully developed and that is compromised by exposure to alcohol. Self-regulation critically depends on two factors: ability and motivation to regulate the appetitive response tendency. The motivational aspect is often still weak in heavy drinking adolescents, who typically do not recognize their drinking as problematic. Motivation to regulate use often develops only years later, after the individual has encountered serious alcohol-related problems. Unfortunately, at that point behavioral change becomes harder due to several neurocognitive adaptations that result from heavy drinking. As we document, there is preliminary support for the central elements of the model (appetitive motivation vs. self-regulation), but there is a paucity of research directly addressing these mechanisms in human adolescents. Further, we emphasize that adolescent alcohol use primarily takes place in a social context, and that therefore studies should not solely focus on intra-individual factors predicting substance use and misuse but also on interpersonal social factors. Finally, we discuss implications of the model for interventions.

Adolescent↗
PubMed2005

The neuronal histamine H(1) and pro-opiomelanocortin-melanocortin 4 receptors: independent regulation of food intake and energy expenditure.

Hypothalamic neuronal histamine and its H(1) receptor (H(1)-R) form part of the leptin signaling pathway in the brain, and regulate body weight and adiposity by affecting food intake and energy expenditure. The pro-opiomelanocortin (POMC)-melanocortin 4 receptor (MC4-R) is also important for leptin signaling. We investigated whether and how these two neuronal pathways interact in regulating energy metabolism. From studies of agouti yellow (A(y)/a) obese mice, a model of a defect in POMC-MC4-R signaling, we concluded that the histamine H(1)-R signaling pathway is independent of the POMC-MC4-R complex in regulating food intake, energy metabolism, and adiposity.

Animals↗
PubMed2004

Salt appetite: a neurohormonal viewpoint.

Sodium is a key component of virtually every mammalian physiological function. As such, many animals have evolved specialized mechanisms for detecting and ameliorating deficits in body sodium, including the development of a robust salt appetite, where normally aversive concentrations of salt are readily consumed during periods of sodium deprivation. Here, we review research spanning more than half a century focusing on the condition and detection of sodium deprivation, the important and unique function of taste in sodium homeostasis, as well as the neurohormonal interactions leading to behaviors aimed at the reversal of sodium deficits. Based on the present literature, we propose a model for the interaction of forebrain and brainstem systems for the mediating circuitry giving rise to salt appetite and discuss the remarkable parallel between what is known about the neurohormonal interactions that regulate salt appetite and those involved in energy homeostasis.

Animals↗
PubMed2004

Leptin receptor signaling and the regulation of mammalian physiology.

While the hormone leptin and its receptor were discovered relatively recently, a great deal is already known about the molecular details of leptin receptor (LR) signaling and physiologic regulation. While multiple alternatively spliced LR isoforms exist, only the long (LRb) form associates with the Janus kinase 2 (Jak2) tyrosine kinase to mediate intracellular signaling. LRb initiates signaling via three major mechanisms: 1) Tyr(985) of LRb recruits SH2-containing tyrosine phosphatase (SHP-2); 2) Tyr(1138) of LRb recruits signal transducer and activator of transcription 3 (STAT3); and 3) tyrosine phosphorylation sites on the receptor-associated Jak2 likely recruit numerous undefined signaling proteins. The Tyr(985) --> SHP-2 pathway is a major regulator of extracellular signal-regulated kinase (ERK) activation during leptin signaling in cultured cells, while the Tyr(1138) --> STAT3 pathway induces the feedback inhibitor, suppressor of cytokine signaling 3 (SOCS3), as well as important positive effectors of leptin action. The Jak2-dependent activation of the insulin receptor substrate (IRS) protein --> phosphatidylinositol 3-kinase (PI3'-K) pathway appears to regulate membrane potential in LRb-expressing neurons and contributes to the regulation of feeding. The Tyr(1138) --> STAT3 pathway mediates transcriptional regulation of the hypothalamic melanocortin pathway in vivo. This pathway is required for the regulation of appetite and energy expenditure by leptin. Interestingly, the Tyr(1138) --> STAT3 pathway does not strongly regulate neuropeptide Y (NPY) and thus is not required for the control of reproduction and growth. Thus, other as-yet-undefined leptin receptor signals are central to these and perhaps other aspects of leptin action.

Alternative Splicing↗