NMU-R1

This research would also support the biological explanation of AN as if an individual has damage to their hypothalamus then it could result in reduced feeding which would then result in dramatic weight loss, as seen in sufferers of AN. However, this theory is reductionist as it suggests that the only explanation of AN is a biological reason, and it ignores other factors; like things such as stress or sexual abuse which can both lead to AN.

Ghrelin, commonly referred to as the “hunger hormone,” is a 28-amino acid peptide that has many important roles in human digestion including regulation of growth hormone release, enhancement of appetite, and increase of food intake (1). This gut-derived peptide could play an extremely important role in the altered eating behaviors of patients with eating disorders. Increased fasting plasma ghrelin levels have been consistently reported in underweight patients with anorexia nervosa. Circulating levels of this hormone have also been found to be enhanced in symptomatic bulimic patients, while also being blunted in response to balanced meals (4).

Under conditions of stress, the nervous system, via the SAM (sympathetic-adrenal-medullary) and HPA (hypothalamic-anterior pituitary-adrenal cortex) systems, produces neurotransmitters and hormones (such as cortisol and catecholamines) that bind to receptors on immune system cells;

acute effects of leptin on synaptic plasticity in the arcuate nucleus of the hypothalamus. The arcuate nucleus is one of the key targets of circulating hormones such as leptin. At least two distinct populations of neurons with opposing actions on food intake residein the arcuate nucleus, " (p.63). Pinto's data is ultimately described as helpful but also created many more questions, probably more than it answered.

There has been research showing that serotonin, a brain chemical, influences a person's eating behavior. If there is a deficiency of the neurotransmitter serotonin this could cause cravings for sweets and other

They found out that a tracer amount of Corticosterone put in mice became more abundantly in the hippocampus of adrenalectomized rats and was bounded with high affinity to MR but not GR receptors. Also, MR receptors had high affinity to cortisol than to Corticosterone and showed a greater degree of plasticity in response to neurotrophic peptides. Moreover, corticosterone has maintained through MR receptors, and the corticosterone maintained excitability in the hippocampal neurons and had high excitatory tone over an inhibitory GABAergic network surrounding CRH-producing neurons in the PVN. They said that MR antagonist disinhibits basal and induce stress during the hypothalamus- pituitary-adrenal activation through the receptors interferes with negative feedback and prolonged stress cause hypothalamus -pituitary- adrenal

The brain has many things that it does for our bodies to maintain a balance. The energy balance is regulated by the central nervous system. In order for the brain to regulate energy it must has a sufficient amount of food intake as well as the output, such as exercise. Both of these depend on one another and can affect the over all balance. When food is digested it sends neurotransmitters to the brain to tell whether a person needs more or whether the are full. Even though the communication is very strong there can be things that can disrupt the communication and cause problems within the balance. An oversupply of nutrients within the diet can lead to lepton and insulin resistance. The brain regulating energy is important for overall health

This system is comprised of Pro-opiomelanocortin (POMC) and AgRP neurons of the arcuate hypothalamus (Arc), neuropeptides α-MSH and AgRP, and central melanocortin receptors (MCRs) MC3R and MC4R. POMC and AgRP neurons monitor energy state and change their activity to alter feeding and body weight. When energy needs are met, POMC neurons release α-MSH which acts as an agonist on MC3R and MC4R. AgRP is released in response to an energy deficit and acts as an inverse agonist/antagonist of the central MCRs. Activation of POMC and AgRP neuron signaling has an opposite effect on feeding behavior such that the stimulation of POMC neurons or injection of MCR agonist decreases food intake and body weight27-29 , whereas AgRP neuron activation, central administration or overexpression of AgRP stimulates food intake and weight gain27,30-33. In addition to neuropeptide-mediated signaling, both POMC and AgRP neurons are also capable of fast neurotransmission via Glutamate and/or GABA34-36 and this neurotransmission has been suggested to play an important role in the ability of POMC and AgRP neurons to control feeding27,32. Although much is known about the role of AgRP and POMC neurons in the regulation of feeding and body weight, there is still much to be learned about the larger role these neurons play in energy homeostasis, including their interactions with non-homeostatic circuits, and a better understanding of the role GABA and Glutamate released from POMC and AgRP neurons play in feeding

Ghrelin is the first hormone to be identified that increases feeding when administered peripherally. All of the other known orexigenic peptide transmitters such as neuropeptide Y, orexin, agoutirelated peptide (AGRP), melanocortin-concentrating hormone, and galanin stimulate feeding only when administered into the brain. The observations that circulating ghrelin levels surge suddenly before a meal and fall sharply after a meal, suggest that ghrelin serves as a signal for initiation of feeding. Interestingly, ghrelin increases the number but not the size of meals. However, ghrelin does not only play a role in regulating short-term feeding, but it also regulates body weight over the long-term (Cummings et al.,

We cannot get essential fatty acids from low-fat foods which are omega-3s and omega-6s. They play roles in mood and behavior. In studying the effects of a low-fat diet on macaque monkeys, scientist discovered that such diets promoted antisocial behavior. They fed one group of monkeys with a luxury diet enriched with fats and other groups of monkeys with low-fat foods. The researchers discovered that fat-eating group groomed each other more often and spent more time within touching distance than low-fat group. Also high-fat diet seems to make monkeys friendlier. In observing the antisocial behavior of the low-fat group, researchers theorized that perhaps a low-fat diets affects fats in the brain, thereby altering production of serotonin, and the brain messenger molecule. A lack of serotonin is known to cause aggression. Another research that reported in the British Journal of Nutrition, January 1998, researchers tested humans in a similar way. They chose twenty healthy male and female volunteers, half of whom were put on a 41 percent fat diet and other half were put on a 25 percent fat diet. After four weeks, they switched to low fat and vice versa. (All meals were prepared at the University conducting the study.) Result showed that anger, hostility, and depression declined slightly during the high-fat period, but increased during the low-fat period-- significantly, where anger and hostility were concerned. Researchers took

In vitro: It was found that alpha-endorphin could block the ovalbumin (OA)-specific IgM-PFC response. It seemed that the neuropeptide was capable of blocking the production and secretion of antigen-specific T cell helper factor. Moreover, alpha-endorphin was shown to be able to inhibit the transition of B cells into PFC that usually occured

This study has also demonstrated from their results that glucose, insulin or leptin that are present in the breast milk or are derived from the maternal circulation has an influence on the development of the neural network that regulates the appetite of the offspring in the rats. Thus in rodents the programming of appetite may occur in the litter-bearing, however, from the species in non-litter-bearing such as sheep the major fat depots and hypothalamic neuropeptide expression occur before birth (Muhlhausler et al., 2004).

This methodology was able to successfully label ~90% of Mcpt5-EYFP cells in the dermis and did not alter mast cell degranulation. Similar to the studies detailed above40,59, intravital imaging of mast cell degranulation highlighted the extravasation of vascular dyes. Interestingly, the vascular leakage occurred before any detectable release of labelled mast cell granules, probably mediated by histamine release after activation. Post-degranulation, few of the mast granules appeared to be transported further into the tissue, akin to a previous report60 where intact mast cell granules travelled to draining lymph nodes. Fluorescent avidin based labelling of mast cells in the IL-10 GFP reporter strain showed the presence of predominantly Av.SRho+GFP- mast cells under homeostasis. Post-challenge, mast cells were identified as a source of IL-10 within the activated tissue with more than 50% of avidin labelled mast cells expressing GFP24. However, within 2 days, other immune cells contributed to the production of IL-10 with mast cells only constituting approximately 10-15% of GFP+ cells within the inflamed tissue. The presence of mast cells and IL-10 was intimately linked to the suppression of inflammation during severe contact hypersensitivity.

There are multiple ways to be guided to an eating disorder other than the media. “Eating behavior is a complex process controlled by the neuroendocrine system of which the Hypothalamus-pituitary-adrenal-axis (HPA axis) is a major component” (News Medical). Psychological research is very important to patients who have an eating disorder. Throughout the research in the paper, researchers have come to a conclusion that some of the qualities in the brain a person has a certain level

Food coma, or in medical terms “Postprandial somnolence” is a real scientific phenomenon. There are physiological explanations