Neuropeptide Y hormone, appetite, weight influence
Feb 22 2016 by Ray Sahelian, M.D.
The hypothalamus and other brain regions that control energy homeostasis contain neuronal populations that produce specific neuropeptides which have experimental effects on feeding behavior and body weight. Neuropeptides exert anabolic effects, notably stimulation of feeding and increased body weight. For more information on peptides. Neuropeptide Y is an appetite stimulant.
Neuropeptide Y (NPY) information
Neuropeptide Y neurons in the hypothalamic arcuate nucleus are inhibited by leptin and insulin, and thus are stimulated in states of energy deficit and fat loss, e.g., underfeeding. such neuronal overactivity contributes to enhanced hunger and food-seeking activity under these conditions.
Fat cells in abdomen can make
A rodent study indicates that fat cells within the abdomen produce neuropeptide Y, an appetite stimulant that was previously thought to originate only in the brain. Rats that are bred to be heavy around the middle produce substantially more neuropeptide Y in their belly-fat cells than thin rats. This excess neuropeptide Y stimulates the production of fat-cell precursors, which mature into full-fledged fat, creating a vicious cycle by which excess belly fat leads to more belly fat. The FASEB Journal, 2008.
The lateral hypothalamic area contains specific neuronal populations that affect feeding in different ways. Neurons expressing the appetite-stimulating peptide orexin A are stimulated by starvation (but not food restriction) and by hypoglycemia, but only if food is withheld. Orexin neurons are apparently activated by low glucose but are promptly inhibited by visceral feeding signals, probably mediated via vagal sensory pathway and the nucleus of the solitary tract; a short-term role in initiating feeding seems most likely.
Melanin concentrating hormone
Other lateral hypothalamic area neurons express melanin-concentrating hormone, which transiently increases food intake when injected centrally. Melanin concentrating hormone neurons may be regulated by leptin, insulin and glucose. Glucose-sensing neurons in the hypothalamus and elsewhere are sensitive to other cues of nutritional state, including visceral satiety signals (transmitted via the vagus) and orexin.
Neuroeptides and Appetite
During the past decade, a detailed understanding has emerged of the aminergic and peptidergic neural pathways present within the brain that regulate appetite. Central among the peptide regulators is neuropeptide Y (NPY), a potent orexigenic agent that acts through five different receptor subtypes.
A neuropeptide essential for wakefulness and appetite also appears to enhance the brain's appetite for cocaine. Drug addiction may be related to the neural circuits that control appetite. In studies with rats, orexin A, a neuro peptide produced in the lateral hypothalamus, strengthens the potential for addiction by enhancing synaptic connections between neurons in the lateral hypothalamus and dopaminergic neurons in the ventral tegmental area of the brain. This connection helps provide the "synaptic plasticity" important for full-fledged addiction.
Nutr Rev. 2013. Ghrelin, neuropeptide Y, and other feeding-regulatory peptides active in the hippocampus: role in learning and memory. The hippocampus is a brain region of primary importance for neurogenesis, which occurs during early developmental states as well as during adulthood. Increases in neuronal proliferation and in neuronal death with age have been associated with drastic changes in memory and learning. Numerous neurotransmitters are involved in these processes, and some neuropeptides that mediate neurogenesis also modulate feeding behavior. Concomitantly, feeding peptides, which act primarily in the hypothalamus, are also present in the hippocampus. This review aims to ascertain the role of several important feeding peptides in cognitive functions, either through their local synthesis in the hippocampus or through their actions via specific receptors in the hippocampus. A link between neurogenesis and the orexigenic or anorexigenic properties of feeding peptides is discussed.
Protection from chemotherapy
BMB Rep. 2016. Neuropeptide Y protects cisplatin-induced nephrotoxicity by regulating the p53-dependent apoptosis pathway. Cisplatin is a platinum-based chemotherapeutic drug used to treat various types of cancers. However, the use of cisplatin is limited by its negative effects on normal tissues, particularly nephrotoxicity. Various mechanisms, such as DNA adduct formation, mitochondrial dysfunction, oxidative stress, and apoptosis are critically involved in the adverse effects induced by cisplatin treatment. Several studies have suggested that neuropeptide Y (NPY) is involved in neuroprotection as well as restoration of bone marrow dysfunction from chemotherapy induced nerve injury. However, the role of NPY in chemotherapy-induced nephrotoxicity has not been studied. Here, we show that NPY rescues renal dysfunction by reducing the expression of pro-apoptotic proteins in cisplatin induced nephrotoxicity, and this effect is mediated by the Y1 receptor. Therefore, we suggest that NPY protects the kidney against cisplatin nephrotoxicity and may be a useful agent for preventing and treating cisplatin-induced nephrotoxicity.
I wonder if you have done any research on the Russian brain improving substance called "Semax", I have heard lots of it but it doesn't seem to come available to the western world.
According to one website, Semax is a neuropeptide developed from a short fragment of ACTH, Pro8-Gly9-Pro10 ACTH(4-10) and is a neuroactive peptide with unique neuroregulatory properties. I am not familiar with this product.