Also the role of hypothalamic peptides in food intake control and energy consumption has recently received greater attention. In particular, the so called aminostatic mechanism has been widely accepted, highlighting the close relationship between the serotoninergic system and feeding behaviour, thus allowing an effective therapeutic approach to some clinical conditions. A great number of clinical and experimental studies have brought to light many scarcely known aspects of feeding behaviour, showing the essential neuropeptide and neurotransmitter role. The development of new theoretical models has rendered problems more complex, especially in relation to etiopathogenesis, nosographic classification and to therapeutic strategies. Recently, researchers have invested greater interest in studies concerning body-weight, appetite, and feeding behaviour illnesses. Indeed, some enzymes (such as fructose-1,6-bisphosphase and protease inhibitor), gut hormones and brain are involved in the perturbation of appetite and body weight. This review discusses the biochemical mechanisms involved in the regulation of appetite and body weight, and explores a suite of well characterized and intensely investigated enzymes, anorexigenic and orexigenic gut hormones, and their appetite-regulating capabilities. With this realization has come increased effort to understand the intricate interplay between enzymes, gut hormones (such as ghrelin, leptin, cholecystokinin, neuropeptide Y, glucagon-like peptide 1 etc.) and the central nervous system, and their roles in food intake regulation through appetite modulation. To regulate food intake, the brain must alter appetite. It is well known that physical activity and food intake regulation are the two most important factors involved in body weight control. As the obesity prevalence approaches epidemic proportions, the necessity to unravel the mechanisms regulating appetite and weight gain have garnered significant attention. Among current treatments, gastrointestinal (GI) surgery remains the only approach capable of achieving significant weight loss results with long-term sustainability. As is generally true for the development of therapeutics for substance use disorder, there are multiple preclinically promising specific compounds against (meth)amphetamine, for which further development and clinical trials are badly needed.Īmphetamine use disorder Catecholamine Dopamine Monoamine transporter Neurotransmitter release Protein kinase.The overwhelming increase in the prevalence of overweight and obesity in recent years represents one of the greatest threats to the health of the developed world and part of the developing world. Thus, treatments are discussed that target DAT, VMAT2, PKC, CaMKII, and OCT3. The second part deals with requirements in amphetamine's effect on the kinases PKC, CaMKII, and ERK, whereas the third part focuses on where we are in developing anti-amphetamine therapeutics. In the first part of this review, the interaction of amphetamine with the dopamine transporter (DAT), crucially involved in its behavioral effects, is covered, as well as the role of dopamine synthesis, the vesicular monoamine transporter VMAT2, and organic cation 3 transporter (OCT3). There is a plethora of amphetamine derivatives exerting stimulant, euphoric, anti-fatigue, and hallucinogenic effects all structural properties allowing these effects are contained within the amphetamine structure.
0 Comments
Leave a Reply. |