Açlık ve Tokluk Metabolizması
Özet
Besin alımı, bireyin metabolik durumuna ilişkin geri bildirimi merkezi sinir sistemine (MSS) ileten farklı organlar ve sistemler tarafından düzenlenir ve MSS tarafından kontrol edilir. Yemek yeme epizodlarının başlatılması, süresi (yemeğin sonlanması) ve zamanlaması (öğünler arasındaki süre), bilinçli ve bilinçsiz nöroendokrin süreçlere bağlıdır. Bu süreçlerin bir kısmı iç ortamdan (örneğin hormonal sinyaller), diğer kısmı ise çevreden gelen ve duyular (örneğin görme, koku, tat) aracılığıyla çözümlenen sinyallerden kaynaklanır. Bu düzenleme birbirine bağlı ancak farklı homeostatik ve hedonik yolakları içeren sistemlerden oluşur. Tokluk sinyalleri, kolesistokinin (CCK), glukagon benzeri peptid-1 (GLP-1), oksintomodulin (OXM), peptid YY (PYY) ve pankreatik peptit (PP) gibi peptidler ile adipoz dokudan leptin salınımı aracılığıyla düzenlenir ve hipotalamusun arkuat çekirdeğindeki (ARC) proopiomelanokortin (POMC) ve kokain ve amfetamin düzenlemeli transkript (CART) nöronlarını etkileyerek anoreksijenik mekanizmaları devreye sokar. Benzer şekilde açlık sinyalleri gastrointestinal sistemden salgılanan ghrelin hormonu ile ARC’deki Neuropeptid Y (NPY) ve Agouti-İlgili Peptid (AgRP) nöronlarının aktivasyonu aracılığıyla düzenlenir. Dahası, hipotalamusta biyojenik aminlerin de anoreksijenik ve oreksijenik etkileri bulunmaktadır. Açlık ve tokluk sinyalleri hem ödül odaklı hem de nöroendokrin mekanizmaları içerdiğinden bu sistemlerin etkileşimlerini ve birleştirilmesini inceleyen araştırmalar obezite ve bozuk yeme davranışlarının tedavisinde etkili olabilir.
Food intake is regulated by different organs and systems that transmit feedback to the central nervous system (CNS) regarding the individual's metabolic status, and is controlled by the CNS. The initiation, duration (termination of the meal), and timing (interval between meals) of eating episodes depend on conscious and unconscious neuroendocrine processes. Some of these processes originate from the internal environment (e.g. hormonal signals), while others originate from signals from the environment that are decoded through the senses (e.g. vision, smell, taste). This regulation consists of interconnected systems that include distinct homeostatic and hedonic pathways. Satiety signals are regulated by peptides such as cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), oxyntomodulin (OXM), peptide YY (PYY), and pancreatic peptide (PP) via leptin release from adipose tissue, and activate anorexigenic mechanisms by affecting proopiomelanocortin (POMC) and cocaine and amphetamine regulated transcript (CART) neurons in the arcuate nucleus (ARC) of the hypothalamus. Similarly, hunger signals are regulated by ghrelin hormone secreted from the gastrointestinal tract via activation of Neuropeptide Y (NPY) and Agouti-Related Peptide (AgRP) neurons in the ARC. Furthermore, biogenic amines in the hypothalamus also have anorexigenic and orexigenic effects. Because hunger and satiety signals involve both reward-driven and neuroendocrine mechanisms, research examining the interactions and integration of these systems may be effective in treating obesity and disordered eating behaviors.
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