Diyabetin Patofizyolojisi
Özet
Diabetes mellitus (DM), insülin üretiminin veya etkisinin azalmasıyla gelişen, karbonhidrat, yağ ve protein metabolizmasını bozan kronik bir hastalıktır. En yaygın türü olan tip 2 diyabet (T2DM); insülin direnci, yetersiz insülin salgılanması, inkretin hormon defekti, karaciğerde glikoz üretiminin artması ve lipit metabolizması bozuklukları gibi çoklu mekanizmalarla ortaya çıkar. İnsülin direnci nedeniyle glikoz hücre içine giremez ve hücre içi hipoglisemi gelişirken, pankreas bu durumu kompanse etmek için aşırı çalışarak zamanla beta hücre işlevini kaybeder. Tip 1 diyabette ise beta hücrelerinde otoimmün hasar sonucu mutlak bir insülin eksikliği söz konusudur. T2DM hastalarında inkretin etkisi bozulmakta, insülin sinyallerinin baskılanamaması nedeniyle karaciğerde glikoz üretimi artmakta ve serbest yağ asitlerinin yükselmesiyle dislipidemi tablosu tetiklenmektedir. Bu lipit değişiklikleri hastaların kardiyovasküler riskini artırdığı için hayati önem taşır. Tedavi edilmediğinde yaşam kalitesini düşüren bu kronik süreçte, sağlıklı beslenme, düzenli egzersiz ve yaşam tarzı değişiklikleri patolojik oluşumları engellemede en kritik başarı faktörleridir.
Diabetes mellitus (DM) is a chronic disease characterized by impaired carbohydrate, lipid, and protein metabolism due to a deficiency or reduced effectiveness of insulin production. Type 2 diabetes (T2DM), the most prevalent form, arises through multiple mechanisms including insulin resistance, inadequate insulin secretion, incretin hormone defects, increased hepatic glucose production, and lipid metabolism disorders. Due to insulin resistance, glucose cannot enter the cells, leading to intracellular hypoglycemia, while the pancreas overworks to compensate, eventually exhausting beta-cell function over time. In type 1 diabetes, however, an absolute insulin deficiency occurs as a result of autoimmune destruction of beta cells. In T2DM patients, the incretin effect is impaired, hepatic glucose production increases because insulin signaling cannot be suppressed, and elevated free fatty acids trigger dyslipidemia. These lipid alterations are vital as they increase the cardiovascular risk of patients. In this chronic process that reduces quality of life if left untreated, healthy nutrition, regular exercise, and lifestyle modifications are the most critical success factors in preventing pathological outcomes.
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