Diabetesa gaixotasun inflamatorio gisa

Abstract

Diabetesa gaixotasun kronikoa da, prebalentzia handikoa, zeinetan pankreak ez duen behar adina intsulina sortzen edo organismoak sortzen duen intsulina ez duen eraginkortasunez erabiltzen. Kontrolatu gabeko diabetesaren ondorioa hipergluzemia da, denborarekin organo eta sistema asko larriki kaltetzen dituena, nerbioak eta odol-hodiak batez ere. 2 motako diabetesa (DT2) diabetes motarik ohikoena da, non ehunek ez dioten intsulinari eraginkortasunez erantzuten. Egoera horri intsulinarekiko erresistentzia deritzo. Obesitatea, munduko asaldura metabolikorik ohikoena da, eta DT2 garatzeko arrisku-faktore nagusienetako bat. Obesitatea diabetesarekin lotzen duten mekanismoak oraindik argi ez badaude ere, azken urteotan hanturak indarra hartu du funtsezko faktore gisa. Paziente diabetikoek zitokina proinflamatorioen maila altuak dituzte, eta horrek gradu baxuko hantura kroniko orokortua eragiten du, gantz-ehunean sortzen duena. Hantura kroniko horrek alterazioak eragiten ditu intsulinaren seinaleztapen-jauzian eta, ondorioz, intsulinarekiko erresistentzia eta hipergluzemia dakar. Gaur egungo tratamenduaren helburu nagusia gluzemia normalizatzea da, farmako hipogluzemiatzaileen bidez. Hala ere, sistema immunearen modulazioak, TNF-α eta IL-b bezalako zitokinen blokeoaren bidez, medikamentuak garatzeko aukera berri interesgarriak irekitzen ditu.; Diabetes is a chronic, highly prevalent disease that occurs when the pancreas does not produce enough insulin or does not effectively use the insulin it produces. The effect of uncontrolled diabetes is hyperglycemia, which over time severely damages many organs and systems, especially nerves and blood vessels. Type 2 diabetes is the most common type of diabetes, in which the tissues do not respond effectively to insulin, a condition known as insulin resistance. Obesity is the most common metabolic disorder in the world and is one of the main risk factors for the development of T2DM. Although the mechanisms linking obesity and diabetes are still unclear, inflammation has emerged in the last years as a key factor. Diabetic patients have high levels of pro-inflammatory cytokines, originating in adipose tissue, leading to chronic generalized low-grade inflammation. This chronic inflammation causes alterations in insulin signaling, leading to insulin resistance and hyperglycemia. Although the main goal of current treatment is to normalize glycaemia withhypoglycemic drugs, modulation of the immune system, by blocking cytokines such as TNF-α or IL-1β, is an interesting therapeutic target that may open up new possibilities for drug development.