Fruktozla oluşturulan metabolik sendromda renin-anjiyotensin sistemi

Abstract

Fruktozun işlenmiş gıdalarda yaygın olarak kullanılması insülin direnci, abdominal obezite, hipertrigliseridemi ve hipertansiyon ile karakterize olan metabolik sendromun artmasına neden olmaktadır. Fruktozla oluşturulan metabolik sendrom tip 2 diyabet, kardiyovasküler hastalıklar ve alkole bağlı olmayan yağlı karaciğer hastalığı (NAFLD) gibi çeşitli hastalıklara zemin hazırlamaktadır. Renin-anjiyotensin sistemi (RAS), kan basıncının düzenlenmesi, sıvı-elektrolit homeostazı, hücre büyümesi ve glikoz homeostazı üzerinde önemli rollere sahiptir. Renin ve anjiyotensin dönüştürücü enzim (ACE) tarafından anjiyotensinojenden türetilen anjiyotensin I (Agt I) ve anjiyotensin II (Agt II), RAS'ın temel bileşenleridir. Deneysel ve klinik çalışmalar, aşırı fruktoz tüketiminin RAS aktivasyonunu artırdığını göstermiştir. Fruktozla oluşturulan metabolik sendromda artan Agt II, insülin sinyal yolunu bozarak insülin direncini başlatmakta ve böylece tip 2 diyabet, hipertansiyon ve NAFLD'e zemin hazırlamaktadır. Anjiyotensin dönüştürücü enzim 2 (ACE2) tarafından Agt II'den oluşturulan anjiyotensin 1-7 (Agt 1-7), insülin direnci ve hepatik yağ birikimi üzerinde düzenleyici etkilerin yanı sıra Agt II'ye karşı dengeleyici etkilere sahiptir.

Keywords

• fruktoz
• metabolik sendrom
• insulin direnci
• renin-anjiyotensin sistemi

The renin-angiotensin system in fructose-induced metabolic syndrome

Abstract

The widespread use of fructose in processed foods is accepted to cause an increase in metabolic syndrome characterized by insulin resistance, abdominal obesity, hypertriglyceridemia, and hypertension. Fructose-induced metabolic syndrome is also associated with various diseases such as type 2 diabetes, cardiovascular diseases, and non-alcoholic fatty liver disease (NAFLD). The renin-angiotensin system (RAS) has essential roles in blood pressure regulation, fluid-electrolyte homeostasis, cell growth, and glucose homeostasis. Angiotensin I (Agt I) and angiotensin II (Agt II), which are derived from angiotensinogen by renin and angiotensin-converting enzyme (ACE), respectively, are essential players of RAS. Experimental and clinical studies showed that excessive fructose consumption causes activation in RAS. Increased Agt II in fructose-induced metabolic syndrome initiates insulin resistance by disrupting the insulin signaling pathway and thus predisposes to type 2 diabetes, hypertension and NAFLD. Angiotensin 1-7 (Agt 1-7), which is formed from Agt II by angiotensin-converting enzyme 2 (ACE2) has contra-balancing effects to Agt II as well as regulatory effects on insulin resistance and hepatic fat accumulation.

Keywords

• fructose
• metabolic syndrome
• insulin resistance
• renin-angiotensin system

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