Chronic exposure to elevated levels

Chronic exposure to elevated levels of glucose and free fatty acids (FFAs) causes β-cell dysfunction and may induce β-cell apoptosis in type 2 diabetes. Exposure to high glucose has dual effects, triggering initially “glucose hypersensitization” and later apoptosis, via different mechanisms. High glucose, however, does not induce or activate IL-1β, NF-κB, or inducible nitric oxide synthase in rat or human β-cells in vitro or in vivo in Psammomys obesus. FFAs may cause β-cell apoptosis via ER stress, which is NF-κB and NO independent. Thus, cytokines and nutrients trigger β-cell death by fundamentally different mechanisms, namely an NF-κB–dependent mechanism that culminates in caspase-3 activation for cytokines and an NF-κB–independent mechanism for nutrients. This argues against a unifying hypothesis for the mechanisms of β-cell death in type 1 and type 2 diabetes and suggests that different approaches will be required to prevent β-cell death in type 1 and type 2 diabetes.

Kết quả (Anh) 1:

Chronic exposure to elevated levels of glucose and free fatty acids (FFAs) causes β-cell dysfunction and may induce β-cell apoptosis in type 2 diabetes. Exposure to high glucose has dual effects, triggering initially "glucose hypersensitization" and later apoptosis, via different mechanisms. High glucose, however, does not induce or activate IL-1 β, NF-κB, or inducible nitric oxide synthase in rat or human β-cells in vitro or in vivo in Psammomys obesus. FFAs may cause β-cell apoptosis via the ER stress, which is NF-κB and NO independent. Thus, cytokines and β-cell death trigger nutrients by fundamentally different mechanisms, namely an NF-κB-dependent mechanism that culminates in caspase-3 activation for cytokines and an NF-κB-independent mechanism for nutrients. This argues against a unifying hypothesis for the mechanisms of β-cell death in type 1 and type 2 diabetes and suggests that different approaches will be required to prevent β-cell death in type 1 and type 2 diabetes.

Kết quả (Anh) 2:

Chronic exposure to elevated levels of glucose and free fatty acids (FFAs), β-cell dysfunction Causes induce β-cell and sew type 2 diabetes in apoptosis. Exposure to high glucose has dual effects, initially triggering "glucose hypersensitization" and later apoptosis, via khác Mechanisms. High glucose, Tuy nhiên, does not induce IL-1β or activate NF-κB, inducible nitric oxide synthase or in rat or human β-cells in vitro or in vivo in sand rat. FFAs β-cell apoptosis sewing cause, via ER stress, NF-κB mà independent and NO. Thì, cytokines and nutrients trigger β-cell death by fundamentally khác Mechanisms, NF-κB namely security-dependent mechanism in caspase-3 mà culminates for activation of NF-κB cytokines and an independent mechanism for nutrients-. This hypothesis argues với a Unifying for the Mechanisms of β-cell death in type 1 and type 2 diabetes and đề nghị khác mà Approaches to Prevent required sẽ β-cell death in type 1 and type 2 diabetes.