Abstract
Insulin resistance, closely linked to inflammation, is recognized as a key factor in the onset and aggravation of diabetes, cardio-renal syndrome, hypertension, and obesity. In the renal proximal tubule, insulin resistance may increase renal sodium reabsorption, leading to hypertension, edema and sometimes heart failure. Recently some anti-diabetic agents have been shown to have effects on the transporters in renal proximal tubule. Because renal proximal tubule mediates about 70% of sodium reabsorption, it is quite important to clarify the function of renal proximal tubule under insulin resistance and inflammation.
Highlights
The relationship between inflammation and diabetes had been described long ago by the fact that anti-inflammatory drugs such as salicylates decrease blood glucose level [1]
These results suggest that the insulin/WNK-oxidative stress-responsive kinase-1 (OSR1)/ SPS1-related proline-alanine-rich kinase (SPAK)-Na+-Cl− cotransporter (NCC) system may play an important role in Na+ retention and hypertension, and may be another therapeutic target in hypertension associated with insulin resistance
We have discussed the relationship between insulin resistance and inflammation in the context of the onset of hypertension
Summary
The relationship between inflammation and diabetes had been described long ago by the fact that anti-inflammatory drugs such as salicylates decrease blood glucose level [1]. JNK pathway induces serine phosphorylation of insulin-related substrate (IRS-1) [8,9,10,11]. Phosphorylated IRS-1 itself induces insulin resistance by direct blocking of insulin signaling pathway through IRS-1 [10,11]. Duced insulin resistance and inflammation are promoted by JNK in macrophage [12]. The signals from proinflammatory factors such as TNF-α and interleukin (IL)-1, via IKKβ complex, activate NFκB complex. IKKβ/NFκB pathway is triggered by PI3K/AKT signaling [17,18,19]. These pathways inducing insulin resistance are triggered by such factors as TNF-α, IL-1, endoplasmic reticulum (ER) stress, oxidative stress, and lipids [1].
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