Abstract
A safe and effective approach is needed to prevent and reduce the incidence of diabetes worldwide. The hypoglycemic efficacy of salicylic acid (salsalate, SAL), which has anti-inflammatory properties, has been empirically demonstrated in studies conducted at the Joslin Diabetes Center and elsewhere. Here, we investigated the potential role of SAL in preventing the onset of diabetes in Zucker diabetic fatty (ZDF) rats and attempted to elucidate its underlying mechanisms. ZDF and Zucker lean (ZL) rats were administered a high-fat diet with or without SAL intervention, and their relative rates of diabetes were compared. Our results showed that all rats in the placebo group developed diabetes, whereas only 10% of the SAL-treated rats presented with impaired glucose tolerance (IGT). None of the latter progressed to diabetes. Relative to the untreated rats, SAL lowered plasma glucagon and insulin while improving insulin sensitivity and β-cell function. SAL may protect against hyperglycemia by increasing the microbial diversity, ameliorating gut dysbiosis, restoring intestinal epithelial cell connections, inhibiting endotoxin influx into the blood, and attenuating inflammation. Together, these findings suggest that SAL may be a candidate prophylactic therapy against diabetes. The protective role of SAL may be attributed to its ability to reduce intestinal inflammation and improve gut dysbiosis.
Highlights
According to International Diabetes Federation (IDF) data, as of 2017, there were 451 million people with diabetes worldwide
Zucker diabetic fatty (ZDF) rats had normal glucose tolerance at age 6 weeks but their blood glucose levels were comparatively higher at each measurement point than those of Zucker lean (ZL) rats (p > 0.05) (Figure 1C)
We calculated the ratios of rats with abnormal glucose tolerance to those with normal glucose tolerance based on oral glucose tolerance test (OGTT) results
Summary
According to International Diabetes Federation (IDF) data, as of 2017, there were 451 million people with diabetes worldwide. It was estimated that there are 374 million people with impaired glucose tolerance (IGT) who are at high risk of becoming diabetic (Cho et al, 2018). In “leaky gut syndrome”, dysbiosis may increase intestinal permeability, activate the innate immune system, modulate lipid and glucose metabolism, trigger low-grade inflammation, cause insulin resistance, and induce T2D (Sabatino et al, 2017). These findings have raised the hope of identifying anti-inflammatory agents that are valid therapeutic targets for T2D
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