Two weeks of high glucose intake is enough to induce intestinal mucosal damage and disturb the balance of the gut microbiota of rats.

Abstract

High glucose plays a critical role in diabetes. However, the point when high glucose induces diabetes and the organ that triggers the initiation of diabetes remain to be elucidated. The aim of the present study was to clarify the damage induced on different organs of rats, when administered a 2-week infusion of dietary glucose. SD rats (12 weeks old) were randomly divided into normal diet, high glucose infusion (IHG) and oral high glucose (OHG) groups. The levels of fasting blood sugar, tumor necrosis factor (TNF)-α and interleukin (IL)-6 were assessed. Intestine, kidney and liver samples were collected for pathological examination. Feces were collected from the rats for gut microbiota assessment. The results indicated that short-term high glucose induced hyperglycemia that lasted for at least 2 weeks after cessation of high glucose intake. Short-term high glucose also clearly increased the serum levels of IL-6 and TNF-α, led to jejunum mucosa injury and obvious steatosis in hepatocytes, and disturbed the balance of the gut microbiota. OHG led to swelling and necrosis of individual intestinal villi. IHG led to the necrosis and disappearance of cells in the upper layer of the intestinal mucosa. The lesions were confined to the mucosa. A degree of glomerular cell swelling and apoptosis were also observed. Short-term high glucose intake induced lesions in the liver, kidney and intestine, disturbed the balance of the gut microbiota and may consequently induce diabetes complications.