Intestinal parasitic infection-induced intestinal wall cytoskeleton dysfunction in diabetes mellitus

Abstract

Background: The gastrointestinal tract (GIT) could harbor intestinal parasitic infections (IPIs) alongside a dense and diverse microbial community, termed GIT microbiome. We examined the role of IPI-related changes in intestinal echoanatomy in the pathophysiology of type 2 diabetes mellitus (T2DM). Methods: The study included 95 subjects (44 males and 51 females). The diagnosis was based on clinical presentation and laboratory tests, including serial stool microscopy for IPIs, and for diabetes, measurement of hemoglobin A1C, fasting or random blood glucose level, or oral glucose tolerance testing. The B-mode ultrasound grayscale and color images using a high-frequency phased array transducer of 7.5 MHz of the duodenum and colon were obtained with and without water contrast. The duodenal wall thickness was used as measurement endpoint. Results: Eighty consecutive patients had at least one type of IPIs in serial stool microscopy, and 15 were healthy persons. Among the 80 IPI patients, 52 (65%) were diabetic, and 28 (35%) patients were nondiabetic. We demonstrated normal duodenum and colon echoanatomy in healthy persons. In patients with IPIs, the duodenal wall thickness (6.87 ± 2.09 mm) was greater than that in healthy persons (3.5 ± 1.07 mm) (P < 0.001). In diabetic patients, the duodenal wall thickness (7.23 ± 2.1 mm) was greater than that in nondiabetic patients (5.26 ± 2.07 mm) (P < 0.001). There were main effects of age and obesity but not sex. Antiparasitic treatment of IPIs alongside antidiabetic drugs improved control of fasting blood sugar. Conclusion: Ultrasound duodenography and colonography demonstrated IPI-induced intestinal wall thickening with rearrangement of the cytoskeleton, causing malfunction of the glucose transporter system which resulted in T2DM.