Supplementary Table 1 and Supplementary Table 2

The abnormalities of gastrointestinal (GI) slow waves play key roles in the pathophysiology of diabetic gastroparesis that is highly prevent in type 2 diabetes (T2D). While relatively well-investigated in diabetic enteric neuropathy, abnormalities and progressive impairments of gastric slow waves (GSW) and duodenal slow waves (DSW) are under-investigated during the progression of T2D. The aim of this study was to explore alterations in GSW and DSW during the development of diabetes induced by high fat diet (HFD) followed with a low dose of streptozotocin (STZ). Weekly recordings of the slow waves from healthy, pre-diabetic to diabetes stages exhibited a progressively decreased percentage of normal slow waves (%NSW) starting after HFD feeding (pre-diabetic stage) in the fasting state and starting after STZ injection (diabetic stage) in the postprandial state. The postprandial increase in the power of slow waves observed in normal control rats was absent starting from 2 weeks after HFD and persisted after STZ. The mechanism might be attributed to both progressively increased blood glucose (BG) and the impaired autonomic function in view of the following results: 1) The %NSW was negatively correlated with the fasting BG; 2) During the oral glucose tolerance test, %NSW of DSW and BG exhibited a positive correlation in rats with HbA1C <5.0%, but a negative correlation in rats with HbA1C ≥ 5.0%; 3) In comparison with baseline (healthy stage) of the same cohort, plasma pancreatic polypeptide (PP, reflecting vagal activity) was progressively decreased whereas, plasma norepinephrine (NE, reflecting sympathetic activity) was progressively increased.