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Abstract Background: Intestinal dysmotility in type 2 diabetes mellitus (T2DM) may involve impaired cholinergic and incretin-mediated regulation

The pivotal role of central dysfunctional, insulin-resistant adipose tissue to the evolution of advanced fibrosis in patients with T2D and NAFLD, beyond body mass index (BMI) or steatosis, has been well established [5]

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These effects on digestive motility mean that intestinal contents move more slowly, potentially allowing more time for bacterial metabolism of sulfur compounds