Abstract
BackgroundGastroparesis is a recognized complication of diabetes but its pathogenic mechanism incompletely understood. Our aim was to determine whether HIF-1α and VEGF are secreted from gastric tissue is a fundamental factor that drives diabetic gastroparesis.MethodsDiabetes was induced in Sprague-Dawley by a single intraperitoneal injection of 65 mg/kg streptozotocin. After 4 and 12 weeks, rats were euthanized for assaying body weight, blood glucose, gastric acid secretion and gastric emptying. Morphologic changes in gastric mucosa were observed by the light microscope. Expression of HIF-1α and VEGF were assessed using immunohistochemistry, RT-PCR and Western blot analyses.ResultsCompared with control group, blood glucose were significantly increased and body weight were markedly decreased in streptozotocin-induced diabetes. Gastric emptying was significantly decreased in diabetic rats compared to the control group at different times. The number of parietal cells was obviously decreased, and vacuolated degeneration in diabetic rats. Gastric acid secretion in diabetic group was significantly decreased, and expression of HIF-1α and VEGF were significantly increased in the diabetic group.ConclusionThese results indicated that overexpression of HIF-1α and VEGF in the gastric mucosa and played a pivotal role in the progression of diabetic gastroparesis.
Highlights
Gastroparesis is a recognized complication of diabetes but its pathogenic mechanism incompletely understood
Type 1 diabetes mellitus (T1DM) patient had more serious gastric emptying delays [2] lead to unsatisfactory glycemic control [3] and may be the first sign that the patient is developing gastroparesis
Blood glucose, gastric acid secretion and gastric emptying in STZ-induced DM rats In diabetic rats, markedly decreased in body weight at the end of weeks 4 and 12 was observed compared with the control group (Fig. 1a)
Summary
Gastroparesis is a recognized complication of diabetes but its pathogenic mechanism incompletely understood. Our aim was to determine whether HIF-1α and VEGF are secreted from gastric tissue is a fundamental factor that drives diabetic gastroparesis. Diabetic gastroparesis (DGP) is a chronic and potential complication of diabetes [1]. The pathophysiology of DGP is a complex and multifactorial and remains to be determined, several studies suggested that DGP is associated with hyperglycemia, changes in gastrointestinal hormones, and microvascular lesions [4]. Parietal cells are an established source of secreted acid and appear to be key regulators of gastric gland homeostasis. Parietal cells are play an important act in maintaining the normal structure and function of gastric mucosa, and play a major role in regulating gastrointestinal motility [5]. Chronic DM leads to marked changes in gastrointestinal function, decreased
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