透過您的圖書館登入
IP:18.221.236.119
  • 期刊
  • OpenAccess

Adaptation of Gastrointestinal Motility to Diabetes Mellitus

並列摘要


Gastrointestinal (GI) motility is defined by the movement of the digestive system and the transit of the contents within it. Delayed gastric emptying indicates the symptoms included nausea and vomiting, especially in diabetes mellitus (DM). Clinically, diabetic patients may experience upper GI symptoms such as epigastric fullness, nausea and heartburn, and lower GI symptoms such as constipation, diarrhea and fecal incontinence. Insulin-dependent diabetes mellitus patients showed more delayed gastric emptying than non-insulin-dependent diabetes mellitus patients. During insulin stimulation, the GI motility is changed and accelerated. In diabetic gastroparesis, motilin, incretins (glucagon-like peptide-1and glucose-dependent insulinotropic polypeptide) are also a group of GI hormones that cause an increase in the amount of insulin released from the beta cells and are discussed in the article. Ghrelin, secreted in hunger, is found chiefly from the oxyntic glands in the stomach and are often referred to as growth hormone secretagogues. It plays a much newer role in the development of metabolic syndrome as it modifies glucose as well as insulin metabolism, blood pressure levels, and adipogenesis in diabetes. The rapid gastric emptying may be due to the rising levels of ghrelin and growth hormone secretagogue receptor (GHSR) in the hypothalamus during early hyperglycemia. The duration of hyperglycemia is affected by the rising ratio of ghrelin/obestatin. Diabetic diarrea, celiac disease, as well as mechanic obstruction, were also general GI problems in hyperglycemia. Delayed gastric emptying of solids in diabetic patients with autonomic neuropathy was proven in our study, implying the gastric electrical stimulation improved the gastric motility in streptozotocin-induced diabetic rats. Clinically, prokinetic agents, including D2 receptor antagonist, motilin receptor agonists and 5-hydroxytryptamine receptor 4 receptor agonists, are generally used to improve the gastroparesis. We conclude that the mechanism between GI motility and DM may be related to the treatment of gastroparesis, the neuropathic disorders, and the roles of endocrine cell in diabetic gastroenteropathy. Further studies on the role of GHSR or some drugs for complications in clinical diabetes should be conducted.

並列關鍵字

GI motility DM gastroparesis neuropathic disorders ghrelin

延伸閱讀


  • 陳美芳、王瑞霞、洪敏南、林立人、黃啓泉、陳淑玲、邱慧卿(2010)。Convergence of the Diabetes Mellitus and Tuberculosis Epidemics內科學誌21(5),344-349。https://doi.org/10.6314/JIMT.2010.21(5).06
  • 張峰義、周明淵、蕭孟芳(1989)。Diabetes Mellitus and InfectionJournal of Medical Sciences10(1),1-6。https://www.airitilibrary.com/Article/Detail?DocID=10114564-198902-201308020003-201308020003-1-6
  • 鄭淑鎂(2014)。Cancer-associated Diabetes Mellitus中國鍼灸學雜誌2(1),145-154。https://doi.org/10.6528/CAMS.2014.0009
  • Migdalis, I., Leslie, D., Papanas, N., Valensi, P., & Vlassara, H. (2014). Diabetes Mellitus. International Journal of Endocrinology, 2014(), 47-52-005. https://doi.org/10.1155/2014/108419
  • 吳篤安(1995)。Genetics of Diabetes MellitusJournal of Medical Sciences16(2),73-82。https://www.airitilibrary.com/Article/Detail?DocID=10114564-199510-201306210003-201306210003-73-82