Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic gastropathy is a term that encompasses a number of neuromuscular dysfunctions of the stomach, including abnormalities of gastric contractility, tone, and myoelectrical activity in patients with diabetes. These abnormalities range from tachygastrias to antral hypomotility and frank gastroparesis. Diabetic gastropathies may be acutely produced during hyperglycemia. Symptoms of chronic diabetic gastropathy include chronic nausea, vague epigastric discomfort, postprandial fullness, early satiety, and vomiting. Because these symptoms are nonspecific, other disorders such as mechanical obstruction of the gastrointestinal tract, gastroesophageal reflux disease, cholecystitis, pancreatitis, mesenteric ischemia, and drug effects should be considered. Neuromuscular abnormalities of the stomach may be assessed noninvasively with gastric emptying tests, electrogastrography, and ultrasound. Gastrokinetic agents such as metoclopramide, cisapride, domperidone, and erythromycin increase fundic or antral contractions and/or eradicate gastric dysrhythmias. Diet and glucose control also are important in the management of diabetic gastropathy. As the pathophysiology of diabetic gastropathy is better understood, more specific and improved treatments will evolve.
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PMID:Diabetic gastropathy: gastric neuromuscular dysfunction in diabetes mellitus: a review of symptoms, pathophysiology, and treatment. 1038 75

Diabetic neuropathy is a most-convoluted complication. Diabetic gastropathy, ulcers, diarrhea, and bladder dysfunction are the major peripheral neuropathies. Peripheral neuropathies have been the primary neuroscience focus of diabetes research. In contrast to the periphery, the brain is not usually thought to be a target of chronic diabetic complications. However, the impact of diabetes mellitus on the central nervous system has recently gained attention. It is well known that diabetes or hyperglycemia influences the sensitivity of laboratory animals to various pharmacological agents. An increased sensitivity of hyperglycemic or diabetic animals to barbiturates and a decreased sensitivity of D-amphetamine, p-chloroamphetamine, and carbon tetrachloride have been demonstrated. Furthermore, it was reported that mice and rats with streptozotocin-induced diabetes and spontaneously diabetic mice are significantly less sensitive than non-diabetic mice to the antinociceptive effect of morphine. However, little information is available regarding the mechanism responsible for these changes. It is well established that anxiety and depression are common in patients with diabetes. Moreover, diabetic animals showed significantly more anxiogenic activity than non-diabetic animals did. However, the mechanisms through which diabetes may contribute to the development of, or be a risk factor for, psychiatric disorders are not clear. We provide an overview of our current understanding of the effects of streptozotocin-induced diabetes on the opioid receptor and the benzodiazepine receptor.
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PMID:[Modifications of several pharmacological actions by diabetes: effects on the opioid receptor agonist and benzodiazepines]. 1237 65

Background Diabetic gastropathy is a complex neuromuscular dysfunction of the stomach that commonly occurs in diabetes mellitus. Diabetic patients often present with upper gastrointestinal symptoms, such as epigastric discomfort or pain. The aim of this study was to assess gastric sensation in streptozocin-induced diabetes mellitus (DM) rats and to determine the contribution of C-C motif chemokine receptor 2 (CCR2) signaling to gastric hyperalgesia. Results DM rats showed signs of neuropathy (cutaneous mechanical hyperalgesia) from two weeks after streptozocin administration until the end of the experiment. Accelerated solid gastric emptying was observed at two weeks after streptozocin administration compared to the controls. Intense gastric hyperalgesia also developed in DM rats at two weeks after streptozocin administration, which was significantly reduced after intrathecal administration of the CCR2 antagonist INCB3344. Immunochemical analysis indicated that CCR2 expression was substantially upregulated in small and medium-sized dorsal root ganglia neurons of DM rats, although the protein level of monocyte chemoattractant protein-1, the preferred ligand for CCR2, was not significantly different between the control and DM groups. Conclusions These data suggest that CCR2 activation in nociceptive dorsal root ganglia neurons plays a role in the pathogenesis of gastric hyperalgesia associated with diabetic gastropathy and that CCR2 antagonist may be a promising treatment for therapeutic intervention.
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PMID:CCR2 upregulation in DRG neurons plays a crucial role in gastric hyperalgesia associated with diabetic gastropathy. 2935 16