期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 106, 期 3, 页码 373-384出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI8273
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资金
- NIDA NIH HHS [K05 DA000074, DA-00266, P50 DA000266, DA-00074] Funding Source: Medline
- NIMH NIH HHS [F30 MH012545] Funding Source: Medline
Gastrointestinal dysfunction is common in diabetic patients. In genetic (nonobese diabetic) and toxin-elicited (streptozotocin) models of diabetes in mice, we demonstrate defects in gastric emptying and nonadrenergic, noncholinergic relaxation of pyloric muscle, which resemble defects in mice harboring a deletion of the neuronal nitric oxide synthase gene (nNOS). The diabetic mice manifest pronounced reduction ill pyloric nNOS protein and mRNA, The decline of nNOS in diabetic mice does not result from loss of myenteric neurons. nNOS expression and pyloric function are restored to normal levels by insulin treatment. Thus diabetic gastropathy in mice reflects an insulin-sensitive reversible loss of nNOS. In diabetic animals, delayed gastric emptying can be reversed with a phosphodiesterase inhibitor, sildenafil, These findings have implications for novel therapeutic approaches and may clarify the etiology of diabetic gastropathy.
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