Failure of glucose to elicit a normal secretory response in fetal pancreatic beta cells results from glucose insensitivity of the ATP-regulated K+ channels.

• DOI: 10.1073/pnas.86.12.4505
• Publication Date: 2006-05-31T10:56:58Z
• Authors: P Rorsman; P Arkhammar; K Bokvist; C Hellerström; T Nilsson; M Welsh; N Welsh; P O Berggren
• Keywords: Carbohydrate Metabolism; BETA (programming language); Adenosine triphosphate

Fetal pancreatic beta cells demonstrate a deficient insulin release in response to glucose, but the underlying mechanism at cellular level is unknown. By using from 21-day fetal rats we made an attempt clarify mechanism(s) behind this reduced glucose response. In addition measuring release, metabolism, and ATP content, ATP-regulated K+ channels (G channels) voltage-activated Ca2+ currents were investigated with patch-clamp technique. It was thus demonstrated that not sensitive otherwise had similar characteristics as those of adult cells. Also, However, judged measurements both oxidation utilization, metabolism impaired addition, there no increase even when stimulated for 30 min. therefore concluded attenuated glucose-induced due immature resulting regulation ATP-sensitive channels. These findings may be relevant understanding stimulus-secretion coupling associated non-insulin-dependent diabetes.