Failure of glucose to elicit a normal secretory response in fetal pancreatic beta cells results from glucose insensitivity of the ATP-regulated K+ channels.
Fetal pancreatic beta cells demonstrate a deficient insulin release in response to glucose, but the underlying mechanism at the cellular level is unknown. By using beta cells from 21-day fetal rats we made an attempt to clarify the mechanism(s) behind this reduced glucose response. In addition to me...
Prif Awduron: | Rorsman, P, Arkhammar, P, Bokvist, K, Hellerström, C, Nilsson, T, Welsh, M, Welsh, N, Berggren, P |
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Fformat: | Journal article |
Iaith: | English |
Cyhoeddwyd: |
1989
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Eitemau Tebyg
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DEFECTIVE REGULATION OF GLUCOSE-REGULATED AND ATP-REGULATED K-CHANNELS RESULTS IN DISTURBED GLUCOSE SENSITIVITY IN FETAL B-CELLS
gan: Rorsman, P, et al.
Cyhoeddwyd: (1988) -
GLUCOSE DOES NOT BLOCK ATP-REGULATED K+-CHANNEL ACTIVITY IN FETAL B-CELLS
gan: Welsh, M, et al.
Cyhoeddwyd: (1987) -
Direct evidence for opposite effects of D-glucose and D-glyceraldehyde on cytoplasmic pH of mouse pancreatic beta-cells.
gan: Arkhammar, P, et al.
Cyhoeddwyd: (1986) -
Glucose-induced increase in cytoplasmic pH in pancreatic beta-cells is mediated by Na+/H+ exchange, an effect not dependent on protein kinase C.
gan: Juntti-Berggren, L, et al.
Cyhoeddwyd: (1991) -
Inhibition of ATP-regulated K+ channels precedes depolarization-induced increase in cytoplasmic free Ca2+ concentration in pancreatic beta-cells.
gan: Arkhammar, P, et al.
Cyhoeddwyd: (1987)