PMID- 1846745
OWN - NLM
STAT- MEDLINE
DCOM- 19910308
LR  - 20181130
IS  - 1044-1549 (Print)
IS  - 1044-1549 (Linking)
VI  - 4
IP  - 2
DP  - 1991 Feb
TI  - Influence of streptozotocin-induced diabetes on adenylate cyclase activity in 
      cultured type II pneumocytes.
PG  - 108-14
AB  - Previous studies with cultured type II pneumocytes from streptozotocin-induced 
      diabetic rats demonstrated altered surfactant synthesis and secretion. The 
      effects of the diabetic state were reversed by in vivo but not in vitro insulin 
      treatment. In the current study, cultured type II pneumocytes from control and 
      streptozotocin-induced diabetic rats were demonstrated to possess approximately 
      17,500 and 8,500 receptors per cell, respectively. High-affinity binding sites 
      were determined to have a dissociation constant of 0.429 nM and 0.203 nM for 
      control and diabetic cells, respectively. Functional capacity of the insulin 
      receptors was determined by the initial rates of 2-deoxy-D-glucose uptake. Uptake 
      was stimulated by insulin in a dose-dependent manner and was not significantly 
      altered by the diabetic state. This would suggest that the insulin receptor was 
      present and functioning in cells isolated from diabetic rats. Basal adenylate 
      cyclase activity of type II cell homogenates from diabetic rats was shown to be 
      16% of that for controls. In addition, isoproterenol, guanosine 5'-triphosphate 
      (GTP), and NaF were unable to stimulate adenylate cyclase activity. However, 
      forskolin, which directly activates the catalytic subunit of adenylate cyclase, 
      was able to increase the cellular content of cyclic adenosine monophosphate 
      (cAMP) in this model. This would suggest that some step prior to adenylate 
      cyclase but not the catalytic subunit was altered by the diabetic state. But 
      forskolin was unable to restore surfactant secretion, suggesting that in addition 
      to adenylate cyclase, other processes are affected by the diabetic state. The 
      effects of the diabetic state on adenylate cyclase and surfactant secretion were 
      reversed by in vivo but not in vitro insulin treatment.
FAU - Brown, L A
AU  - Brown LA
AD  - Department of Pediatrics, Emory University, Atlanta, Georgia 30322.
LA  - eng
GR  - HL-38358/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
RN  - 0 (Insulin)
RN  - 0 (Pulmonary Surfactants)
RN  - 1F7A44V6OU (Colforsin)
RN  - 5W494URQ81 (Streptozocin)
RN  - 86-01-1 (Guanosine Triphosphate)
RN  - 8ZYQ1474W7 (Sodium Fluoride)
RN  - 9G2MP84A8W (Deoxyglucose)
RN  - E0399OZS9N (Cyclic AMP)
RN  - EC 2.7.10.1 (Receptor, Insulin)
RN  - EC 4.6.1.1 (Adenylyl Cyclases)
RN  - L628TT009W (Isoproterenol)
SB  - IM
MH  - Adenylyl Cyclases/*metabolism
MH  - Animals
MH  - Cells, Cultured
MH  - Colforsin/pharmacology
MH  - Cyclic AMP/metabolism
MH  - Deoxyglucose/metabolism
MH  - Diabetes Mellitus, Experimental/*enzymology/metabolism
MH  - Guanosine Triphosphate/metabolism
MH  - Insulin/pharmacology
MH  - Isoproterenol/pharmacology
MH  - Lung/*enzymology/pathology
MH  - Pulmonary Surfactants/metabolism
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Receptor, Insulin/metabolism
MH  - Sodium Fluoride/pharmacology
MH  - Streptozocin
EDAT- 1991/02/01 00:00
MHDA- 1991/02/01 00:01
CRDT- 1991/02/01 00:00
PHST- 1991/02/01 00:00 [pubmed]
PHST- 1991/02/01 00:01 [medline]
PHST- 1991/02/01 00:00 [entrez]
AID - 10.1165/ajrcmb/4.2.108 [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 1991 Feb;4(2):108-14. doi: 10.1165/ajrcmb/4.2.108.