TY - JOUR
T1 - Insulin and glucagon binding to isolated hepatocytes of egyptian sand rats (Psammomys obesus)
T2 - Evidence for an insulin receptor defect
AU - Mandarino, Lawrence
N1 - Funding Information:
Acknowledgements-The author gratefully acknowledges the technical assistance of B. Brick and J. King and valuable discussions with Dr J. E. Gerich and Dr P. H. Bennett. This work was supported in part by NIH Training Grant AM-7147-04, NIH contract NOI-AM-6-2206, and the Mayo Foundation.
PY - 1984
Y1 - 1984
N2 - 1. 1. To determine whether a defect in insulin bincling could contribute to insulin resistance in Egyptian sand rats (Psammomys obesus), insulin bincling to isolated hepatocytes from euglycemic sand rats was compared to that of normal Sprague-Dawley rats (Rattus norvegiens). Because of its potential importance in glucoregulation, glucagon bincling to hepatocytes from these species was also measured. 2. 2. Hepatocytes of sand rats exhibit an almost complete lack of insulin receptors compared to hepatocytes from Sprague-Dawley rats, whereas there are numerous high affinity glucagon binding sites on sand rat hepatocytes. 3. 3. The lack of insulin bincling to sand rat tissues is sufficient to entirely explain the insulin resistance seen in this species. Glucagon may be primarily responsible for glucose homeostasis in Psammomys obesus.
AB - 1. 1. To determine whether a defect in insulin bincling could contribute to insulin resistance in Egyptian sand rats (Psammomys obesus), insulin bincling to isolated hepatocytes from euglycemic sand rats was compared to that of normal Sprague-Dawley rats (Rattus norvegiens). Because of its potential importance in glucoregulation, glucagon bincling to hepatocytes from these species was also measured. 2. 2. Hepatocytes of sand rats exhibit an almost complete lack of insulin receptors compared to hepatocytes from Sprague-Dawley rats, whereas there are numerous high affinity glucagon binding sites on sand rat hepatocytes. 3. 3. The lack of insulin bincling to sand rat tissues is sufficient to entirely explain the insulin resistance seen in this species. Glucagon may be primarily responsible for glucose homeostasis in Psammomys obesus.
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U2 - 10.1016/0300-9629(84)90589-9
DO - 10.1016/0300-9629(84)90589-9
M3 - Article
C2 - 6147232
AN - SCOPUS:0021161572
SN - 0300-9629
VL - 78
SP - 519
EP - 523
JO - Comparative Biochemistry and Physiology -- Part A: Physiology
JF - Comparative Biochemistry and Physiology -- Part A: Physiology
IS - 3
ER -