TY - JOUR
T1 - Diabetes-induced suppression of IGF-1 and its receptor mRNA levels in rat superior cervical ganglia
AU - Sami Bitar, Milad
AU - Pilcher, Charles W.T.
AU - Khan, Islam
AU - Waldbillig, Robert J.
PY - 1997/11/1
Y1 - 1997/11/1
N2 - Insulin-like growth factor-I (IGF-I) is implicated in the development, survival and maintenance of function of sympathetic and sensory neurons. These neurons are affected at an early stage during the course of diabetes. Reverse transcriptase polymerase chain reaction (RT-PCR) based assay revealed that rat superior cervical ganglia (SCG) express mRNA transcripts for IGF-I and its receptor. Moreover, specific membrane protein binding sites of IGF-I within the SCG have also been demonstrated using competition-inhibition and affinity cross-linking techniques. An induction of diabetes with streptozotocin (STZ, 55 mg/kg, i.v.) produced a marked decrease in the SCG levels of mRNA transcripts for IGF-I and its receptor. Concentrations of circulating IGF-I and its receptor protein within the SCG were also reduced in this disease state. Insulin treatment partially prevented diabetes- related alterations in circulating IGF-I and the SCG-IGF-I system. Overall, the data described in this study may be of value in understanding the pathogenetic mechanisms(s) responsible for the development of diabetic sympathetic neuropathy.
AB - Insulin-like growth factor-I (IGF-I) is implicated in the development, survival and maintenance of function of sympathetic and sensory neurons. These neurons are affected at an early stage during the course of diabetes. Reverse transcriptase polymerase chain reaction (RT-PCR) based assay revealed that rat superior cervical ganglia (SCG) express mRNA transcripts for IGF-I and its receptor. Moreover, specific membrane protein binding sites of IGF-I within the SCG have also been demonstrated using competition-inhibition and affinity cross-linking techniques. An induction of diabetes with streptozotocin (STZ, 55 mg/kg, i.v.) produced a marked decrease in the SCG levels of mRNA transcripts for IGF-I and its receptor. Concentrations of circulating IGF-I and its receptor protein within the SCG were also reduced in this disease state. Insulin treatment partially prevented diabetes- related alterations in circulating IGF-I and the SCG-IGF-I system. Overall, the data described in this study may be of value in understanding the pathogenetic mechanisms(s) responsible for the development of diabetic sympathetic neuropathy.
KW - Diabetes mellitus
KW - IGF-I
KW - IGF-I receptor
KW - Superior cervical ganglia
UR - http://www.scopus.com/inward/record.url?scp=0031418450&partnerID=8YFLogxK
U2 - 10.1016/S0168-8227(97)00077-6
DO - 10.1016/S0168-8227(97)00077-6
M3 - Article
C2 - 9483370
AN - SCOPUS:0031418450
VL - 38
SP - 73
EP - 80
JO - Diabetes Research and Clinical Practice
JF - Diabetes Research and Clinical Practice
SN - 0168-8227
IS - 2
ER -