Growth Hormone Secretion, Serum, and Cerebral Spinal Fluid Insulin and Insulin-Like Growth Factor-l Concentrations in Pigs with Streptozotocin-Induced Diabetes Mellitus

C. R. Barb, N. M. Cox, C. A. Carlton, W. J. Chang, R. F. Randle

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Diabetes mellitus was induced using streptozotocin in five gilts between 8 and 12 weeks of age. Gilts were maintained with exogenous insulin (INS) except during experimental periods. Four litter-mate gilts served as controls. At 9 months of age, all gilts were ovariectomized, and 30 days after ovariectomy, Experiment (Exp) 1 was conducted. Jugular vein catheters were inserted and blood samples were collected every 10 min for 8 hr. Experiment 2 was conducted when gilts were 11 months of age. Venous blood and cerebrospinal fluid (CSF) samples were collected in the absence (Phase I) or presence (Phase II) of INS therapy. In Experiment 1, plasma glucose concentrations were greater (P < 0.05) in diabetic (465 × 17 mg/100 ml) than in control (82 mg × 17 mg/100 ml) gilts, whereas serum INS was lower (P < 0.0001) in diabetic gilts (0.3 × 0.02 vs 0.9 × 0.05 ng/ml) and insulin-like growth factor-l was similar in diabetic and control gilts (32 × 3 vs 43 × 4 ng/ml, respectively). Mean serum GH concentration was 2-fold greater (P < 0.02) in diabetics (2.8 × 0.4 ng/ml) than in control gilts (1.2 × 0.2 ng/ml). Diabetic gilts exhibited a greater (P < 0.05) number of GH pulses than control gilts (3.2 × 0.4 vs 1.5 × 0.3/8 hr, respectively). In addition, GH pulse magnitude was markedly elevated (P < 0.02) in diabetic (5.8 × 0.4 ng/ml) compared with control gilts (3.3 × 0.6 ng/ml). Mean basal serum GH concentrations were greater (P < 0.07) in diabetic (2.2 × 0.5 ng/ml) compared with control gilts (1.0 × .1 ng/ml). In Experiment 2, CSF concentrations of insulin-like growth factor-l, INS, GH, and protein were similar for diabetic and control gilts in both phases. Serum GH levels were similar for diabetics and controls in Phase I, but were greater (P < 0.05) in diabetics than in controls in Phase II. CSF glucose levels were greater in diabetic than in control gilts in both the presence (P < 0.003) and absence (P < 0.0002) of INS therapy, whereas plasma glucose was greater (P < 0.003) in diabetic than in control gilts in the absence of INS, but returned to control concentrations in the presence of INS. However, serum GH levels were unchanged after INS therapy in the diabetic gilts. In conclusion, altered GH secretion in the diabetic gilt may, in part, be due to elevated CSF glucose concentrations, which may alter GH-releasing hormone and/or somatostatin secretion from the hypothalamus.

Original languageEnglish (US)
Pages (from-to)223-228
Number of pages6
JournalProceedings of the Society for Experimental Biology and Medicine
Volume201
Issue number2
DOIs
StatePublished - Nov 1992

Fingerprint

Experimental Diabetes Mellitus
Somatomedins
Streptozocin
Medical problems
Growth Hormone
Diabetes Mellitus
Swine
Insulin
Fluids
Serum
Cerebrospinal Fluid
Cerebrospinal fluid
Glucose
Jugular Veins
Ovariectomy
Somatostatin
Blood
Experiments
Hypothalamus
Plasmas

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

@article{c183537c2a844d29814e275a6f100d2a,
title = "Growth Hormone Secretion, Serum, and Cerebral Spinal Fluid Insulin and Insulin-Like Growth Factor-l Concentrations in Pigs with Streptozotocin-Induced Diabetes Mellitus",
abstract = "Diabetes mellitus was induced using streptozotocin in five gilts between 8 and 12 weeks of age. Gilts were maintained with exogenous insulin (INS) except during experimental periods. Four litter-mate gilts served as controls. At 9 months of age, all gilts were ovariectomized, and 30 days after ovariectomy, Experiment (Exp) 1 was conducted. Jugular vein catheters were inserted and blood samples were collected every 10 min for 8 hr. Experiment 2 was conducted when gilts were 11 months of age. Venous blood and cerebrospinal fluid (CSF) samples were collected in the absence (Phase I) or presence (Phase II) of INS therapy. In Experiment 1, plasma glucose concentrations were greater (P < 0.05) in diabetic (465 × 17 mg/100 ml) than in control (82 mg × 17 mg/100 ml) gilts, whereas serum INS was lower (P < 0.0001) in diabetic gilts (0.3 × 0.02 vs 0.9 × 0.05 ng/ml) and insulin-like growth factor-l was similar in diabetic and control gilts (32 × 3 vs 43 × 4 ng/ml, respectively). Mean serum GH concentration was 2-fold greater (P < 0.02) in diabetics (2.8 × 0.4 ng/ml) than in control gilts (1.2 × 0.2 ng/ml). Diabetic gilts exhibited a greater (P < 0.05) number of GH pulses than control gilts (3.2 × 0.4 vs 1.5 × 0.3/8 hr, respectively). In addition, GH pulse magnitude was markedly elevated (P < 0.02) in diabetic (5.8 × 0.4 ng/ml) compared with control gilts (3.3 × 0.6 ng/ml). Mean basal serum GH concentrations were greater (P < 0.07) in diabetic (2.2 × 0.5 ng/ml) compared with control gilts (1.0 × .1 ng/ml). In Experiment 2, CSF concentrations of insulin-like growth factor-l, INS, GH, and protein were similar for diabetic and control gilts in both phases. Serum GH levels were similar for diabetics and controls in Phase I, but were greater (P < 0.05) in diabetics than in controls in Phase II. CSF glucose levels were greater in diabetic than in control gilts in both the presence (P < 0.003) and absence (P < 0.0002) of INS therapy, whereas plasma glucose was greater (P < 0.003) in diabetic than in control gilts in the absence of INS, but returned to control concentrations in the presence of INS. However, serum GH levels were unchanged after INS therapy in the diabetic gilts. In conclusion, altered GH secretion in the diabetic gilt may, in part, be due to elevated CSF glucose concentrations, which may alter GH-releasing hormone and/or somatostatin secretion from the hypothalamus.",
author = "Barb, {C. R.} and Cox, {N. M.} and Carlton, {C. A.} and Chang, {W. J.} and Randle, {R. F.}",
year = "1992",
month = "11",
doi = "10.3181/00379727-201-43503",
language = "English (US)",
volume = "201",
pages = "223--228",
journal = "Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)",
issn = "1535-3702",
publisher = "Society for Experimental Biology and Medicine",
number = "2",

}

TY - JOUR

T1 - Growth Hormone Secretion, Serum, and Cerebral Spinal Fluid Insulin and Insulin-Like Growth Factor-l Concentrations in Pigs with Streptozotocin-Induced Diabetes Mellitus

AU - Barb, C. R.

AU - Cox, N. M.

AU - Carlton, C. A.

AU - Chang, W. J.

AU - Randle, R. F.

PY - 1992/11

Y1 - 1992/11

N2 - Diabetes mellitus was induced using streptozotocin in five gilts between 8 and 12 weeks of age. Gilts were maintained with exogenous insulin (INS) except during experimental periods. Four litter-mate gilts served as controls. At 9 months of age, all gilts were ovariectomized, and 30 days after ovariectomy, Experiment (Exp) 1 was conducted. Jugular vein catheters were inserted and blood samples were collected every 10 min for 8 hr. Experiment 2 was conducted when gilts were 11 months of age. Venous blood and cerebrospinal fluid (CSF) samples were collected in the absence (Phase I) or presence (Phase II) of INS therapy. In Experiment 1, plasma glucose concentrations were greater (P < 0.05) in diabetic (465 × 17 mg/100 ml) than in control (82 mg × 17 mg/100 ml) gilts, whereas serum INS was lower (P < 0.0001) in diabetic gilts (0.3 × 0.02 vs 0.9 × 0.05 ng/ml) and insulin-like growth factor-l was similar in diabetic and control gilts (32 × 3 vs 43 × 4 ng/ml, respectively). Mean serum GH concentration was 2-fold greater (P < 0.02) in diabetics (2.8 × 0.4 ng/ml) than in control gilts (1.2 × 0.2 ng/ml). Diabetic gilts exhibited a greater (P < 0.05) number of GH pulses than control gilts (3.2 × 0.4 vs 1.5 × 0.3/8 hr, respectively). In addition, GH pulse magnitude was markedly elevated (P < 0.02) in diabetic (5.8 × 0.4 ng/ml) compared with control gilts (3.3 × 0.6 ng/ml). Mean basal serum GH concentrations were greater (P < 0.07) in diabetic (2.2 × 0.5 ng/ml) compared with control gilts (1.0 × .1 ng/ml). In Experiment 2, CSF concentrations of insulin-like growth factor-l, INS, GH, and protein were similar for diabetic and control gilts in both phases. Serum GH levels were similar for diabetics and controls in Phase I, but were greater (P < 0.05) in diabetics than in controls in Phase II. CSF glucose levels were greater in diabetic than in control gilts in both the presence (P < 0.003) and absence (P < 0.0002) of INS therapy, whereas plasma glucose was greater (P < 0.003) in diabetic than in control gilts in the absence of INS, but returned to control concentrations in the presence of INS. However, serum GH levels were unchanged after INS therapy in the diabetic gilts. In conclusion, altered GH secretion in the diabetic gilt may, in part, be due to elevated CSF glucose concentrations, which may alter GH-releasing hormone and/or somatostatin secretion from the hypothalamus.

AB - Diabetes mellitus was induced using streptozotocin in five gilts between 8 and 12 weeks of age. Gilts were maintained with exogenous insulin (INS) except during experimental periods. Four litter-mate gilts served as controls. At 9 months of age, all gilts were ovariectomized, and 30 days after ovariectomy, Experiment (Exp) 1 was conducted. Jugular vein catheters were inserted and blood samples were collected every 10 min for 8 hr. Experiment 2 was conducted when gilts were 11 months of age. Venous blood and cerebrospinal fluid (CSF) samples were collected in the absence (Phase I) or presence (Phase II) of INS therapy. In Experiment 1, plasma glucose concentrations were greater (P < 0.05) in diabetic (465 × 17 mg/100 ml) than in control (82 mg × 17 mg/100 ml) gilts, whereas serum INS was lower (P < 0.0001) in diabetic gilts (0.3 × 0.02 vs 0.9 × 0.05 ng/ml) and insulin-like growth factor-l was similar in diabetic and control gilts (32 × 3 vs 43 × 4 ng/ml, respectively). Mean serum GH concentration was 2-fold greater (P < 0.02) in diabetics (2.8 × 0.4 ng/ml) than in control gilts (1.2 × 0.2 ng/ml). Diabetic gilts exhibited a greater (P < 0.05) number of GH pulses than control gilts (3.2 × 0.4 vs 1.5 × 0.3/8 hr, respectively). In addition, GH pulse magnitude was markedly elevated (P < 0.02) in diabetic (5.8 × 0.4 ng/ml) compared with control gilts (3.3 × 0.6 ng/ml). Mean basal serum GH concentrations were greater (P < 0.07) in diabetic (2.2 × 0.5 ng/ml) compared with control gilts (1.0 × .1 ng/ml). In Experiment 2, CSF concentrations of insulin-like growth factor-l, INS, GH, and protein were similar for diabetic and control gilts in both phases. Serum GH levels were similar for diabetics and controls in Phase I, but were greater (P < 0.05) in diabetics than in controls in Phase II. CSF glucose levels were greater in diabetic than in control gilts in both the presence (P < 0.003) and absence (P < 0.0002) of INS therapy, whereas plasma glucose was greater (P < 0.003) in diabetic than in control gilts in the absence of INS, but returned to control concentrations in the presence of INS. However, serum GH levels were unchanged after INS therapy in the diabetic gilts. In conclusion, altered GH secretion in the diabetic gilt may, in part, be due to elevated CSF glucose concentrations, which may alter GH-releasing hormone and/or somatostatin secretion from the hypothalamus.

UR - http://www.scopus.com/inward/record.url?scp=0026673558&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026673558&partnerID=8YFLogxK

U2 - 10.3181/00379727-201-43503

DO - 10.3181/00379727-201-43503

M3 - Article

C2 - 1409737

AN - SCOPUS:0026673558

VL - 201

SP - 223

EP - 228

JO - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)

JF - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)

SN - 1535-3702

IS - 2

ER -