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Am J Physiol Endocrinol Metab 283: E937-E945, 2002; doi:10.1152/ajpendo.00014.2002
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Vol. 283, Issue 5, E937-E945, November 2002

Impaired glucose homeostasis in insulin-like growth factor-binding protein-3-transgenic mice

Josef V. Silha1, Yaoting Gui1, and Liam J. Murphy1,2

1 Departments of Physiology and 2 Internal Medicine, University of Manitoba, Winnipeg R3E 0W3, Canada

Glucose homeostasis was examined in male transgenic (Tg) mice that overexpressed the human insulin-like growth factor (IGF)-binding protein (IGFBP)-3 cDNA, driven by either the cytomegalovirus (CMV) or the phosphoglycerate kinase (PGK) promoter. The Tg mice of both lineages demonstrated increased serum levels of human (h) IGFBP-3 and total IGF-I compared with wild-type (Wt) mice. Fasting blood glucose levels were significantly elevated in 8-wk-old CMV-binding protein (CMVBP)-3- and PGK binding protein (PGKBP)-3-Tg mice compared with Wt mice: 6.35 ± 0.22 and 5.22 ± 0.39 vs. 3.99 ± 0.26 mmol/l, respectively. Plasma insulin was significantly elevated only in CMVBP-3-Tg mice. The responses to a glucose challenge were significantly increased in both Tg strains: area under the glucose curve = 1,824 ± 65 and 1,910 ± 115 vs. 1,590 ± 67 mmol · l-1 · min for CMVBP-3, PGKBP-3, and Wt mice, respectively. The hypoglycemic effects of insulin and IGF-I were significantly attenuated in Tg mice compared with Wt mice. There were no differences in adipose tissue resistin, retinoid X receptor-alpha , or peroxisome proliferator-activated receptor-gamma mRNA levels between Tg and Wt mice. Uptake of 2-deoxyglucose was reduced in muscle and adipose tissue from Tg mice compared with Wt mice. These data demonstrate that overexpression of hIGFBP-3 results in fasting hyperglycemia, impaired glucose tolerance, and insulin resistance.

insulin resistance; diabetes; resistin; peroxisome proliferator-activated receptor-gamma


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