Insulin-dependent diabetes mellitus decreases osteoblastogenesis associated with the inhibition of Wnt signaling through increased expression of Sost and Dkk1 and inhibition of Akt activation

Int J Mol Med. 2011 Sep;28(3):455-62. doi: 10.3892/ijmm.2011.697. Epub 2011 May 11.

Abstract

Insulin-dependent diabetes mellitus (IDDM) is known to be associated with an increased risk of osteopenia. However, the cellular and molecular mechanisms for IDDM-induced alterations of the bone are not well understood. The effects of IDDM on bone metabolism were investigated using rats rendered diabetic by an injection of streptozotocin (STZ). After 4 weeks, the diabetic rats exhibited bone loss, low levels of osteocalcin, insulin-like growth factor-I (IGF-I) and bone alkaline phosphatase (ALP) activity with normal levels of bone tartrate-resistant acid phosphatase (TRAP) and cathepsin K activity, and urinary excretion of deoxypyridinoline (Dpd). Histological analysis showed a decrease in the number of osteoblasts with a normal number of osteoclasts in the metaphysis of the proximal tibia. The decreased expression of ALP, osteoclacin and collagen mRNA was associated with a decrease in the expression of runt-related transcription factor 2 (Runx2), Osterix and distal-less homeobox 5 (Dlx5) and an unaltered expression of bone morphogenic protein-2 (BMP2). The protein levels of Runx2, phosphorylated glycogen synthase kinase 3β (GSK3β), active β-catenin and β-catenin decreased. The activation of Akt was inhibited. The mRNA and protein levels of sclerosteosis (Sost) and Dickkopf 1 (Dkk1), inhibitors of Wnt signaling, increased. The mRNA expression of IGF-I and the IGF-I receptor (IGF-IR) was suppressed. These changes observed in the bone of diabetic rats were reversed by treatment with insulin, but not by normalization of the circulating IGF-I levels by treatment with IGF-I. These results suggest that insulin-deficiency in IDDM decreases osteoblastogenesis associated with inhibition of Wnt signaling through the increased expression of Sost and Dkk1 and the inhibition of Akt activation.

MeSH terms

  • Acid Phosphatase / metabolism
  • Alkaline Phosphatase / metabolism
  • Amino Acids / urine
  • Animals
  • Bone Morphogenetic Protein 2 / genetics
  • Bone Morphogenetic Protein 2 / metabolism
  • Bone Morphogenetic Proteins / genetics*
  • Bone Morphogenetic Proteins / metabolism
  • Cathepsin K / metabolism
  • Core Binding Factor Alpha 1 Subunit / genetics
  • Core Binding Factor Alpha 1 Subunit / metabolism
  • Diabetes Mellitus, Experimental / metabolism
  • Diabetes Mellitus, Type 1 / metabolism*
  • Female
  • Genetic Markers / genetics*
  • Glycogen Synthase Kinase 3
  • Glycogen Synthase Kinase 3 beta
  • Homeodomain Proteins / genetics
  • Homeodomain Proteins / metabolism
  • Insulin-Like Growth Factor I / metabolism
  • Intercellular Signaling Peptides and Proteins / genetics*
  • Intercellular Signaling Peptides and Proteins / metabolism
  • Isoenzymes / metabolism
  • Osteoblasts / cytology
  • Osteoblasts / metabolism
  • Osteocalcin / metabolism
  • Proto-Oncogene Proteins c-akt / antagonists & inhibitors
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Rats
  • Rats, Wistar
  • Signal Transduction
  • Tartrate-Resistant Acid Phosphatase
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Wnt Proteins / antagonists & inhibitors
  • Wnt Proteins / metabolism*
  • beta Catenin / metabolism

Substances

  • Amino Acids
  • Bmp2 protein, rat
  • Bone Morphogenetic Protein 2
  • Bone Morphogenetic Proteins
  • Core Binding Factor Alpha 1 Subunit
  • Distal-less homeobox proteins
  • Dkk1 protein, rat
  • Genetic Markers
  • Homeodomain Proteins
  • Intercellular Signaling Peptides and Proteins
  • Isoenzymes
  • Runx2 protein, rat
  • Sost protein, rat
  • Transcription Factors
  • Wnt Proteins
  • beta Catenin
  • Osteocalcin
  • Insulin-Like Growth Factor I
  • deoxypyridinoline
  • Glycogen Synthase Kinase 3 beta
  • Gsk3b protein, rat
  • Proto-Oncogene Proteins c-akt
  • Glycogen Synthase Kinase 3
  • Alkaline Phosphatase
  • Acid Phosphatase
  • Tartrate-Resistant Acid Phosphatase
  • Cathepsin K