TY - JOUR
T1 - Mouse models of type 1 diabetes and their use in skeletal research
AU - Kalaitzoglou, Evangelia
AU - Fowlkes, John L
AU - Thrailkill, Kathryn M
N1 - Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.
PY - 2022/6/27
Y1 - 2022/6/27
N2 - PURPOSE OF REVIEW: In this review, we describe the three primary mouse models of insulin-deficiency diabetes that have been used to study the effects of type 1 diabetes (T1D) on skeletal outcomes. These models include streptozotocin (chemically)-induced diabetes, autoimmune-mediated diabetes (the nonobese diabetes mouse), and a mutation in the insulin gene (the Akita mouse). We then describe the skeletal findings and/or skeletal phenotypes that have been delineated using these models.RECENT FINDINGS: Humans with T1D have decreased bone mineral density and an increased risk for fragility fracture. Mouse models of insulin-deficiency diabetes (hereafter denoted as T1D) in many ways recapitulate these skeletal deficits. Utilizing techniques of microcomputed tomography, bone histomorphometry, biomechanical testing and fracture modeling, bone biomarker analysis, and Raman spectroscopy, mouse models of T1D have demonstrated abnormalities in bone mineralization, bone microarchitecture, osteoblast function, abnormal bone turnover, and diminished biomechanical properties of bone.SUMMARY: Mouse models have provided significant insights into the underlying mechanisms involved in the abnormalities of bone observed in T1D in humans. These translational models have provided targets and pathways that may be modifiable to prevent skeletal complications of T1D.
AB - PURPOSE OF REVIEW: In this review, we describe the three primary mouse models of insulin-deficiency diabetes that have been used to study the effects of type 1 diabetes (T1D) on skeletal outcomes. These models include streptozotocin (chemically)-induced diabetes, autoimmune-mediated diabetes (the nonobese diabetes mouse), and a mutation in the insulin gene (the Akita mouse). We then describe the skeletal findings and/or skeletal phenotypes that have been delineated using these models.RECENT FINDINGS: Humans with T1D have decreased bone mineral density and an increased risk for fragility fracture. Mouse models of insulin-deficiency diabetes (hereafter denoted as T1D) in many ways recapitulate these skeletal deficits. Utilizing techniques of microcomputed tomography, bone histomorphometry, biomechanical testing and fracture modeling, bone biomarker analysis, and Raman spectroscopy, mouse models of T1D have demonstrated abnormalities in bone mineralization, bone microarchitecture, osteoblast function, abnormal bone turnover, and diminished biomechanical properties of bone.SUMMARY: Mouse models have provided significant insights into the underlying mechanisms involved in the abnormalities of bone observed in T1D in humans. These translational models have provided targets and pathways that may be modifiable to prevent skeletal complications of T1D.
U2 - 10.1097/MED.0000000000000737
DO - 10.1097/MED.0000000000000737
M3 - Article
C2 - 35749285
SN - 1752-296X
JO - Current Opinion in Endocrinology, Diabetes and Obesity
JF - Current Opinion in Endocrinology, Diabetes and Obesity
ER -
