Abstract
Background Type 2 diabetes is characterized by insulin resistance in various insulin target cells, such as hepatocytes, myoblasts and adipocytes [1]. The recent realization that the osteoblast is an insulin target cell involved in the control of whole-body glucose homeostasis [2] suggests the possibility that impaired insulin signaling in osteoblasts contributes to the development of type 2 diabetes.
Highlights
Type 2 diabetes is characterized by insulin resistance in various insulin target cells, such as hepatocytes, myoblasts and adipocytes [1]
Glucose metabolism and insulin sensitivity were determined by Glucose tolerance test (GTT) and Insulin tolerance tests (ITT)
Showing normal glucose metabolism when fed on normal diet, InsRosb+/- mice developed more severe insulin resistance in comparison to control mice fed the same high fat diet (HFD) as evidenced by higher levels of blood glucose and serum insulin, decreased ability to clear glucose in GTT and more resistance to insulin in ITT
Summary
Type 2 diabetes is characterized by insulin resistance in various insulin target cells, such as hepatocytes, myoblasts and adipocytes [1]. The recent realization that the osteoblast is an insulin target cell involved in the control of whole-body glucose homeostasis [2] suggests the possibility that impaired insulin signaling in osteoblasts contributes to the development of type 2 diabetes
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