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Project

Metabolic fate of glucose in osteolineage cells in normal conditions and hyperglycemia.

Bone loss and bone fragility often lead to fractures which cause important morbidity. The current therapies halt further bone loss, but drugs increasing bone mass are scarce. Additional osteo-anabolic strategies are therefore needed. Hormones and growth factors can instruct osteolineage cells to proliferate and become matrix-producing osteoblasts, but this activation is only effective when sufficient nutrients are present. Osteoblasts are known to consume much glucose, but insight is lacking on how glucose is metabolized and which metabolic pathways support the anabolic responses of osteolineage cells. In addition, high glucose levels, as observed in diabetes mellitus, lead to bone fragility by incompletely understood mechanisms. Possibly, changes in the metabolic profile of osteolineage cells contribute to the bone pathology. Based on our preliminary data, we hypothesize that the way glucose is metabolized in osteolineage cells is critical for normal bone formation and may become disturbed by high glucose levels. We will thoroughly characterize glucose metabolism in osteolineage stages in normal and hyperglycemic conditions and prove its importance for bone homeostasis by a genetic approach in mice. The knowledge gathered from this project will hopefully improve our insight in the nutritional requirements of a bone anabolic response.

Date:1 Jan 2020 →  31 Dec 2023
Keywords:Bone loss, bone fragility, Metabolic fate of glucose, osteolineage cells, hyperglycemia
Disciplines:Musculo-skeletal systems, Medical biochemistry and metabolism not elsewhere classified, Metabolic diseases