Osteogenesis imperfecta (OI), commonly called "brittle bone disease", is a genetic disorder characterised by increased bone fragility and decreased bone density due to quantitative and/or qualitative abnormalities of type I collagen.
Also known as "brittle bone disease", osteogenesis imperfecta (OI) is a genetic disorder characterised by increased bone fragility and low bone mass density due to quantitative and/or qualitative abnormalities of type I collagen [1, 2].
Furthermore, we identified chromosomal abnormalities of type B1 for the first time.
Therefore, dietary UF can be regarded as a therapeutic agent to prevent some of the abnormalities of type 2 diabetes.
In addition, obesity exacerbates the metabolic abnormalities of type 2 diabetes, in particular, hyperglycemia, dyslipidemia, and hypertension (3).
The type III and IV OI children with documented structural abnormalities of type I collagen have significant abnormalities in pulmonary function which are independent of functional cardiac abnormalities.
Because of the complex underlying pathophysiology responsible for the metabolic abnormalities of type 2 diabetes, combination therapy may be required very early.
Therefore, muscle ATP turnover rates reflect prevailing substrate availability, and defects in mitochondrial function are unlikely to underlie and initiate the metabolic abnormalities of type 2 diabetes.
Many of these measures are abnormal in relatives of type 2 diabetes individuals, but it is not clear that any of these tests are adequately specific or sensitive to understand abnormalities of type 2 diabetes and pre-diabetes.
Roughly 40%to50%0% of patients with diabetes meet criteria for obesity [ 26, 46], and obesity is likely to exacerbate symptoms and metabolic abnormalities of type 2 diabetes, increase the risk of complications, and complicate the goal of achieving glycemic control [ 47- 50].
