Abstract
OBJECTIVE:To test whether swimming training benefits femoral neck strength in young diabetic rats under insulin therapy.METHODS:A total of 60 male Wistar rats (age: 40 days) were divided equally into the following six groups: control sedentary, control exercise, diabetic sedentary, diabetic exercise, diabetic sedentary plus insulin and diabetic exercise plus insulin. Diabetes was induced with a unique intraperitoneal injection (60 mg/kg body weight) of streptozotocin. Seven days after the injection and after 12 hours of fasting, the animals with blood glucose levels ≥300 mg/dL were considered diabetic. Seven days after the induction of diabetes, the animals in the exercise groups were subjected to progressive swimming training (final week: 90 min/day; 5 days/week; 5% load) for eight weeks. The animals in the insulin groups received a daily dose of insulin (2-4 U/day) for the same period.RESULTS:Severe streptozotocin-induced diabetes reduced the structural properties of the femoral neck (trabecular bone volume, trabecular thickness and collagen fiber content). The femoral neck mechanical properties (maximum load and tenacity) were also impaired in the diabetic rats. Insulin therapy partially reversed the damage induced by diabetes on the structural properties of the bone and mitigated the reductions in the mechanical properties of the bone. The combination of therapies further increased the femoral neck trabecular bone volume (∼30%), trabecular thickness (∼24%), collagen type I (∼19%) and type III (∼13%) fiber contents, maximum load (∼25%) and tenacity (∼14%).CONCLUSIONS:Eight weeks of swimming training potentiates the recovery of femoral neck strength in young rats with severe streptozotocin-induced diabetes under insulin therapy.
Highlights
The risk of high hip fracture in people with type 1 diabetes mellitus (T1DM) is thought to be caused by poorer bone quality, which is related to impaired bone structure and tissue integrity [1,2,3]
Insulin therapy partially restored the BWs of the diabetic rats, and the difference in BW between the diabetic insulin-treated rats and nontreated rats was significant from week 7 on
The diminished secretion and/or action of insulin, which is associated with the formation of advanced glycation end-products (AGEs) induced by oxidative stress and hyperglycemia, debilitates new bone formation by decreasing osteoblast activity and increasing osteoclast activity, reducing bone mass [21,22]
Summary
The risk of high hip fracture in people with type 1 diabetes mellitus (T1DM) is thought to be caused by poorer bone quality, which is related to impaired bone structure and tissue integrity [1,2,3]. Received for publication on June 22, 2018. Accepted for publication on January 9, 2019. Poor bone quality has been reported in adolescents with T1DM [8] and in a young rat model of streptozotocin (STZ)-induced diabetes; the characteristics of poor bone quality included impaired structure and mechanical properties of the femoral neck and impaired resistance to fracture [9,10]. Fractures of the femoral neck account for over 50% of the hip fractures that occur in populations with elevated bone fragility (i.e., osteoporosis) [11]
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