Obesity-related changes in bone structural and material properties in hyperphagic OLETF rats and protection by voluntary wheel running

Hinton, Pamela S.; Shankar, Kartik; Eaton, Lynn M.; Rector, R. Scott

doi:10.1016/j.metabol.2015.04.004

Cited by 24 publications

(22 citation statements)

References 71 publications

(99 reference statements)

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“…Weight bearing exercise preserves bone strength (74) while improving insulin sensitivity (75,76). Exercise improved insulin sensitivity and reduced bone loss in Otsuka Long-Evans Tokushima Fatty Rats (77). Both acute bouts of exercise and long-term training improved insulin sensitivity and increased serum OC in obese men (78,79).…”

Section: Exercisementioning

confidence: 99%

Complex interplay among adiposity, insulin resistance and bone health

Tonks

Samocha-Bonet

et al. 2018

Clinical Obesity

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Obesity and osteoporosis are common public health problems. Paradoxically, while obesity is associated with higher bone density, type 2 diabetic obese individuals have an increased fracture risk. Although obesity and insulin resistance co-exist, some obese individuals remain insulin-sensitive. We suggest that the apparent paradox relating obesity, bone density and fracture risk in type 2 diabetes may be at least partly influenced by differences in bone strength and quality between insulin-resistant and insulin-sensitive obese individuals. In this review, we focus on the complex interplay between, adiposity, insulin resistance and osteoporotic fracture risk and suggest that this is an important area of study that has implications for individually tailored and targeted treatment to prevent osteoporotic fracture in obese type 2 diabetic individuals.

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Section: Exercisementioning

confidence: 99%

Complex interplay among adiposity, insulin resistance and bone health

Tonks

Samocha-Bonet

et al. 2018

Clinical Obesity

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“…We used a longitudinal, parallel study design to test the hypothesis that OLETF‐T2D rats would have reduced insulin‐stimulated bone blood flow and deteriorated trabecular microarchitecture, cortical geometry, and biomechanical properties. The hyperphagic OLETF rat progressively accumulates excess body fat, which leads to insulin resistance and eventually hyperglycemia and T2D after skeletal maturity . This accurately parallels what occurs in humans who are overweight during adolescence and develop metabolic complications in adulthood …”

Section: Methodsmentioning

confidence: 69%

“…Whole‐bone and tissue‐level biomechanical properties of the right femur were assessed using torsional loading to failure, as described . Briefly, the proximal and distal ends of the right femur were affixed in cement to a steel holder, with crossbars at each end.…”

Section: Methodsmentioning

confidence: 99%

Insulin‐Stimulated Bone Blood Flow and Bone Biomechanical Properties Are Compromised in Obese, Type 2 Diabetic OLETF Rats

et al. 2017

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Type 2 diabetes (T2D) increases skeletal fragility and fracture risk; however, the underlying mechanisms remain to be identified. Impaired bone vascular function, in particular insulin‐stimulated vasodilation and blood flow is a potential, yet unexplored mechanism. The purpose of this study was to determine the effects of T2D on femoral biomechanical properties, trabecular microarchitecture, and insulin‐stimulated bone vasodilation by comparison of hyperphagic Otsuka Long‐Evans Tokushima Fatty (OLETF) rats with normoglycemic control OLETF rats. Four‐week old, male OLETF rats were randomized to two groups: type 2 diabetes (O‐T2D) or normoglycemic control (O‐CON). O‐T2D were allowed ad libitum access to a rodent chow diet and O‐CON underwent moderate caloric restriction (30% restriction relative to intake of O‐T2D) to maintain normal body weight (BW) and glycemia until 40 weeks of age. Hyperphagic O‐T2D rats had significantly greater BW, body fat, and blood glucose than O‐CON. Total cross‐sectional area (Tt.Ar), cortical area (Ct.Ar), Ct.Ar/Tt.Ar, and polar moment of inertia of the mid‐diaphyseal femur adjusted for BW were greater in O‐T2D rats versus O‐CON. Whole‐bone biomechanical properties of the femur assessed by torsional loading to failure did not differ between O‐T2D and O‐CON, but tissue‐level strength and stiffness adjusted for BW were reduced in O‐T2D relative to O‐CON. Micro–computed tomography (μCT) of the distal epiphysis showed that O‐T2D rats had reduced percent bone volume, trabecular number, and connectivity density, and greater trabecular spacing compared with O‐CON. Basal tibial blood flow assessed by microsphere infusion was similar in O‐T2D and O‐CON, but the blood flow response to insulin stimulation in both the proximal epiphysis and diaphyseal marrow was lesser in O‐T2D compared to O‐CON. In summary, impaired insulin‐stimulated bone blood flow is associated with deleterious changes in bone trabecular microarchitecture and cortical biomechanical properties in T2D, suggesting that vascular dysfunction might play a causal role in diabetic bone fragility. © 2017 The Authors. JBMR Plus Published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.

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“…136,137 More recently, voluntary exercise has been shown to influence the bone marrow microenvironment in diet-induced obese mice, mainly by reducing fat accumulation in the bone marrow. 62 Interestingly, while exercise reduced MAT in these obese mice, it simultaneously increased bone mass.…”

Section: Combating Obesity With Mechanical Signalsmentioning

confidence: 99%

“…135 The influence of exercise on bone has been extensively shown in both rodent and human models to improve skeletal outcomes that are affected by obesity and diabetes, including BMD and structural, material, and biomechanical properties. 136,137 More recently, voluntary exercise has been shown to influence the bone marrow microenvironment in diet-induced obese mice, mainly by reducing fat accumulation in the bone marrow. 62 Interestingly, while exercise reduced MAT in these obese mice, it simultaneously increased bone mass.…”

Section: Exercise As a Treatment Modalitymentioning

confidence: 99%

Mechanical signals protect stem cell lineage selection, preserving the bone and muscle phenotypes in obesity

Frechette

Krishnamoorthy

Pamon

et al. 2017

Annals of the New York Academy of Sciences

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The incidence of obesity is rapidly rising, increasing morbidity and mortality rates worldwide. Associated comorbidities include type 2 diabetes, heart disease, fatty liver disease, and cancer. The impact of excess fat on musculoskeletal health is still unclear, although it is associated with increased fracture risk and a decline in muscular function. The complexity of obesity makes understanding the etiology of bone and muscle abnormalities difficult. Exercise is an effective and commonly prescribed non-pharmacological treatment option, but it can be difficult or unsafe for the frail, elderly, and morbidly obese. Exercise alternatives, such as low-intensity vibration (LIV), have potential for improving musculoskeletal health, particularly in conditions with excess fat. LIV has been shown to influence bone marrow mesenchymal stem cell differentiation toward higher-order tissues (i.e., bone) and away from fat. While the exact mechanisms are not fully understood, recent studies utilizing LIV both at the bench and in the clinic have demonstrated its efficacy. Here, we discuss the current literature investigating the effects of obesity on bone, muscle, and bone marrow and how exercise and LIV can be used as effective treatments for combating the negative effects in the presence of excess fat.

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Obesity-related changes in bone structural and material properties in hyperphagic OLETF rats and protection by voluntary wheel running

Cited by 24 publications

References 71 publications

Complex interplay among adiposity, insulin resistance and bone health

Complex interplay among adiposity, insulin resistance and bone health

Insulin‐Stimulated Bone Blood Flow and Bone Biomechanical Properties Are Compromised in Obese, Type 2 Diabetic OLETF Rats

Mechanical signals protect stem cell lineage selection, preserving the bone and muscle phenotypes in obesity

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