Obesity and Diabetes Damage Bones, but Exercise May Counter Effect

Obesity and Diabetes Damage Bones, but Exercise May Counter Effect

Researchers at the University of Missouri-Columbia have linked obesity and type 2 diabetes to several health issues, including increased risk of bone fractures. In a new animal study, the MU investigators examined how development of obesity and insulin resistance contribute to bone-fracture risk and the potential role of exercise in protecting bone health.

The research team determined that while obesity and type 2 diabetes negatively affect bone health, exercise can simultaneously prevent both weight gain and diabetes and increase bone strength, and that these findings could inform interventions to improve bone health among individuals with obesity and/or type 2 diabetes.

HintonP“Researchers once thought obesity was protective of bone because with more body mass, individuals have more bone mass; more bone mass typically decreases risk of osteoporosis and associated fractures,” says Dr. Pam Hinton, an associate professor in the MU Department of Nutrition and Exercise Physiology, in a release. “What we’ve come to realize is that the bone of people with obesity and Type 2 diabetes isn’t good quality bone. These individuals have an increased risk of fractures, so that extra body weight isn’t protective.”

Dr. Hinton’s lab at MU investigates interactive effects of nutrition and physical activity on bone health, in particular, studying the effects of energy balance on bone turnover during weight loss and weight maintenance in overweight individuals. In addition, Dr. Hinton is studying the efficacy of exercise-based interventions to increase bone mineral density in osteopenic males.

Dr. Hinton and her colleagues examined how the development of obesity and type 2 diabetes affect bone structure, formation, and strength over time. Specifically, the research team studied the bones of rats that had a predisposition to overeat, causing them to gain weight and become insulin resistant. “This pattern of weight gain and insulin resistance parallels the development of obesity and Type 2 diabetes in humans,” Dr. Hinton observes.

The MU researchers’ findings were published in the journal Metabolism in a paper entitled Obesity-related changes in bone structural and material properties in hyperphagic OLETF rats and protection by voluntary wheel running (August 2015, Vol.64(8):905916, doi:10.1016/j.metabol.2015.04.004) co-authored by Dr. Hinton and her MU colleague Lynn M. Eaton.

In their 36-week study using the Otsuka Long-Evans Tokushima Fatty (OLETF) rat model of 1) sedentary, hyperphagic, male OLETF rats (OLETF-SED), 2) exercise-treated OLETF rats (OLETF-EX) and 3) sedentary non-hyperphagic controls (LETO-SED), the investigators allowed half of the rats programmed to overeat to do so and voluntarily exercise on running wheels, while the other half remained sedentary. A control group of non-overeating rats also remained sedentary. Bones from rats in the three respective groups were examined a 13, 20, and 40 weeks of age (n = 58 animals per group per timepoint) to determine how early in the development of obesity and diabetes their bones were negatively affected.

The investigators found negative skeletal effects of excessive adiposity and insulin resistance early in progressive obesity development, with lasting negative impacts on intrinsic and extrinsic bone strength. However, they observed that exercise protected against obesity-associated skeletal changes with marked benefits on the biomechanical properties of bone.

At 13 weeks, OLETF-SED rats had lower total body BMC and BMD and serum P1NP compared with LETO-SED rats. Differences in total body BMC and BMD between OLETF-SED and LETO-SED persisted at 20 weeks, with reductions in total and cortical BMD of the tibia. OLETF-SED also had lesser femur diameter, cross-sectional area, polar moment of area, and torque at fracture than LETO-SED. The researchers observed that body mass and fat as percentages were significantly greater in OLETF-SED rats versus controls. OLETF-SED rats were insulin resistant at 13 and 20 weeks, with overt diabetes by 40 weeks, and also had lesser femur diameter, cross-sectional area, polar moment of area, and torque at fracture than LETO-SED. By 40 weeks, OLETF-SED rats had elevated bone resorption and reduced intrinsic bone strength. OLETF-EX rats did not show the excessive weight gain, obesity, insulin resistance or diabetes observed in OLETF-SED, and also had greater BMD than OLETF-SED, and structural and material properties of the femur were significantly increased in OLETF-EX relative to OLETF-SED and LETO-SED.

“As the rats continued to grow, all groups increased their bone mass, but the rats that were obese and sedentary didn’t accumulate as much bone mass relative to their body weight,” Dr. Hinton says. “So, decreased bone formation, loss of bone mass and decreased bone strength all were present in the obese, diabetic, sedentary rats. However, the rats that exercised did not lose bone strength. In fact, the rats that ran on the wheels had stronger bones than the normal-weight controls.”

“This study doesn’t explain how exercise increased bone quality,” Dr. Hinton continues. “The animals in the exercise group were healthier; they didn’t develop the same insulin resistance and diabetes, which might explain why the bones of the exercising rats were healthier. Once we can identify why bones in individuals with obesity and Type 2 diabetes are weaker and how they become weaker, we can start developing more treatments through lifestyle and behavioral changes.”

The Hinton Lab’s research was supported with resources and facility use at the Harry S. Truman Memorial Veterans Hospital in Columbia, and partially supported by a VA Career Development Award (VHA-DCA2 1299-01;RSR) and by the Department of Nutrition and Exercise Physiology.

The MU Department of Nutrition and Exercise Physiology is jointly administered by the College of Agriculture, Food and Natural Resources, the College of Human Environmental Sciences and the School of Medicine, and is the only department at MU that spans three colleges.

HardinC“This unique configuration poises and challenges us to be a model of interdisciplinary research and education on campus,” says Professor and Chair Christopher Hardin, PhD, in a letter from the chair. “Our research programs are grant funded both nationally and locally and include research in human exercise physiology and metabolism, bone density and exercise, vitamin D and bone growth, lipid and carbohydrate metabolism, molecular mineral nutrition, and obesity research.”

 

Sources:
University of Missouri-Columbia
Metabolism journal

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