Article Details

An Investigation About Improving Insulin Resistance Through Voluntary Physical Activity to Prevent and Control Diabetes |

Manish Mahajan, in International Journal of Information Technology and Management | IT & Management


Diabetes is related to both insulin and glucose levels inthe bloodstream. Normally, when an individual ingests carbohydrates or proteinat rest, the pancreas releases insulin, an endocrine hormone made in andreleased by the pancreatic beta cells that stimulates the uptake of circulatingglucose into muscle and fat tissues. Without adequate levels of insulin andinsulin action, blood glucose levels can rise to abnormally high levels,contributing over time to the development of health complications. Thus, theprimary goal of all diabetes management is effective control of blood glucosewithin normal or nearly normal levels. Physical inactivity and a sedentary lifestyle are riskfactors for the development of type 2 diabetes. Here, we identified the effects8 weeks of voluntary physical activity had on the prevention of insulin resistancein mouse skeletal muscles and liver (a hallmark of T2D). To do this, 8 week oldC57BL/6J mice with (RUN) and without (SED) voluntary access to running wheelswere fed a standard rodent chow ad libitum for 8 weeks. In the liver, there wasa 2.5-fold increase in insulin stimulated AktSER473 phosphorylation,and a threefold increase in insulin-stimulated (0.5 U/kg) GSKβSER9phosphorylation in RUN compared to SED mice. Although not induced in skeletalmuscles, there was a twofold increase in SOCS3 expression in SED compared toRUN mice in the liver. There was no difference in the glucose tolerance testbetween groups. This study was the first to show differences in liverinsulin sensitivity after 8 weeks of voluntary physical activity, and increasedSOCS3 expression in the liver of sedentary mice compared to active mice. Thesefindings demonstrate that even in young mice that would normally be consideredhealthy, the lack of physical activity leads to insulin resistance representingthe initial pathogenesis of impaired glucose metabolism leading to type 2diabetes.