Building on previous research and medical observations that established the negative physical health consequences of insulin resistance (IR), a team of researchers from Tübingen, Germany, embarked on a scientific journey to try to determine how brain insulin sensitivity can be restored in human subjects. Their results were published in JCI Insight.
Stephanie Kullmann, lead author of the study who works at the Institute of Diabetes Research and Metabolic Diseases (IDM) of Helmholtz Center Munich at the University of Tübingen and the Department of Diabetology and Endocrinology at Tübingen University Hospital, both in Germany, and colleagues explored the impact on insulin sensitivity, metabolism, and behavior, if any, that an intervention including exercise would have. Understanding that the adverse impact of diminished insulin sensitivity, or “insulin resistance” includes changes in body fat distribution and that it sabotages long-term weight maintenance, the team focused on exercise interventions.
“The exercise intervention increased the insulin-stimulated activity in brain regions that are responsible, among other things, for the perception of hunger and satiety and for the interaction of motivation, reward, emotion and exercise behavior,” said Dr. Kullmann. He elaborated on this, saying, “In the insulin resistant state, in rodents, altered insulin-evoked activity is present in the hypothalamus, cortex, hippocampus, amygdala, cerebellum, striatum and midbrain. Disruption of insulin receptors in the brain results in obesity-associated IR.”
The exercise intervention they implemented was an 8-week aerobic training program that was reported to boost the insulin action to that of an individual who was in a healthy weight zone. This enhanced brain insulin sensitivity was measured using functional MRI, combined with intranasal administration of insulin, before and after the intervention. The subjects included 14 women and seven men (n = 21) who ranged in age from 21 to 59 years and with BMI ranges between 27.5 to 45.5 kg/m2, which defines overweight or obese status. All participants were reported to be living a sedentary lifestyle.
The authors wrote, “Improved brain insulin action correlated with increased mitochondrial respiration in skeletal muscle, reductions in visceral fat and hunger, as well as improved cognition. Mediation analyses suggest that improved brain insulin responsiveness helps mediate the peripheral exercise effects leading to healthier body fat distribution and reduced perception of hunger.”
According to Martin Heni, last author of the study, “The study suggests that insulin resistance in the brain may be reversible and could be a viable therapeutic target to restore central nervous system regulation of metabolism and body weight and counteract adverse effects of obesity.”
The team concluded that their study “demonstrates that an 8-week exercise intervention in sedentary individuals can restore insulin action in the brain. Hence, the ameliorating benefits of exercise toward brain insulin resistance may provide an objective therapeutic target in humans in the challenge to reduce diabetes risk factors.”
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