The presentation brings to light the association between diabetes and obesity with brain plasticity and the impact of nutrition when observed as per changes in the human circadian rhythm.

Obesity and diabetes have an enormous impact on the central nervous system. Both diseases can lead to structural abnormalities involving both causing a significant reduction in the gray and white matter. 

Brain plasticity can be measured using a new psychophysical technique, which is based on binocular rivalry which is a specific form of perceptual instability that occurs when two different images are simultaneously displayed to the two eyes. Obese non-diabetic individuals show a progressive reduction in brain plasticity that is inversely and significantly correlated with body mass index and insulin resistance. It is possible to restore brain plasticity in around 6 with bariatric surgery where the reduction of body weight is associated with a significant reduction of brain glucose uptake in several cortical and subcortical brain areas. This point towards a reversible brain glucose hypermetabolism that is strictly dependent on the body weight. Brain elasticity also significantly correlates with the changes of leptin and active GLP1.  With respect to the role of GLP1 in neuroplasticity, it was observed that brain plasticity was significantly increased by mixed meal ingestion while it did not significantly change during GLP1 administration.

The human body has its own internal circadian clock which has 24-hour circadian rhythms in order to adapt to our physiological behavior. A proper functioning of the circadian clock helps to maintain our metabolic health whereas some disturbances in circadian clock lead to an increased risk of metabolic diseases, such as obesity or diabetes.  The master clock, which is located in the hypothalamus and the peripheral clock, is present in all organs of our body.

Circadian rhythms are autonomous and can work without any stimuli from the environment.

Chronic nutrition is a novel scientific discipline which investigates the complex interaction between the circadian clock and metabolism and nutrition. Pre-clinical studies with respect to time restricted eating which is intermittent fasting characterized by the shortening of the eating window and prolongation of fasting time accordingly, have shown protection from obesity, glucose intolerance and other metabolic pathologies. In a study on early time restricted eating (eTRE) -8 a.m. and 4 p.m. and late term restricted eating (lTRE) -1 p.m. and 9 p.m, late term restricted eating was associated with decreased postprandial glucose and unchanged insulin levels and insulin sensitivity. Whereas in eTREgroup, insulin secretion index decreased and postprandial glucose increased. However, there was no change in mean 24-hr glucose after each intervention. Nonesterified fatty acids increased after eTRE, no change in LDL cholesterol and triglycerides, HDL increased after both interventions. eTRE and lTRE differently affect selective molecular pathway in adipose tissue.

In conclusion, metabolic disorders such as diabetes and obesity have a close neurological connection and any changes in the body’s circadian clock can have metabolic changes which can impact these two disorders. Chrononutritional strategies (e.g., TRE) are promising approaches to combat obesity and diabetes and need to be investigated in further studies.

Abstract S27 European Association for the Study of Diabetes (EASDInternational Congress 2022, 19th – 23rd Sept. 2022, Stockholm







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