BRAIN INSULIN SENSITIVITY IS LINKED TO ADIPOSITY AND BODY FAT DISTRIBUTION
Brain insulin action regulates eating behaviour and energy, flexes throughout the body. However, numerous people are brain insulin resistant. How brain insulin responsiveness affects long-term weight and body fat composition in humans is still unknown. High brain insulin sensitivity before lifestyle intervention associates with a more pronounced reduction in total and visceral fat during the programmme. High brain insulin sensitivity is also associated with less regain of fat mess during a nine year follow-up.
Cross-sectional, strong insulin responsiveness of the hypothalamus associates with less visceral fat while subcutaneous fat is unrelated. Our result indicates that high brain insulin sensitivity is linked to weight loss during lifestyles intervention and associates with a favourable body fat distribution. Since visceral fat is strongly linked to diabetes, cardiovascular risk and cancer, these finding have implication beyond metabolic diseases and indicate the necessity of strategies to resolve brain insulin resistance.
There is accumulating evidence that the human brain represents an insulin sensitive organ. Initial studies in animals identified a crucial role of brain insulin in the regulation of food intake. This function holds true in humans where insulin affects important neuronal functions that underline eating behaviour. Finally, insulin delivery to the human brain modulates food intake.
Recent imaging, studies characterized a limited number of cortical and sub-cortical brain regions that respond to the peptide hormone including the hypothalamus. Insulin also impacts the functional interconnection of these areas, which underlines its importance in the control of larger networks within the brain. Of note, not every brain responds equally to insulin. A substantial number of people display an attenuated or absent insulin response, an observation often referred to as brain insulin resistance. A number of factors that associate with brain insulin resistance hove been identified so far. These range from alternations at the blood brain barrier to genetics. Among them, obesity is the best studied in animals and humans. Although, for most of these factors, including obesity, it is still unclear whether they are causes or consequences of brain insulin resistance.
Besides, controlling higher brain functions, insulin also influences outflows that modulate peripheral energy metabolism. Based on research in animals, experimental studies in humans suggested that brain insulin affects peripheral lipid metabolism in visceral adipose tissue and liver.
More importantly, insulin delivery to the brain improves whole body insulin sensitivity by suppressing endogenous glucose production and stimulating glucose uptake into peripheral tissues. Research in animals and human identified the hypothalamus as one crucial region for this process. As brain insulin resistance also impairs the central nervous control over peripheral energy metabolism, if has been hypothesized that this imperilment could result in altered substrate distribution with preferential energy accumulation in unfavorable fat depots.
Whether body fat accumulation has detrimental effects on cardiometabolic health is mainly determined by its location. This observation has led to the concept of metabolic healthy obesity with energy storage mainly in the subcutaneous compartment versus unhealthy obesity, with fat accumulation mainly in the visceral space.
Mrs. Queen Alex-Aleybe