Olanzapine increases AMPK-NPY orexigenic signaling by disrupting H1R-GHSR1a interaction in the hypothalamic neurons of mice.

Second generation antipsychotics, particularly olanzapine, induce severe obesity, which is associated with their antagonistic effect on the histamine H1 receptor (H1R). We have previously demonstrated that oral administration of olanzapine increases the concentration of neuropeptide Y (NPY) in the hypothalamus of rats, accompanied by hyperphagia and weight gain. However, it is unclear if the increased NPY after olanzapine administration is due to its direct effect on hypothalamic neurons and its H1R antagonistic property.

Progress in Research on Brain Development and Function of Mice During Weaning.

Lactation is a critical phase for brain function development. New dietary experiences of mouse caused by weaning can regulate brain development and function, increase their response to food and environment, and eventually give rise to corresponding behavioral changes. Changes in weaning time induce the alteration of brain tissues morphology and molecular characteristics, glial cell activity and behaviors in the offspring.

Alterations to the microbiota-colon-brain axis in high-fat-diet-induced obese mice compared to diet-resistant mice.

Obesity is underpinned by both genetic and environmental factors, including a high-saturated-fat diet. Some mice develop diet-induced obesity (DIO), but others remain diet resistant (DR) despite intake of the same high-saturated-fat diet, a phenomenon that mimics characteristics of the human obese phenotype. Microbiota-colon-brain axis regulation is important for energy metabolism and cognition.